Category Archive Healthcare

Eczema – Causes, Symptoms, Diagnosis, Treatment

Eczema is a common, chronic, non-infectious skin condition. The main symptom of this inflammatory disease is a very itchy rash. It often affects children. In many cases eczema gets better as the years go by, and it may go away for a while or disappear altogether. Acute flare-ups can really affect quality of life. The itching can be especially bad, making it difficult to concentrate and sleep well. Some people are embarrassed if their rash is visible to others. By taking good care of your skin, using medication and avoiding irritants and other things that can trigger the eczema, it is usually possible to relieve the symptoms at least enough to live a fairly normal life.

World Allergy Organization (WAO) revised nomenclature in 2003, eczema (also known as atopic dermatitis) is a chronic, relapsing, and itchy inflammatory skin condition. In the acute stage, eczematous lesions are characterised by poorly defined erythema with surface change (oedema, vesicles, and weeping). In the chronic stage, lesions are marked by skin thickening (lichenification). Although lesions can occur anywhere on the body, infants often have eczematous lesions on their cheeks and outer limbs before they develop eczema in the typical flexural areas such as behind the knees and in the folds of the elbow and neck. About 50% of people suffering from eczema also become sensitised to environmental allergens, such as house dust mite, and may then be classified as having atopic eczema under the revised WAO nomenclature.

Types of Eczema

Atopic dermatitis can be grouped into three clinical stages, although these may be difficult to reproduce in the individual patient [].

  • Atopic Dermatitis of Infancy – Infants experience eczema that is often localised to the face, scalp, and extensor aspects of the arms and legs, but it can also be widespread. The lesions are characterised by erythema, papules, vesicles, excoriations, oozing, and formation of crusts.
  • Atopic Dermatitis of Childhood – In toddlers and older children, the eczema lesions tend to shift location so that they are often confined to the flexures of the elbows and knees as well as the wrists and ankles, although it can occur at any site. In general, the eczema becomes drier and lichenified with excoriations, papules, and nodules.
  • Atopic Dermatitis of Adolescence and Adulthood – In adult patients, the lesions frequently localise to the face and neck, head-and-neck dermatitis, and a considerable portion of patients, around 30%, develop atopic hand eczema, which may interfere with workplace activities.

There are at least 11 distinct types of skin conditions that produce eczema. In order to develop a rational treatment plan, it is important to distinguish them. This is often not easy.

  • Atopic dermatitis – This health condition has a genetic basis and produces a common type of eczema. Atopic dermatitis tends to begin early in life in those with a predisposition to inhalant allergies, but it probably does not have an allergic basis. Characteristically, rashes occur on the cheeks, neck, elbow and knee creases, and ankles.
  • Irritant dermatitis – This occurs when the skin is repeatedly exposed to excessive washing or toxic substances.
  • Allergic contact dermatitis – After repeated exposures to the same substance, an allergen, the body’s immune recognition system becomes activated at the site of the next exposure and produces a dermatitis. An example of this would be poison ivy allergy.
  • Stasis dermatitis – It commonly occurs on the swollen lower legs of people who have poor circulation in the veins of the legs.
  • Fungal infections – This can produce a pattern identical to many other types of eczema, but the fungus can be visualized with a scraping under the microscope or grown in culture.
  • Scabies – It’s caused by an infestation by the human itch mite and may produce a rash very similar to other forms of eczema.
  • Pompholyx (dyshidrotic eczema) – This is a common but poorly understood health condition which classically affects the hands and occasionally the feet by producing an itchy rash composed of tiny blisters (vesicles) on the sides of the fingers or toes and palms or soles.
  • Lichen simplex chronicus – It produces thickened plaques of skin commonly found on the shins and neck.
  • Nummular eczema -his is a nonspecific term for coin-shaped plaques of scaling skin most often on the lower legs of older individuals.
  • Xerotic (dry skin) eczema – The skin will crack and ooze if dryness becomes excessive.
  • Seborrheic dermatiti – It produces a rash on the scalp, face, ears, and occasionally the mid-chest in adults. In infants, in can produce a weepy, oozy rash behind the ears and can be quite extensive, involving the entire body.

Pathophysiology

A number of molecular mechanisms and cell types are thought to be important in atopic eczema and these are reviewed in detail elsewhere.] Microscopically, the characteristic appearance of eczema is fluid between the cells in the epidermis (spongiosis). When severe, this fluid eventually disrupts the adjacent cells in the epidermis to form small collections of fluid, which are visible to the naked eye as vesicles. In the chronic phase, atopic eczema is characterised by gross thickening of the epidermis (acanthosis) and a lymphocytic infiltrate in the dermis. The pathophysiology of atopic eczema may be related to abnormal gene expression of immune cells as they infiltrate and remain in the mucosal surfaces and skin. There appears to be a failure to switch off the natural predominance of type 2 helper (Th2) lymphocytes that normally occurs in infancy, leading to an abnormal response of cytokines (chemical messengers) to a variety of stimuli. This failure to achieve the normal balance of type 1 helper (Th1) and Th2 cells may be a result of mutations in the interleukin-18 gene ]r other genes,] for example those that produce receptors for the innate immune system. Defects in the composition of the skin barrier leading to dry skin and enhanced penetration of irritants and allergens are also thought to be critical.,]

Causes of Eczema

  • Irritants – wool or synthetic clothing, soaps, detergents, perspiration, disinfectants and topical antimicrobials, and many chemical reagents
  • Contact allergens – preservatives in topical medications, perfume-based products, metals and latex
  • foods/dietary factors – cow’s milk, eggs, peanuts, tree nuts, wheat, soya, fish, shellfish and (rarely) others such as sesame, kiwi and legumes
  • Inhalant allergens (aero-allergens) – house dust mites (Dermatophagoides pteronyssinus and D. farinae), animal dander, cockroach, tree and grass pollens, and moulds
  • Microbial colonisation and/or infection – Staphylococcus aureus, streptococcus species, Candida albicansPityrosporum yeasts, herpes simplex (colonisation and infection associated with atopic eczema in children is considered separately in
  • Climate – extremes of temperature and humidity, and seasonal variation in the pattern of atopic eczema
  • Environmental factors – hard water, cooking with gas, proximity to road traffic, and environmental tobacco smoke
  • Familial factors – genetics, family size and sibling order
  • Social class (higher incidence in more affluent social classes)
  • Concurrent illness and disruption to family life – teething, psychological stress and lack of sleep.

Symptoms of Eczema

Clinical features of atopic dermatitis

Major features

  • Dry, sensitive skin
  • Red, inflamed skin
  • Very bad itching
  • Dark colored patches of skin
  • Rough, leathery or scaly patches of skin
  • Oozing or crusting
  • Areas of swelling
  • Pruritus – Facial and extensor involvement in infants and children; flexural involvement with lichenification in adults
  • Chronic or chronic, relapsing course – Personal or family history of atopy, including asthma, allergic rhinitis, atopic dermatitis
  • Xerosis – Palmar hyperlinearity, ichthyosis, keratosis pilaris
  • Immediate skin test reactivity, elevated serum IgE – Cutaneous infection, including Staphylococcus aureus and Herpes simplex virus
  • Nipple eczema – Cheilitis, Pityriasis alba
  • White dermatographism, delayed blanching
  • Perifollicular accentuation
  • Anterior subcapsular cataracts
  • Itch when sweating
  • Non-specific hand or foot dermatitis
  • Recurrent conjunctivitis
  • Dennie-Morgan folds
  • Keratoconus
  • Facial erythema or pallor

Diagnosis of Eczema

UK Working Party Diagnostic Criteria for Atopic Dermatitis

An individual must have an itchy skin condition (or parental report of scratching or rubbing) in the last 12 months, plus three or more of the following:
(i) a history of involvement of the skin creases (fronts of elbows, behind knees, fronts of ankles, around neck, or around eyes)
(ii) a personal history of asthma or hay fever (or history of atopic disease in a first-degree relative if a child is aged under 4 years)
(iii) a history of a generally dry skin in the last year
(iv) onset under the age of 2 years (not used if a child is aged under 4 years) or visible flexural dermatitis (including dermatitis affecting cheeks or forehead and outer aspects of limbs in children under 4 years)

Research criteria for assessing severity in eczema

Symptom severity scoring systems
The SCORing Atopic Dermatitis (SCORAD) index
Total score is calculated from:
Extent of affected areas: calculated as a percentage of total body area (from chart)
Intensity of a typical lesion (each scored 0 = none, 1 = mild, 2 = moderate, 3 = severe):
Erythema
Oedema/papulation
Oozing/crust
Excoriation
Lichenification
Dryness of unaffected areas
Subjective symptoms:
Pruritus (0–10 visual analogue scale)
Sleep loss (0–10 visual analogue scale)
SCORAD = extent score/5 + 7 × intensity score/2 + subjective symptoms score
Half of all people with eczema score between 28 and 54 points. For a simple guide to using SCORAD in practice, see http://adserver.sante.univ-nantes.fr/Scorad_Course/How.html (last accessed 8 March 2011)
Six Area, Six Sign Atopic Dermatitis severity index (SASSAD)
Six sites of the body are assessed for each of 6 features, each one scoring 0 to 3 for increasing severity:
Erythema
Exudation
Excoriation
Dryness
Cracking
Lichenification
The SASSAD scale correlates with global assessments of disease severity, but not with quality-of-life scores
Eczema Area and Severity Index (EASI)
Includes an assessment of the extent of disease of different anatomic sites on a Likert scale
Includes an assessment of the intensity of lesions, i.e., erythema, oedema/induration/papulation, excoriation, and lichenification, each one scoring 0 to 3 for increasing severity
Total EASI score ranges from 0 to 72 with higher scores indicating more severe eczema
Patient-oriented Eczema Measure (POEM)
Measures the frequency of occurrence of the following eczema signs and symptoms during the previous week
Dryness
Itching
Flaking
Cracking
Sleep loss
Bleeding
Weeping
POEM score ranges from 0 to 28, with higher scores indicating more severe eczema

Atopy patch test

  • Compared with the DBPCFC] test, the atopy patch test (erythema[rx]usually with infiltration) had high specificity (81–96%) for any reaction (immediate, delayed, or immediate and delayed combined) to cow’s milk, egg and soya. Specificity for any reaction to wheat was more variable (35–94%). Compared with an open food challenge, the specificity results for any reaction were more variable for cow’s milk, egg, wheat and peanut.
  • Compared with DBPCFC or an open food challenge, sensitivity results for any reaction to a single food (cow’s milk, egg, wheat, soya and peanut) were more variable. Sensitivity and specificity results compared with DBPCFC were both more variable when considered for several foods together (no data compared with an open food challenge).

Skin prick test

  • Compared with the DBPCFC test the skin prick test (wheal size 3 mm or greater) had high sensitivity (90–95%) for diagnosing an immediate response to fish and peanut, or to several foods together (results from one study); specificityresults for these foods were more variable.
  • The sensitivity and specificity for detecting any reaction (immediate, delayed, or combined and compared with DBPCFC) to all other allergens tested (cow’s milk, wheat and soya) were more wide-ranging across studies. Compared with an open food challenge, sensitivity and specificity results for any reaction (immediate, delayed, or combined) to all allergens were also more variable.

Specific IgE

  • The sensitivity of specific IgE (more than 0.35 ku/l) for detecting any reaction (immediate, delayed, or combined) to cow’s milk and egg was high (83–100%) compared with the DBPCFC test. Sensitivity for detecting an immediate reaction to wheat, soya, fish and peanut compared with DBPCFC was also high (94–97%; one study only). Sensitivity for a combined immediate and delayed reaction to wheat or soya was more variable (no data for delayed reactions).
  • Specificity results for each of the allergens alone or when considered together were more variable. Compared with an open food challenge, both sensitivity and specificity results were less consistent across all foods tested. The specific IgE level indicative of a positive test ranged from 0.35–99 ku/l in the open challenge studies.

Effect of changing test parameters

  • The available data for each type of test do not show consistency in sensitivity or specificity results. This might reflect the way the particular tests were undertaken or the criteria used to define positive test results. Several studies have considered whether changing certain parameters of a test affects their diagnostic accuracy in children with atopic eczema.,x,]
  • The accuracy of the atopy patch test varied according to the size of the chamber used for occlusion, the vehicle and concentration used to apply the allergen to the skin, and according to which skin sign was taken to indicate a positive test. [ = 3/EL = DS III]

Differential diagnosis for atopic dermatitis

  • Contact dermatitis
  • Seborrheic dermatitis
  • Drug reactions
  • Infantile psoriasis
  • Scabies
  • Nutritional deficiencies – zinc/biotin
  • Acrodermatitis enteropathica
  • Netherton syndrome
  • Icthyosis vulgaris
  • Peeling skin disorder, type B
  • Severe dermatitis, multiple allergies and metabolic wasting (SAM) syndrome
  • Primary immunodeficiency diseases* & Omenn syndrome
  • Lymphocytic-variant Hypereosinophilic syndrome (HES)
  • Cutaneous T cell lymphoma

Treatment of Eczema

Eczema is a chronic condition. Treatment cannot cure it, but regular skin care and medication can help to keep the itching and rash at bay. The main treatment options are:

  • Basic treatment –  Lipid-replenishing and moisturizing products (emollients) are generously applied to the skin at least twice a day to keep it from drying out. This can help relieve itching and protect the skin from germs and irritants.
  • Special soaps, liquid cleansers and shampoos – Normal soaps and products like shampoo or shower gel contain various substances that can dry out your skin. Special cleansing products without these substances are available to get around this problem. But basic treatment with emollients can usually compensate for the loss of moisture caused by normal soaps.
  • Steroid creams – Eczema flare-ups are usually treated with steroid creams because they can relieve the itching and inflammation. They are typically used only for acute symptoms. But they are sometimes used at regular intervals together with moisturizing skin care products (basic treatment): for example, as a “weekend treatment” where a steroid cream is applied on one or two days a week.
  • Pimecrolimus and tacrolimus –  Pimecrolimus and tacrolimus are two other medicines that can be used to treat eczema. They are not approved for use in children under the age of two years, though. These two medicines are also applied to the skin in a cream or ointment, and can be used if steroid products are not an option. This might be the case if steroid treatment is not tolerated or is ineffective. Pimecrolimus and tacrolimus may also be an option for long-term treatment of sensitive skin in the face and neck area. They can also be used on one or two days per week only, as described above.
  • Other eczema treatment options include wet wrap – radiation and medications that suppress certain immune responses. Tablets containing these medicines are used if other treatments don’t work, or if the eczema is very severe or affects large areas of skin. Because they have an effect throughout the entire body, they may have more extensive side effects than topical treatments.
  • Allergy medications (antihistamines)-are also commonly used to relieve itching. But research has now shown that they are not suitable for treating eczema, whether used as tablets or a cream.

People often try out herbal products or dietary supplements, such as evening primrose oil, borage oil, vitamin B6, vitamin E and zinc. But research hasn’t shown that these products are effective.

Dealing with dryness

  • Bath oils and products containing oatmeal are useful and prevent the drying of the skin that bathing can induce. Bath oils that contain antiseptic may have added benefit in certain cases but have a tendency to overdry and sometimes actually irritate the skin. The child should have either a bath with additive or a short shower. It is essential to find a suitable moisturiser that can be applied all over twice a day whether or not there is active eczema. Creams containing cetomacrogol, emulsifying ointment, and creams or ointments with lanolin can be used. If a product stings the skin it must be abandoned. The most likely irritant in emollient creams is the stabiliser propylene glycol. Products that contain urea almost always sting broken skin and are unsuitable in these children.

Use of wet dressings

  • Wet dressings are useful in children with severe widespread eczema.] This is essentially an inpatient procedure but can be used for short periods at home. A water based emollient is applied all over; a corticosteroid cream (rather than ointment in this case because cream is more water miscible) is applied to the areas of active eczema. The creams are covered with a double layer of wrapping, the innermost of which is wetted with tepid water. The material may be cotton sheeting covered with a crepe bandage, though an easier alternative is the use of a double layer of tubular elasticated bandage. The procedure is repeated three times a day. This treatment is usually effective in clearing the eczema in three or four days.

Avoidance of allergens

  • House dust mite is the most important allergen. Avoidance measures have to be carried out assiduously and must include encasing the mattress and pillows as well as dealing with the top covers, either by encasement or by hot (>60°C) washing.
  • If food allergy is suspected, the child should be referred to a paediatric dietician. In general, it is children with severe atopic eczema who have food allergy or food intolerance. Children with flexural eczema are unlikely to have food allergy, unless the history suggests otherwise.

Topical corticosteroids

  • It is often necessary to spend some time counselling the parents that topical steroid preparations used appropriately are safe. The strength chosen depends on the severity of the eczema and the site affected. The frequency of application depends on the individual product.

Topical antibacterials

  • Staphylococcus aureus is commonly cultured from eczematous skin, and there may be obvious signs of infection. For localised infections, fusidic acid ointment may be effective. To prevent infections it is useful to bathe the child in preparations containing triclosan or benzalkonium chloride.

 Calcineurin Inhibitors

  • Pimecrolimus cream and tacrolimus ointment—also termed topical calcineurin inhibitors—are newer formulations used both for the treatment of acute flares and for maintenance therapy of atopic dermatitis []. Pimecrolimus has the potency of a mild corticosteroid cream, whereas tacrolimus corresponds to a moderate to strong topical corticosteroid. The side effects of corticosteroids, such as thinning of the skin, are not seen with topical calcineurin inhibitors, and this allows daily treatment for longer periods. Topical calcineurin inhibitors can also be used in the proactive treatment strategy.

 Phototherapy

  • Widespread eczema benefits from treatment with UV light. Narrowband UVB light is particularly suitable for treating adults with recalcitrant eczema. Broadband UVA light and a combination of UVA light and the photosensitizing drug psoralene can also be used to treat severe recalcitrant eczema. Difficult-to-treat atopic dermatitis often clears with 1-2 months’ phototherapy three to five times a week, preferably combined with topical corticosteroids. Nevertheless, as phototherapy causes premature aging of the skin and increases the risk of skin cancer in the long run, it should be prescribed with caution.

Topical immunosuppressants

  • Tacrolimus is a potent immunosuppressive drug used in organ transplantation. A topical formulation has been shown to be effective in trials in patients with moderate to severe atopic dermatitis. Two studies specifically related to childhood eczema have confirmed its efficacy.],]The main side effect is a sensation of burning. A concern has been raised as to whether application to skin exposed to sun could increase the long term risk of skin cancer.
  • Pimecrolimus (an ascomycin derivative) is a newer immunosuppressive agent, similar to tacrolimus. Preliminary studies in children look encouraging.]

Outline of available treatments in atopic dermatitis

Topical Phototherapy and systemic therapy
Class: Corticosteroids
Examples*:
Low-potency 
• Hydrocortisone acetate 1% cream/ointment
• Desonide 0.05% cream/ointment
Mid-potency 
• Betamethasone valerate 0.05% or 0.1% cream/ointment
• Mometasone furoate 0.1% cream
• Hydrocortisone valerate 0.2% cream/ointment
High-potency 
• Fluocinonide 0.05% cream/ointment/gel
• Mometasone furoate 0.1% ointment
• Desoximetasone 0.25% cream/ointment/gel
Very-high potency
• Betamethasone dipropionate glycol 0.05% ointment
• Clobetasol propionate 0.05% cream/ointment
• Halobetasol propionate 0.05% cream/ointment
Class: Corticosteroids
Example:
Prednisone
Class: Calcineurin inhibitor
Example:
Cyclosporine A
Class: Anti-metabolites
Examples:
Methotrexate
Azathioprine
Mycophenolate mofetil
Class: Calcineurin inhibitors
Examples:
Tacrolimus 0.03% ointment
Tacrolimus 0.1% ointment
Pimecrolimus 1% cream
Phototherapy
Example:
• Narrow-band UVB (311 nm)
• Broad-band UVB
• Psoralen + UVA photochemotherapy
*For a comprehensive list of topical corticosteroids, organized by potency, available in Canada and available dosage forms, contact the Eczema Society of Canada for the “Topical Treatments in Atopic Dermatitis—Health Care Provider Resource Chart.”

First-line therapy of atopic dermatitis (AD) (based on [], [])

Education Explain/demonstrate how to apply emollients
Various topical medications should be used with intervals
In children > 12 months, use shampoos recommended in AD
When talking to the patient (guardian), make sure the recommendations are understood and followed
Revision of recommendations at least once a year
Prevention Avoid allergens and irritants:
 Tobacco smoke
 Infections
 Wool clothing
 Stress
Skin cleansing Delicate and precise, mechanical cleansing
Detergents with/without aseptic substances
Suitable galenic forms
pH in the range of 6
Fast bath ≤ 5 min, including 2-min bathing in oil at 27–30°C
Adding 1/2 cup of sodium hypochlorite to the bath eliminates itching
Bath salts – facilitate the removal of exfoliated skin, skin scales, particularly beneficial in severe impetiginization
Emollient therapy Application min. 2–3 times a day!
Glycerol is better tolerated than urea or sodium chloride
Propylene glycol can easily cause irritation in young children < 2 years of age and should not be used in these patients
In children < 2 years of age it is recommended to use emollients without protein allergens and haptens
Do not use emollients containing peanut extracts which increase the risk of sensitization and allergies!
Emollients are poorly tolerated in inflammation sites – use the appropriate doses of emollients (250–500 g/week)
Topical corticosteroids.
Mild (Class I)
  •  Hydrocortisone
Moderate (Class II)
  •  Hydrocortison-17-butyrate
  •  Clobetason-17-butyrate
Strong (Class III)
  •  Betamethason-17-valerate
  •  Fluticasone propionate
  •  Betamethasone
  •  Mometasonfuroate
  •  Desoximethasone
  •  Fluocinonide
  •  Fluocinolonacetonide
Very strong (Class IV)
  •  Clobetasol propionate
  • Cyclosporine – is a calcineurin inhibitor that controls T-cell–mediated inflammation by preventing the transcription of inflammatory cytokines.] Cyclosporine A has been found to be effective in the management of severe and refractory AD in adults and children[] However, the risk of serious adverse effects, including hypertension, renal dysfunction and an increased risk of infection, limit it to short-term use[] Cyclosporine A may interact with a number of different medications, and so care must be taken to avoid interactions.
  • Methotrexate azathioprine and mycophenolate mofetil are antimetabolite medications that work as a folate antagonist, purine analog and purine synthesis inhibitor, respectively. These medications have been shown to be variably effective in treatment-resistant AD[ As with cyclosporine, they are immunosuppressive and therefore can increase the risk of infection. They are also each associated with the potential for end-organ damage, including hepatotoxicity and cytopenias. Methotrexate should be used in conjunction with folic acid supplementation to reduce the risk of hematologic adverse events[]
  • Azathioprine – a safer drug for long term use, though it does have several side effects, including nausea, fatigue, myalgia, and liver dysfunction. It is used by paediatric dermatologists in the United Kingdom. It is essential to assay for thiopurine methyl transferase before treatment starts as children deficient in this enzyme will experience marked bone marrow suppression. In most children it is effective at low dosage. The main long term side effect that could theoretically occur (as with ciclosporin) is the development of lymphoma. The advantage of this drug is that it can be used continuously.

Other possibilities include the leukotriene inhibitors zafirlukast] and montelukast, given orally. Chinese herbal medicines have also been used successfully but are not without danger[]

Antihistamines

  • Sedating antihistamines such as alimemazine and promethazine given at bedtime are both useful. The sedation is an important feature of their antipruritic action. It is still debatable whether non-sedating antihistamines such as cetirizine and loratadine are useful because generally the role of histamine in eczema is somewhat limited. However, a large study of the use of cetirizine in adults with atopic eczema showed a significant reduction of clinical manifestations in those treated.]

Cetirizine

  • One double-blind placebo-controlled randomised trial considered the effectiveness of cetirizine in the treatment of mild to moderate pruritus in children aged 6–12 years with  ( = 22). The dosage of cetirizine given was dependent on body weight: 5 mg/kg daily was given to those weighing 30 kg or less, and 10 mg/kg daily to those over 30 kg. After 8 weeks’ treatment there were significant differences between the two groups in terms of clearance of all signs and symptoms of atopic eczema (73% cetirizine versus 18% placebo, P < 0.02), and in use of concomitant therapy (disodium cromoglicate or topical corticosteroids: 18% cetirizine versus 82% placebo, P < 0.01). Severity of pruritus and erythema was also measured in the study, but no numerical results were reported.] [ = 1+]

Chlorphenamine

  • One double-blind RCT compared the effectiveness of chlorphenamine with placebo in children aged 1–12 years who had nocturnal itching and scratching associated with  ( = 151). Treatment was given for 4 weeks. The dosage of chlorphenamine given was 1 mg once daily for children aged 1–5 years and 2 mg once daily for children aged 6–12 years. Where itching was not reduced by the initial dose, a second identical dose was permitted from 3 hours after administration of the first dose. If itching had not improved at the end of the first 2 weeks of treatment then the dosage was doubled (2 mg and 4 mg for children aged 1–5 years and 6–12 years, respectively). Use of emollients and hydrocortisone 1% was permitted during the trial.]

Hydroxyzine versus cyproheptadine

  • One double-blind  evaluated the effects of hydroxyzine and cyproheptadine on pruritus (day and night) in children aged 2–16 years (mean age approximately 8 years) with an acute exacerbation of  ( = 20).]
  • The doses taken were 1.25 mg/kg three times daily (t.d.s.) of hydroxyzine (up to 30 mg t.d.s.), and 0.25 mg/kg t.d.s. cyproheptadine (up to 6 mg t.d.s.). The doses used were higher than those generally used in UK practice. The children were also using an emollient preparation three times daily, but no other medications were permitted.

Clemastine versus ketotifen

  • A double-blind RCT compared the effectiveness of clemastine and ketotifen in children (mean age 9 years) with atopic eczema ( = 284 randomised, 255 analysed). After 4 weeks’ treatment, the proportion of children whose condition was moderately improved based on the investigator’s rating was significantly higher with ketotifen; no other differences in the other six ratings were noted. In terms of individual symptoms, improvement in itching, erythema/papule and excoriation/scratch was found in significantly more children treated with ketotifen (itching 79% versus 57%, erythema/papule 73% versus 58%, excoriation/scratch 70% versus 54%).

Loratadine versus placebo

  • A study evaluating the use of loratadine in conjunction with topical mometasone furoate 1% cream in children with  was identified ( = 50). Although the volume (and not strength) was reported in the paper, it was assumed that the only available proprietary preparation of loratadine was used (5 mg/5 ).
  • The dose given was 5 ml for children who weighed up to 30 kg, and 10 ml for those weighing more than 30 kg. After 15 days’ treatment, there were no significant differences between groups in any outcome (improvement in severity () scores, physician’s assessment of global improvement or pruritus score). Dizziness was reported by one child in each group; there were no reports of drowsiness or difficulty in awakening. [ = 2+]

Antihistamines used preventatively in children with atopic eczema

  • The Early Treatment of the Atopic Child (ETAC) study considered whether cetirizine could prevent the onset of asthma, and also provided longer term safety data for cetirizine. In this double-blind RCT, 18 months’ treatment with cetirizine was compared with placebo in children aged 12–24 months with active atopic eczema ( = 795). The dosage of cetirizine given was 0.25 mg/kg twice daily. Both groups were permitted to use topical or systemicmedication if required.
  • Pityrosporum ovale and tinea (ringworm) infections are no more common in children with  than other children[x,] [sing topical corticosteroids can alter the clinical appearance of tinea infections, allowing low-grade spread of the causal fungus.

Interferon gamma

  • One placebo-controlled double-blind RCT,] an associated long-term follow-up study and five  or case report[x] described the use of interferon gamma to treat atopic eczema]
  • The  included children and adults (age range 3–65 years), with some data reported separately for those aged 3–20 years ( = 83, 25% aged 3–20 years). [ = 1+] However, the relative proportion of people aged 3–20 years differed between groups, with six treated with interferon gamma and 15 treated with ].
  • Interferon gamma 50 /m2/day by subcutaneous injection was self-administered by patients (or carers in the case of children, presumably) for 12 weeks. At the end of treatment, the proportions reporting at least 50% improvement were significantly higher in the interferon gamma than the placebo group (45% versus 21%, P = 0.016 based on the investigator’s assessment, and 53% versus 21%, P = 0.002 based on the patient’s or carer’s assessment). In those aged 3–20 years, the patient/carer ratings were 67% versus 20% (investigator’s assessment was not reported).

Intravenous immunoglobulin

  • One narrative review described literature identified in relation to the use of intravenous (IV) immunoglobulin in children with , which consisted of three publications.] In four children, IV immunoglobulin was used to treat Kawasaki syndrome or idiopathic thrombocytopenia purpura, in which improvement (‘remission’) of their coexisting atopic eczema was noted within 7 days.
  • A case report of an 8-month-old boy treated for thrombocytopenia did not find improvement of his atopic eczema. The third publication reported improvement in ‘skin score’ and in levels of cytokines (including interleukin and interferon levels) in five children with atopic eczema who were treated with IV immunoglobulin. [ = 3]

Mycobacterium vaccae

  • One double-blind  evaluated the effects of killed Mycobacterium vaccae on  in children with moderate to severe disease ( = 166, 93% completed and analysed, aged 5–16 years).] [ = 1−] At 12 or 24 weeks following a single intradermal injection of the preparation (either 1 mg or 0.1 mg, or ), there were no significant differences between groups in any outcome (severity (SASSAD), body surface area affected, patient’s global assessment, pruritus, sleep, topical corticosteroid use, or quality of life (CDLQI)). Overall, 19% had injection-site reactions (induration and erythema), and 13% had atopic eczema that was believed to be due to the injection given (32% reported atopic eczema as an adverse effect overall).

Alclometasone dipropionate 0.05% (moderately potent) versus clobetasone butyrate 0.05% (moderately potent)

  • One double-blind  compared the  of alclometasone dipropionate 0.05% with clobetasone butyrate 0.05% ( = 43). In this small study, improvement in severity of signs and symptoms was not significantly different between groups. Investigator’s rating of the global condition was similar in both groups. Stinging was reported in two children treated with alclometasone.] [ = 1+]

Triamcinolone acetonide cream 0.1% (potent) versus hydrocortisone valerate cream 0.2% (moderately potent)

  • A within-patient (left–right) ] compared 2 weeks’ triamcinolone acetonide 0.1% treatment with hydrocortisone 0.2% ( = 66, 54 completed and analysed). Severity was reported to be improved in both groups, but data were only shown in graphs. Clearance or an ‘excellent response’ was seen in 74% in both groups. Transient stinging was reported in 3% in both groups.x [ = 1−]

Hydrocortisone butyrate 0.1% cream (potent) versus hydrocortisone 1% ointment (mild)

  • One  evaluated two hydrocortisone preparations in a left–right comparison (hydrocortisone butyrate 0.1% cream versus hydrocortisone 1% ointment,  = 40). Treatment was given for 4 weeks. Significantly greater improvements in the global severity of the condition were reported in children treated with hydrocortisone butyrate 0.1%: mean (%) reduction in global severity score after 4 weeks of 2 (73%) versus 1.6 (62%), P < 0.05. Details of any adverse effects were not reported.] [ = 1+]

Betamethasone valerate 0.1% (potent) versus hydrocortisone 1% (mild)

  • One double-blind RCT compared the effectiveness of 3 days’ treatment with betamethasone valerate 0.1% with 7 days’ treatment with hydrocortisone 1% ointment in children with mild to moderate atopic eczema ( = 207).]Treatment was used when needed during an 18 week period.
  • The population consisted predominantly of children from the community in whom atopic eczema was milder than in the 16% recruited from a hospital outpatient clinic. Several outcomes were only reported for the community subgroup

Mometasone furoate 0.1% (potent) versus various hydrocortisone preparations

  • Two RCTs compared mometasone furoate 0.1% with various hydrocortisone preparations in children with moderate to severe atopic eczema.
  • In the first study the comparator was hydrocortisone valerate 0.2% cream (moderate potency  = 219). The children had failed to respond to treatment with a hydrocortisone preparation (assumed to be a mild preparation) over the previous 7 days. It was reported that there were no significant differences between mometasone furoate 0.1% and hydrocortisone valerate 0.2% groups in global improvement (87% versus 78%, P = 0.01) after 3 weeks’ treatment. However, no baseline data were reported and thus it was not possible to determine whether groups were similar other than in the intervention being give.

Fluticasone propionate 0.05% (potent) versus hydrocortisone 1% (mild) or hydrocortisone 17-butyrate 0.1% (potent)

  • One publication reported the outcomes of two RCTs which compared fluticasone propionate 0.05% cream with hydrocortisone 1% ( = 137) or hydrocortisone 17-butyrate 0.1% (n = 128) in children experiencing a flare of .] Treatment was applied twice a day for 2–4 weeks until the atopic eczema was stabilised, followed by intermittent use as required up to twice a day, for up to 12 weeks. Emollients could be used as required.

Prebiotics in the treatment of AD

  • Prebiotics have not been extensively studied in the treatment of AD. One small RCT did find that prebiotics alone lowered the SCORAD index in children with AD []. Overall, however, minimal evidence exists to support the use of prebiotics as a stand-alone therapy.

Synbiotics (combination therapy)

  • A combination of prebiotics and probiotics, known as synbiotics, appears to hold promise in the treatment of AD. A recently published meta-analysis examined all published RCTs of synbiotics for the treatment of AD, using the SCORAD index to evaluate efficacy []. The final analysis included 6 studies with 369 children.
  • The authors concluded that the use of synbiotics for at least 8 weeks with mixed-strain bacterial species had a significant effect on improving the SCORAD index. This effect held only for children aged 1 year or older. Probiotics containing single strains of bacteria did not show a significant effect.
  • The studies included in the analysis used a variety of bacterial strains, some single-strain and some mixed-strain, at differing doses and dosing regimens. The studies also used a variety of prebiotics, such as fructo-oligosaccharides, galacto-oligosaccharides, potato starch and lactose [].
  • We don’t know whether vitamin E or multivitamins reduce symptoms in adults with eczema or whether pyridoxine, zinc supplementation, exclusion diets, or elemental diets are effective in children with eczema, as there are insufficient good-quality studies.
  • Probiotics do not seem to reduce symptoms in children with established eczema.

  • Essential fatty acids, such as evening primrose oil, blackcurrant seed oil, or fish oil, do not seem to reduce symptoms in people with eczema.

We don’t know whether control of house dust mites or maternal dietary restriction can prevent the development of eczema in children.

  • Observational data suggest that exclusive breastfeeding for at least 3 months does not reduce eczema risk and there is no evidence to suggest that exclusive breastfeeding alleviates eczema symptoms, unless a child is allergic to cow’s milk protein.

  • Introduction of probiotics in the last trimester of pregnancy and during breastfeeding may reduce the risk of eczema in the baby, although it remains unclear whether both antenatal and postnatal supplementation together yields the strongest protective effect. It is equally unclear which strains of probiotics are most effective.

Vitamin and mineral supplementation

  • Two placebo-controlled RCTs considered the effectiveness of zinc or vitamin E for .,] The trial involving zinc included children aged 1–16 years who continued with their usual treatments for atopic eczema (emollients and topical corticosteroids). Itch scores were significantly higher in children treated with zinc than with placebo, otherwise there were no significant differences in any outcome at 8 weeks (sleep disturbance, redness, surface area or combined disease severity scores, or in use of other treatments;  = 50, 84% analysed). [ = 1−]
  • The trial of vitamin E included children and adults ( = 96, aged 10–60 years).] Treatment with emollients was continued. Vitamin E or placebo was given for 8 months, after which the global assessment of the condition (classifications not defined) found worsening in 8% of the vitamin E group versus 78% in the placebo group; no change in 12% versus 11%, slight improvement in 20% versus 9%, great improvement in 46% versus 2%, and almost complete remission in 14% versus 0%. No statistical analysis of the data was presented and no adverse effects were reported.[x = 1−]

Probiotics

  • Three double-blind RCTs considered the effectiveness of a milk substitute supplemented with probiotics for the treatment of atopic eczema in infants with suspected cow’s milk allergy.[] The cow’s milk substitute in all three studies was a hydrolysed whey formula, with Lactobacillus added in the intervention group. Two studies had an additional intervention group: one received a mixture of probiotics (LactobacillusBifidobacteriumPropionibacterium) and the other received Lactobacillus rhamnosus. Control groups received the hydrolysed whey formula only. Two studies evaluated 1 month’s use. Of these, the study with three treatment arms found no significant differences between the groups treated with probiotics and the control group in changes in  severity scores ( = 252, 91% completed and analysed). [ = 1−]

 Prevention

  • Moisturise your skin as often as possible, ideally at least 2-3 times each day. The most greasy, non-perfumed moisturiser tolerated is best. This is the most important part of your skin care. Smooth it on in the direction of hair growth. Do not put your fingers back and forth into the pot of moisturiser, as it may become contaminated and be a source of infection. It is best to remove an adequate amount to cover the skin with a spoon or spatula and put this on a saucer or piece of kitchen roll.
  • Wash with a moisturiser instead of soap (known as a soap substitute), and avoid soap, bubble baths, shower gels and detergents.
  • Wear non-powdered non-rubber gloves (e.g vinyl gloves) to protect your hands and avoid contact with irritants, such as when doing housework.
  • Rinse well after swimming and apply plenty of your moisturiser after drying. Make sure that the shower at the swimming pool contains fresh water and not chlorinated water from the swimming pool.
  • Wear comfortable clothes made of materials such as cotton and avoid wearing wool next to your skin.
  • Try to resist the temptation to scratch. It may relieve your itch briefly, but it will make your skin itchier in the long term. Smooth a moisturiser onto itchy skin.
  • Avoid close contact with anyone who has an active cold sore as patients with eczema are at risk of getting a widespread cold sore infection.
  • Do not keep pets to which there is an obvious allergy.
  • Keep cool. Overheating can make eczema itch more.
  • Treat eczema early – the more severe it becomes, the more difficult it is to control.
  • Wash clothes with a non-biological washing powder and use a double rinse cycle to remove detergent residues from the clothing.

References

Eczema

 

Esophageal Candidiasis, Causes, Symptoms, Treatment

Esophageal candidiasis (EC) is one of the most common opportunistic infections in patients with impaired cellular immunity, and it is and the most common gastrointestinal (GI) opportunistic disorder among individuals infected with human immunodeficiency virus (HIV) However, we have sometimes come across EC in healthy individuals without HIV infection. When EC has been found in healthy individuals, predisposing medical conditions have often been identified. Broad-spectrum antibiotics may eliminate certain bacteria that inhibit fungal growth, thereby enhancing Candida overgrowth. Soon after the introduction of H2-receptor antagonists, some isolated cases of digestive Candida were reported.

Causes of Esophageal Candidiasis

  • Invasive candidiasis – is caused by 15 of the more than 150 known species of Candida. These species, all confirmed by isolation from patients, are: C. albicans, C. glabrataC. tropicalisC. parapsilosisC. kruseiC. guilliermondiiC. lusitaniaeC. dubliniensisC. pelliculosaC. kefyrC. lipolytica, C. famata, C. inconspicuaC. rugosa, and C. norvegensis. Over the last 20 – 30 years, C. albicans has been responsible for 95% of infections, with, C. glabrataC. parapsilosisC. tropicalis, and C. krusei causing the majority of the remaining cases.[rx]
  • Recently,C. auris, a species first reported in 2009, has been found to cause invasive candidiasis. C. auris has attracted attention because it can be resistant to the antifungal medications used to treat candidiasis.[rx]
  • Weakened immunity. Oral thrush is more likely to occur in infants and older adults due to reduced immunity. Some medical conditions and treatments can suppress your immune system, such as cancer and its treatments, organ transplantation and required drugs that suppress the immune system, and HIV/AIDS.
  • Diabetes. If you have untreated diabetes or the disease isn’t well-controlled, your saliva may contain large amounts of sugar, which encourages the growth of candida.
  • Vaginal yeast infections. Vaginal yeast infections are caused by the same fungus that causes oral thrush. You can pass the infection to your baby.
  • Medications. Drugs such as prednisone, inhaled corticosteroids, or antibiotics that disturb the natural balance of microorganisms in your body can increase your risk of oral thrush.
  • Other oral conditions. Wearing dentures, especially upper dentures, or having conditions that cause dry mouth can increase the risk of oral thrush.

Symptoms of Esophageal Candidiasis

The symptoms of esophageal thrush include

  • Some patients present with esophageal candidiasis as a first presentation of systemic candidiasis.
  • white lesions on the lining of your esophagus that may look like cottage cheese and may bleed if they’re scraped
  • People with esophageal candidiasis typically present with difficult or painful swallowing. Longstanding esophageal candidiasis can result in weight loss. There is often concomitant thrush in the mouth.
  • Pain or discomfort when swallowing
  • Dry mouth
  • Difficulty swallowing
  • Nausea
  • Vomiting
  • Weight loss
  • Chest pain
  • Creamy white patches on the inside of the cheeks and on surface of the tongue
  • White lesions on the roof of your mouth, tonsils, and gums
  • Cracking in the corner of your mouth
  • Especially red, sensitive, cracking, or itchy nipples
  • Stabbing pains felt deep within the breast
  • Significant pain when nursing or pain between nursing sessions

Diagnosis of Esophageal Candidiasis

These include

  • Endoscopic exam – In this procedure, your doctor examines your esophagus, stomach and upper part of your small intestine (duodenum) using a lighted, flexible tube with a camera on the tip (endoscope).
  • Physical exam – If needed, a physical exam and certain blood tests may be done to try to identify any possible underlying medical condition that could cause thrush in the esophagus.
  • Upper endoscopy – A test in which a long, flexible lighted tube, called an endoscope, is used to view the esophagus.
  • Biopsy – During this test, a small sample of the esophageal tissue is removed and then sent to a laboratory to be examined under a microscope.
  • Upper GI series (or barium swallow) – During this procedure, X-rays are taken of the esophagus after drinking a barium solution. Barium coats the lining of the esophagus and shows up white on an X-ray. This characteristic enables doctors to view certain abnormalities of the esophagus.

Treatment of Esophageal Candidiasis

The current first-line treatment is fluconazole, 200 mg. on the first day, followed by daily dosing of 100 mg. for at least 21 days total. Treatment should continue for 14 days after relief of symptoms. Other therapy options include:

  • Treatment of esophageal candidiasis involves the use of antifungal therapy. Unlike oropharyngeal candidiasis, esophageal candidiasis should always have therapy with systemic agents and not topical agents.
  • The most commonly used medication to treat esophageal candidiasis is oral fluconazole 200 to 400 mg per day for 14 to 21 days.
  • If patients cannot tolerate oral intake, then intravenous Fluconazole 400 mg daily can be used and then deescalated to oral Fluconazole when the patient can tolerate oral medications. Fluconazole 100 to 200 mg three times per week can be used to suppress recurrent esophageal candidiasis. Micafungin 150 mg IV daily has been shown to be non-inferior to fluconazole at 200 mg daily.
  • Itraconazole 200 mg per day orally or Voriconazole 200 mg twice daily for 14 to 21 days are other treatment options.
  • Amphotericin B deoxycholate 0.3 to 0.7 mg/kg daily can be used in patients with refractory candida esophagitis, but it has serious medication side effects and should be avoided if possible. Posaconazole 400 mg twice daily has been effective in refractory esophageal candidiasis as well. 
  • Since esophageal candidiasis is an opportunistic infection and most often seen in immunocompromised persons, the cause of the immunosuppression should be diagnosed and treated as well.
  • nystatin is not an effective treatment for esophageal candidiasis. It can be used as (swish, do not swallow) treatment for oral candidiasis that occurs with the use of asthma pumps.
  • other oral triazoles, such as itraconazole
  • caspofungin, used in refractory or systemic cases
  • amphotericin, used in refractory or systemic cases

Antifungals for oropharyngeal candidiasis

Antifungal agent Form Strength Usage Cost
Topical
Nystatin Pastille 200 000 units 1–2 pastilles, 4 times daily +
Suspension 5 mL swish-and-Swallow, 4 times daily +
+
Clotrimazole Oral troche 10 mg troche Dissolve 1 troche, 5 times daily +
Amphotericin B Suspension 1 mg/mL 1 mL swish-and-swallow, 4 times daily +
Lozenge 100 mg Four times daily +
Tablet 10 mg Four times daily +
Miconazole (Lauriad®) Lauriad 10 mg Apply to gum once daily TBD
Systemic
Ketoconazole Tablet 200 mg 1–2 tablets, once to twice daily +
Fluconazole Tablet 100 mg 1 tablet daily ++
Solution 10 mg/mL 10 mL, once daily ++
Itraconazole Capsule 100 mg 2 capsules, once daily ++
Solution 10 mg/mL 10–20 mL, once daily ++
Posaconazole Suspension 100 mg/2.5 mL 2 tsp daily +++
*Notes: Oral therapy preferred when tolerated. Cost index: (+) inexpensive; (++) modest expense; (+++) expensive; TBD = to be determined.

Antifungals for esophageal candidiasis

Antifungal agent Form Strength Usage
Azoles
Ketoconazole Tablets 200 mg 1–2 tablets, once to twice daily
Fluconazole Tablet 100 mg 1 tablet daily
SolutionIV piggyback 10 mg/mL 10 mL, once daily
100 mg, once daily
Itraconazole Capsule 100 mg 2 capsules, once daily
Solution 10 mg/mL 20 mL, once daily
Posaconazole Suspension 100 mg/2.5 mL 4 tsp, twice daily
Voriconazole Tablet/IV piggyback 200 mg Once daily
Caspofungin Intravenous 50 mg Once daily
Micafungin Intravenous 150 mg Once daily
Anidulafungin Intravenous 50 mg Once daily
Amphotericin B Intravenous 0.3–0.7 mg/kg Once daily

Treatment for Recommendations

  • An echinocandin (caspofungin: loading dose 70 mg, then 50 mg daily; micafungin: 100 mg daily; anidulafungin: loading dose 200 mg, then 100 mg daily) is recommended as initial therapy (strong recommendation; high-quality evidence).
  • Fluconazole, intravenous or oral, 800-mg (12 mg/kg) loading dose, then 400 mg (6 mg/kg) daily is an acceptable alternative to an echinocandin as initial therapy in selected patients, including those who are not critically ill and who are considered unlikely to have a fluconazole-resistant Candida species (strong recommendation; high-quality evidence).
  • Testing for azole susceptibility is recommended for all bloodstream and other clinically relevant Candida isolates. Testing for echinocandin susceptibility should be considered in patients who have had prior treatment with an echinocandin and among those who have infection with C. glabrata or C. parapsilosis (strong recommendation; low-quality evidence).
  • Transition from an echinocandin to fluconazole (usually within 5–7 days) is recommended for patients who are clinically stable, have isolates that are susceptible to fluconazole (eg, C. albicans), and have negative repeat blood cultures following initiation of antifungal therapy (strong recommendation; moderate-quality evidence).
  • For infection due to C. glabrata, transition to higher-dose fluconazole 800 mg (12 mg/kg) daily or voriconazole 200–300 (3–4 mg/kg) twice daily should only be considered among patients with fluconazole-susceptible or voriconazole-susceptible isolates (strong recommendation; low-quality evidence).
  • Lipid formulation amphotericin B (AmB) (3–5 mg/kg daily) is a reasonable alternative if there is intolerance, limited availability, or resistance to other antifungal agents (strong recommendation; high-quality evidence).
  • Transition from AmB to fluconazole is recommended after 5–7 days among patients who have isolates that are susceptible to fluconazole, who are clinically stable, and in whom repeat cultures on antifungal therapy are negative (strong recommendation; high-quality evidence).
  • Among patients with suspected azole- and echinocandin-resistant Candidainfections, lipid formulation AmB (3–5 mg/kg daily) is recommended (strong recommendation; low-quality evidence).
  • Voriconazole 400 mg (6 mg/kg) twice daily for 2 doses, then 200 mg (3 mg/kg) twice daily is effective for candidemia, but offers little advantage over fluconazole as initial therapy (strong recommendation; moderate-quality evidence).Voriconazole is recommended as step-down oral therapy for selected cases of candidemia due to C. krusei (strong recommendation; low-quality evidence).
  • All nonneutropenic patients with candidemia should have a dilated ophthalmological examination, preferably performed by an ophthalmologist, within the first week after diagnosis (strong recommendation; low-quality evidence).
  • Follow-up blood cultures should be performed every day or every other day to establish the time point at which candidemia has been cleared (strong recommendation; low-quality evidence).
  • Recommended duration of therapy for candidemia without obvious metastatic complications is for 2 weeks after documented clearance of Candida species from the bloodstream and resolution of symptoms attributable to candidemia (strong recommendation; moderate-quality evidence).

II. Should Central Venous Catheters Be Removed in Nonneutropenic Patients With Candidemia?

Recommendation

  • Central venous catheters (CVCs) should be removed as early as possible in the course of candidemia when the source is presumed to be the CVC and the catheter can be removed safely; this decision should be individualized for each patient (strong recommendation; moderate-quality evidence).

III. What Is the Treatment for Candidemia in Neutropenic Patients?

Recommendations

  • An echinocandin (caspofungin: loading dose 70 mg, then 50 mg daily; micafungin: 100 mg daily; anidulafungin: loading dose 200 mg, then 100 mg daily) is recommended as initial therapy (strong recommendation; moderate-quality evidence).
  • Lipid formulation AmB, 3–5 mg/kg daily, is an effective but less attractive alternative because of the potential for toxicity (strong recommendation; moderate-quality evidence).
  • Fluconazole, 800-mg (12 mg/kg) loading dose, then 400 mg (6 mg/kg) daily, is an alternative for patients who are not critically ill and have had no prior azole exposure (weak recommendation; low-quality evidence).
  • Fluconazole, 400 mg (6 mg/kg) daily, can be used for step-down therapy during persistent neutropenia in clinically stable patients who have susceptible isolates and documented bloodstream clearance (weak recommendation; low-quality evidence).
  • Voriconazole, 400 mg (6 mg/kg) twice daily for 2 doses, then 200–300 mg (3–4 mg/kg) twice daily, can be used in situations in which additional mold coverage is desired (weak recommendation; low-quality evidence). Voriconazole can also be used as step-down therapy during neutropenia in clinically stable patients who have had documented bloodstream clearance and isolates that are susceptible to voriconazole (weak recommendation; low-quality evidence).
  • For infections due to C. krusei, an echinocandin, lipid formulation AmB, or voriconazole is recommended (strong recommendation; low-quality evidence).
  • Recommended minimum duration of therapy for candidemia without metastatic complications is 2 weeks after documented clearance of Candida from the bloodstream, provided neutropenia and symptoms attributable to candidemia have resolved (strong recommendation; low-quality evidence).
  • Ophthalmological findings of choroidal and vitreal infection are minimal until recovery from neutropenia; therefore, dilated funduscopic examinations should be performed within the first week after recovery from neutropenia (strong recommendation; low-quality evidence).
  • In the neutropenic patient, sources of candidiasis other than a CVC (eg, gastrointestinal tract) predominate. Catheter removal should be considered on an individual basis (strong recommendation; low-quality evidence).
  • Granulocyte colony – stimulating factor (G-CSF)–mobilized granulocyte transfusions can be considered in cases of persistent candidemia with anticipated protracted neutropenia (weak recommendation; low-quality evidence).

IV. What Is the Treatment for Chronic Disseminated (Hepatosplenic) Candidiasis?

Recommendations

  • Initial therapy with lipid formulation AmB, 3–5 mg/kg daily OR an echinocandin (micafungin: 100 mg daily; caspofungin: 70-mg loading dose, then 50 mg daily; or anidulafungin: 200-mg loading dose, then 100 mg daily), for several weeks is recommended, followed by oral fluconazole, 400 mg (6 mg/kg) daily, for patients who are unlikely to have a fluconazole-resistant isolate (strong recommendation; low-quality evidence).
  • Therapy should continue until lesions resolve on repeat imaging, which is usually several months. Premature discontinuation of antifungal therapy can lead to relapse (strong recommendation; low-quality evidence).
  • If chemotherapy or hematopoietic cell transplantation is required, it should not be delayed because of the presence of chronic disseminated candidiasis, and antifungal therapy should be continued throughout the period of high risk to prevent relapse (strong recommendation; low-quality evidence).
  • For patients who have debilitating persistent fevers, short-term (1–2 weeks) treatment with nonsteroidal anti-inflammatory drugs or corticosteroids can be considered (weak recommendation; low-quality evidence).

V. What Is the Role of Empiric Treatment for Suspected Invasive Candidiasis in Nonneutropenic Patients in the Intensive Care Unit?

Recommendations

  • Empiric antifungal therapy should be considered in critically ill patients with risk factors for invasive candidiasis and no other known cause of fever and should be based on clinical assessment of risk factors, surrogate markers for invasive candidiasis, and/or culture data from nonsterile sites (strong recommendation; moderate-quality evidence). Empiric antifungal therapy should be started as soon as possible in patients who have the above risk factors and who have clinical signs of septic shock (strong recommendation; moderate-quality evidence).
  • Preferred empiric therapy for suspected candidiasis in nonneutropenic patients in the intensive care unit (ICU) is an echinocandin (caspofungin: loading dose of 70 mg, then 50 mg daily; micafungin: 100 mg daily; anidulafungin: loading dose of 200 mg, then 100 mg daily) (strong recommendation; moderate-quality evidence).
  • Fluconazole, 800-mg (12 mg/kg) loading dose, then 400 mg (6 mg/kg) daily, is an acceptable alternative for patients who have had no recent azole exposure and are not colonized with azole-resistant Candida species (strong recommendation; moderate-quality evidence).
  • Lipid formulation AmB, 3–5 mg/kg daily, is an alternative if there is intolerance to other antifungal agents (strong recommendation; low-quality evidence).
  • Recommended duration of empiric therapy for suspected invasive candidiasis in those patients who improve is 2 weeks, the same as for treatment of documented candidemia (weak recommendation; low-quality evidence).
  • For patients who have no clinical response to empiric antifungal therapy at 4–5 days and who do not have subsequent evidence of invasive candidiasis after the start of empiric therapy or have a negative non-culture-based diagnostic assay with a high negative predictive value, consideration should be given to stopping antifungal therapy (strong recommendation; low-quality evidence).

VI. Should Prophylaxis Be Used to Prevent Invasive Candidiasis in the Intensive Care Unit Setting?

Recommendations

  • Fluconazole, 800-mg (12 mg/kg) loading dose, then 400 mg (6 mg/kg) daily, could be used in high-risk patients in adult ICUs with a high rate (>5%) of invasive candidiasis (weak recommendation; moderate-quality evidence).
  • An alternative is to give an echinocandin (caspofungin: 70-mg loading dose, then 50 mg daily; anidulafungin: 200-mg loading dose and then 100 mg daily; or micafungin: 100 mg daily) (weak recommendation; low-quality evidence).
  • Daily bathing of ICU patients with chlorhexidine, which has been shown to decrease the incidence of bloodstream infections including candidemia, could be considered (weak recommendation; moderate-quality evidence).

VII. What Is the Treatment for Neonatal Candidiasis, Including Central Nervous System Infection?

What Is the Treatment for Invasive Candidiasis and Candidemia?

Recommendations

  • AmB deoxycholate, 1 mg/kg daily, is recommended for neonates with disseminated candidiasis (strong recommendation; moderate-quality evidence).
  • Fluconazole, 12 mg/kg intravenous or oral daily, is a reasonable alternative in patients who have not been on fluconazole prophylaxis (strong recommendation; moderate-quality evidence).
  • Lipid formulation AmB, 3–5 mg/kg daily, is an alternative, but should be used with caution, particularly in the presence of urinary tract involvement (weak recommendation; low-quality evidence).
  • Echinocandins should be used with caution and generally limited to salvage therapy or to situations in which resistance or toxicity preclude the use of AmB deoxycholate or fluconazole (weak recommendation; low-quality evidence).
  • A lumbar puncture and a dilated retinal examination are recommended in neonates with cultures positive for Candida species from blood and/or urine (strong recommendation; low-quality evidence).
  • Computed tomographic or ultrasound imaging of the genitourinary tract, liver, and spleen should be performed if blood cultures are persistently positive for Candida species (strong recommendation; low-quality evidence).
  • CVC removal is strongly recommended (strong recommendation; moderate-quality evidence).
  • The recommended duration of therapy for candidemia without obvious metastatic complications is for 2 weeks after documented clearance of Candidaspecies from the bloodstream and resolution of signs attributable to candidemia (strong recommendation; low-quality evidence).

What Is the Treatment for Central Nervous System Infections in Neonates?

Recommendations

  • For initial treatment, AmB deoxycholate, 1 mg/kg intravenous daily, is recommended (strong recommendation; low-quality evidence).
  • An alternative regimen is liposomal AmB, 5 mg/kg daily (strong recommendation; low-quality evidence).
  • The addition of flucytosine, 25 mg/kg 4 times daily, may be considered as salvage therapy in patients who have not had a clinical response to initial AmB therapy, but adverse effects are frequent (weak recommendation; low-quality evidence).
  • For step-down treatment after the patient has responded to initial treatment, fluconazole, 12 mg/kg daily, is recommended for isolates that are susceptible to fluconazole (strong recommendation; low-quality evidence).
  • Therapy should continue until all signs, symptoms, and cerebrospinal fluid (CSF) and radiological abnormalities, if present, have resolved (strong recommendation; low-quality evidence).
  • Infected central nervous system (CNS) devices, including ventriculostomy drains and shunts, should be removed if at all possible (strong recommendation; low-quality evidence).

What Are the Recommendations for Prophylaxis in the Neonatal Intensive Care Unit Setting?

Recommendations

  • In nurseries with high rates (>10%) of invasive candidiasis, intravenous or oral fluconazole prophylaxis, 3–6 mg/kg twice weekly for 6 weeks, in neonates with birth weights <1000 g is recommended (strong recommendation; high-quality evidence)
  • Oral nystatin, 100 000 units 3 times daily for 6 weeks, is an alternative to fluconazole in neonates with birth weights <1500 g in situations in which availability or resistance preclude the use of fluconazole (weak recommendation; moderate-quality evidence).
  • Oral bovine lactoferrin (100 mg/day) may be effective in neonates <1500 g but is not currently available in US hospitals (weak recommendation; moderate-quality evidence).

VIII. What Is the Treatment for Intra-abdominal Candidiasis?

Recommendations

  • Empiric antifungal therapy should be considered for patients with clinical evidence of intra-abdominal infection and significant risk factors for candidiasis, including recent abdominal surgery, anastomotic leaks, or necrotizing pancreatitis (strong recommendation; moderate-quality evidence).
  • Treatment of intra-abdominal candidiasis should include source control, with appropriate drainage and/or debridement (strong recommendation; moderate-quality evidence).
  • The choice of antifungal therapy is the same as for the treatment of candidemia or empiric therapy for nonneutropenic patients in the ICU (See sections I and V) (strong recommendation; moderate-quality evidence).
  • The duration of therapy should be determined by adequacy of source control and clinical response (strong recommendation; low-quality evidence).

IX. Does the Isolation of Candida Species From the Respiratory Tract Require Antifungal Therapy?

Recommendation

  • Growth of Candida from respiratory secretions usually indicates colonization and rarely requires treatment with antifungal therapy (strong recommendation; moderate-quality evidence).

X. What Is the Treatment for Candida Intravascular Infections, Including Endocarditis and Infections of Implantable Cardiac Devices?

What Is the Treatment for Candida Endocarditis?

Recommendations

  • For native valve endocarditis, lipid formulation AmB, 3–5 mg/kg daily, with or without flucytosine, 25 mg/kg 4 times daily, OR high-dose echinocandin (caspofungin 150 mg daily, micafungin 150 mg daily, or anidulafungin 200 mg daily) is recommended for initial therapy (strong recommendation; low-quality evidence).
  • Step-down therapy to fluconazole, 400–800 mg (6–12 mg/kg) daily, is recommended for patients who have susceptible Candida isolates, have demonstrated clinical stability, and have cleared Candida from the bloodstream (strong recommendation; low-quality evidence).
  • Oral voriconazole, 200–300 mg (3–4 mg/kg) twice daily, or posaconazole tablets, 300 mg daily, can be used as step-down therapy for isolates that are susceptible to those agents but not susceptible to fluconazole (weak recommendation; very low-quality evidence).
  • Valve replacement is recommended; treatment should continue for at least 6 weeks after surgery and for a longer duration in patients with perivalvular abscesses and other complications (strong recommendation; low-quality evidence).
  • For patients who cannot undergo valve replacement, long-term suppression with fluconazole, 400–800 mg (6–12 mg/kg) daily, if the isolate is susceptible, is recommended (strong recommendation; low-quality evidence).
  • For prosthetic valve endocarditis, the same antifungal regimens suggested for native valve endocarditis are recommended (strong recommendation; low-quality evidence). Chronic suppressive antifungal therapy with fluconazole, 400–800 mg (6–12 mg/kg) daily, is recommended to prevent recurrence (strong recommendation; low-quality evidence).

What Is the Treatment for Candida Infection of Implantable Cardiac Devices?

Recommendations

  • For pacemaker and implantable cardiac defibrillator infections, the entire device should be removed (strong recommendation; moderate-quality evidence).
  •  Antifungal therapy is the same as that recommended for native valve endocarditis (strong recommendation; low-quality evidence).
  • For infections limited to generator pockets, 4 weeks of antifungal therapy after removal of the device is recommended (strong recommendation; low-quality evidence).
  • For infections involving the wires, at least 6 weeks of antifungal therapy after wire removal is recommended (strong recommendation; low-quality evidence).
  • For ventricular assist devices that cannot be removed, the antifungal regimen is the same as that recommended for native valve endocarditis (strong recommendation; low-quality evidence). Chronic suppressive therapy with fluconazole if the isolate is susceptible, for as long as the device remains in place is recommended (strong recommendation; low-quality evidence).

What Is the Treatment for Candida Suppurative Thrombophlebitis?

Recommendations

  • Catheter removal and incision and drainage or resection of the vein, if feasible, is recommended (strong recommendation; low-quality evidence).
  • Lipid formulation AmB, 3–5 mg/kg daily, OR fluconazole, 400–800 mg (6–12 mg/kg) daily, OR an echinocandin (caspofungin 150 mg daily, micafungin 150 mg daily, or anidulafungin 200 mg daily) for at least 2 weeks after candidemia (if present) has cleared is recommended (strong recommendation; low-quality evidence).
  • Step-down therapy to fluconazole, 400–800 mg (6–12 mg/kg) daily, should be considered for patients who have initially responded to AmB or an echinocandin, are clinically stable, and have a fluconazole-susceptible isolate (strong recommendation; low-quality evidence).
  • Resolution of the thrombus can be used as evidence to discontinue antifungal therapy if clinical and culture data are supportive (strong recommendation; low-quality evidence).

XI. What Is the Treatment for Candida Osteoarticular Infections?

What Is the Treatment for Candida Osteomyelitis?

Recommendations

  • Fluconazole, 400 mg (6 mg/kg) daily, for 6–12 months OR an echinocandin (caspofungin 50–70 mg daily, micafungin 100 mg daily, or anidulafungin 100 mg daily) for at least 2 weeks followed by fluconazole, 400 mg (6 mg/kg) daily, for 6–12 months is recommended (strong recommendation; low-quality evidence).
  • Lipid formulation AmB, 3–5 mg/kg daily, for at least 2 weeks followed by fluconazole, 400 mg (6 mg/kg) daily, for 6–12 months is a less attractive alternative (weak recommendation; low-quality evidence).
  • Surgical debridement is recommended in selected cases (strong recommendation; low-quality evidence).

What Is the Treatment for Candida Septic Arthritis?

  • Fluconazole, 400 mg (6 mg/kg) daily, for 6 weeks OR an echinocandin (caspofungin 50–70 mg daily, micafungin 100 mg daily, or anidulafungin 100 mg daily) for 2 weeks followed by fluconazole, 400 mg (6 mg/kg) daily, for at least 4 weeks is recommended (strong recommendation; low-quality evidence)
  • Lipid formulation AmB, 3–5 mg/kg daily, for 2 weeks, followed by fluconazole, 400 mg (6 mg/kg) daily, for at least 4 weeks is a less attractive alternative (weak recommendation; low-quality evidence).
  • Surgical drainage is indicated in all cases of septic arthritis (strong recommendation; moderate-quality evidence).
  • For septic arthritis involving a prosthetic device, device removal is recommended (strong recommendation; moderate-quality evidence).
  • If the prosthetic device cannot be removed, chronic suppression with fluconazole, 400 mg (6 mg/kg) daily, if the isolate is susceptible, is recommended (strong recommendation; low-quality evidence).

XII. What Is the Treatment for Candida Endophthalmitis?

What Is the General Approach to Candida Endophthalmitis?

Recommendations

  • All patients with candidemia should have a dilated retinal examination, preferably performed by an ophthalmologist, within the first week of therapy in nonneutropenic patients to establish if endophthalmitis is present (strong recommendation; low-quality evidence). For neutropenic patients, it is recommended to delay the examination until neutrophil recovery (strong recommendation; low-quality evidence).
  • The extent of ocular infection (chorioretinitis with or without macular involvement and with or without vitritis) should be determined by an ophthalmologist (strong recommendation; low-quality evidence).
  • Decisions regarding antifungal treatment and surgical intervention should be made jointly by an ophthalmologist and an infectious diseases physician (strong recommendation; low-quality evidence).

What Is the Treatment for Candida Chorioretinitis Without Vitritis?

Recommendations

  • For fluconazole-/voriconazole-susceptible isolates, fluconazole, loading dose, 800 mg (12 mg/kg), then 400–800 mg (6–12 mg/kg) daily OR voriconazole, loading dose 400 mg (6 mg/kg) intravenous twice daily for 2 doses, then 300 mg (4 mg/kg) intravenous or oral twice daily is recommended (strong recommendation; low-quality evidence).
  • For fluconazole-/voriconazole-resistant isolates, liposomal AmB, 3–5 mg/kg intravenous daily, with or without oral flucytosine, 25 mg/kg 4 times daily is recommended (strong recommendation; low-quality evidence).
  • With macular involvement, antifungal agents as noted above PLUS intravitreal injection of either AmB deoxycholate, 5–10 µg/0.1 mL sterile water, or voriconazole, 100 µg/0.1 mL sterile water or normal saline, to ensure a prompt high level of antifungal activity is recommended (strong recommendation; low-quality evidence).
  • The duration of treatment should be at least 4–6 weeks, with the final duration depending on resolution of the lesions as determined by repeated ophthalmological examinations (strong recommendation; low-quality evidence).

What Is the Treatment for Candida Chorioretinitis With Vitritis?

Recommendations

  • Antifungal therapy as detailed above for chorioretinitis without vitritis, PLUS intravitreal injection of either amphotericin B deoxycholate, 5–10 µg/0.1 mL sterile water, or voriconazole, 100 µg/0.1 mL sterile water or normal saline is recommended (strong recommendation; low-quality evidence).
  • Vitrectomy should be considered to decrease the burden of organisms and to allow the removal of fungal abscesses that are inaccessible to systemic antifungal agents (strong recommendation; low-quality evidence).
  • The duration of treatment should be at least 4–6 weeks, with the final duration dependent on resolution of the lesions as determined by repeated ophthalmological examinations (strong recommendation; low-quality evidence).

XIII. What Is the Treatment for Central Nervous System Candidiasis?

Recommendations

  • For initial treatment, liposomal AmB, 5 mg/kg daily, with or without oral flucytosine, 25 mg/kg 4 times daily is recommended (strong recommendation; low-quality evidence).
  • For step-down therapy after the patient has responded to initial treatment, fluconazole, 400–800 mg (6–12 mg/kg) daily, is recommended (strong recommendation; low-quality evidence).
  • Therapy should continue until all signs and symptoms and CSF and radiological abnormalities have resolved (strong recommendation; low-quality evidence).
  • Infected CNS devices, including ventriculostomy drains, shunts, stimulators, prosthetic reconstructive devices, and biopolymer wafers that deliver chemotherapy should be removed if possible (strong recommendation; low-quality evidence).
  • For patients in whom a ventricular device cannot be removed, AmB deoxycholate could be administered through the device into the ventricle at a dosage ranging from 0.01 mg to 0.5 mg in 2 mL 5% dextrose in water (weak recommendation; low-quality evidence).

XIV. What Is the Treatment for Urinary Tract Infections Due to Candida Species?

What Is the Treatment for Asymptomatic Candiduria?

Recommendations

  • Elimination of predisposing factors, such as indwelling bladder catheters, is recommended whenever feasible (strong recommendation; low-quality evidence).
  • Treatment with antifungal agents is NOT recommended unless the patient belongs to a group at high risk for dissemination; high-risk patients include neutropenic patients, very low-birth-weight infants (<1500 g), and patients who will undergo urologic manipulation (strong recommendation; low-quality evidence).
  • Neutropenic patients and very low–birth-weight infants should be treated as recommended for candidemia (see sections III and VII) (strong recommendation; low-quality evidence).
  • Patients undergoing urologic procedures should be treated with oral fluconazole, 400 mg (6 mg/kg) daily, OR AmB deoxycholate, 0.3–0.6 mg/kg daily, for several days before and after the procedure (strong recommendation; low-quality evidence).

What Is the Treatment for Symptomatic Candida Cystitis?

Recommendations

  • For fluconazole-susceptible organisms, oral fluconazole, 200 mg (3 mg/kg) daily for 2 weeks is recommended (strong recommendation; moderate-quality evidence).
  • For fluconazole-resistant C. glabrata, AmB deoxycholate, 0.3–0.6 mg/kg daily for 1–7 days OR oral flucytosine, 25 mg/kg 4 times daily for 7–10 days is recommended (strong recommendation; low-quality evidence).
  • For C. krusei, AmB deoxycholate, 0.3–0.6 mg/kg daily, for 1–7 days is recommended (strong recommendation; low-quality evidence).
  • Removal of an indwelling bladder catheter, if feasible, is strongly recommended (strong recommendation; low-quality evidence).
  • AmB deoxycholate bladder irrigation, 50 mg/L sterile water daily for 5 days, may be useful for treatment of cystitis due to fluconazole-resistant species, such as C. glabrata and C. krusei (weak recommendation; low-quality evidence).

What Is the Treatment for Symptomatic Ascending Candida Pyelonephritis?

Recommendations

  • For fluconazole-susceptible organisms, oral fluconazole, 200–400 mg (3–6 mg/kg) daily for 2 weeks is recommended (strong recommendation; low-quality evidence).
  • For fluconazole-resistant C. glabrata, AmB deoxycholate, 0.3–0.6 mg/kg daily for 1–7 days with or without oral flucytosine, 25 mg/kg 4 times daily, is recommended (strong recommendation; low-quality evidence).
  • For fluconazole-resistant C. glabrata, monotherapy with oral flucytosine, 25 mg/kg 4 times daily for 2 weeks, could be considered (weak recommendation; low-quality evidence)
  • For C. krusei, AmB deoxycholate, 0.3–0.6 mg/kg daily, for 1–7 days is recommended (strong recommendation; low-quality evidence).
  • Elimination of urinary tract obstruction is strongly recommended (strong recommendation; low-quality evidence).
  • For patients who have nephrostomy tubes or stents in place, consider removal or replacement, if feasible (weak recommendation; low-quality evidence).

What Is the Treatment for Candida Urinary Tract Infection Associated With Fungus Balls?

Recommendations

  • Surgical intervention is strongly recommended in adults (strong recommendation; low-quality evidence).
  • Antifungal treatment as noted above for cystitis or pyelonephritis is recommended (strong recommendation; low-quality evidence).
  • Irrigation through nephrostomy tubes, if present, with AmB deoxycholate, 25–50 mg in 200–500 mL sterile water, is recommended (strong recommendation; low-quality evidence).

XV. What Is the Treatment for Vulvovaginal Candidiasis?

Recommendations

  • For the treatment of uncomplicated Candida vulvovaginitis, topical antifungal agents, with no one agent superior to another, are recommended (strong recommendation; high-quality evidence).
  • Alternatively, for the treatment of uncomplicated Candida vulvovaginitis, a single 150-mg oral dose of fluconazole is recommended (strong recommendation; high-quality evidence).
  • For severe acute Candida vulvovaginitis, fluconazole, 150 mg, given every 72 hours for a total of 2 or 3 doses, is recommended (strong recommendation; high-quality evidence).
  • For C. glabrata vulvovaginitis that is unresponsive to oral azoles, topical intravaginal boric acid, administered in a gelatin capsule, 600 mg daily, for 14 days is an alternative (strong recommendation; low-quality evidence).
  • Another alternative agent for C. glabrata infection is nystatin intravaginal suppositories, 100 000 units daily for 14 days (strong recommendation; low-quality evidence).
  • A third option for C. glabrata infection is topical 17% flucytosine cream alone or in combination with 3% AmB cream administered daily for 14 days (weak recommendation; low-quality evidence).
  • For recurring vulvovaginal candidiasis, 10–14 days of induction therapy with a topical agent or oral fluconazole, followed by fluconazole, 150 mg weekly for 6 months, is recommended (strong recommendation; high-quality evidence).

XVI. What Is the Treatment for Oropharyngeal Candidiasis?

Recommendations

  • For mild disease, clotrimazole troches, 10 mg 5 times daily, OR miconazole mucoadhesive buccal 50-mg tablet applied to the mucosal surface over the canine fossa once daily for 7–14 days are recommended (strong recommendation; high-quality evidence).
  • Alternatives for mild disease include nystatin suspension (100 000 U/mL) 4–6 mL 4 times daily, OR 1–2 nystatin pastilles (200 000 U each) 4 times daily, for 7–14 days (strong recommendation; moderate-quality evidence).
  • For moderate to severe disease, oral fluconazole, 100–200 mg daily, for 7–14 days is recommended (strong recommendation; high-quality evidence).
  • For fluconazole-refractory disease, itraconazole solution, 200 mg once daily OR posaconazole suspension, 400 mg twice daily for 3 days then 400 mg daily, for up to 28 days are recommended (strong recommendation; moderate-quality evidence).
  • Alternatives for fluconazole-refractory disease include voriconazole, 200 mg twice daily, OR AmB deoxycholate oral suspension, 100 mg/mL 4 times daily (strong recommendation; moderate-quality evidence).
  • Intravenous echinocandin (caspofungin: 70-mg loading dose, then 50 mg daily; micafungin: 100 mg daily; or anidulafungin: 200-mg loading dose, then 100 mg daily) OR intravenous AmB deoxycholate, 0.3 mg/kg daily, are other alternatives for refractory disease (weak recommendation; moderate-quality evidence).
  • Chronic suppressive therapy is usually unnecessary. If required for patients who have recurrent infection, fluconazole, 100 mg 3 times weekly, is recommended (strong recommendation; high-quality evidence).
  • For HIV-infected patients, antiretroviral therapy is strongly recommended to reduce the incidence of recurrent infections (strong recommendation; high-quality evidence).
  • For denture-related candidiasis, disinfection of the denture, in addition to antifungal therapy is recommended (strong recommendation; moderate-quality evidence).

XVII. What Is the Treatment for Esophageal Candidiasis?

Recommendations

  • Systemic antifungal therapy is always required. A diagnostic trial of antifungal therapy is appropriate before performing an endoscopic examination (strong recommendation; high-quality evidence).
  • Oral fluconazole, 200–400 mg (3–6 mg/kg) daily, for 14–21 days is recommended (strong recommendation; high-quality evidence).
  • For patients who cannot tolerate oral therapy, intravenous fluconazole, 400 mg (6 mg/kg) daily, OR an echinocandin (micafungin, 150 mg daily, caspofungin, 70-mg loading dose, then 50 mg daily, or anidulafungin, 200 mg daily) is recommended (strong recommendation; high-quality evidence).
  • A less preferred alternative for those who cannot tolerate oral therapy is AmB deoxycholate, 0.3–0.7 mg/kg daily (strong recommendation; moderate-quality evidence).
  • Consider de-escalating to oral therapy with fluconazole 200–400 mg (3–6 mg/kg) daily once the patient is able to tolerate oral intake (strong recommendation; moderate-quality evidence).
  • For fluconazole-refractory disease, itraconazole solution, 200 mg daily, OR voriconazole, 200 mg (3 mg/kg) twice daily either intravenous or oral, for 14–21 days is recommended (strong recommendation; high-quality evidence).
  • Alternatives for fluconazole-refractory disease include an echinocandin (micafungin: 150 mg daily; caspofungin: 70-mg loading dose, then 50 mg daily; or anidulafungin: 200 mg daily) for 14–21 days, OR AmB deoxycholate, 0.3–0.7 mg/kg daily, for 21 days (strong recommendation; high-quality evidence)
  • Posaconazole suspension, 400 mg twice daily, or extended-release tablets, 300 mg once daily, could be considered for fluconazole-refractory disease (weak recommendation; low-quality evidence).
  • For patients who have recurrent esophagitis, chronic suppressive therapy with fluconazole, 100–200 mg 3 times weekly, is recommended (strong recommendation; high-quality evidence).
  • For HIV-infected patients, antiretroviral therapy is strongly recommended to reduce the incidence of recurrent infections (strong recommendation; high-quality evidence).

Risk Factors

Patients with the following conditions, treatments or situations are at increased risk for invasive candidiasis.[rx][rx][rx]

  • Critical illness
  • Long-term intensive care unit stay
  • Abdominal surgery (aggravated by anastomotic leakage or repeat laparotomies)
  • Immunosuppressive diseases
  • Acute necrotizing pancreatitis
  • Malignant hematologic disease
  • Solid-organ transplantation
  • Hematopoietic stem cell transplantation
  • Solid-organ tumors
  • Neonates (especially low birth weight and preterm infants)
  • Broad-spectrum antibiotic treatment
  • Central venous catheter
  • Internal prosthetic device
  • Total parenteral nutrition
  • Hemodialysis
  • Glucocorticoid use
  • Chemotherapy
  • Noninvasive Candida colonization (particularly if multifocal)

Transmission

Invasive candidiasis is a nosocomial infection with the majority of cases associated with hospital stays.[rx]

Prevention

These measures may help reduce your risk of developing candida infections

  • Rinse your mouth – If you need to use a corticosteroid inhaler, be sure to rinse your mouth with water or brush your teeth after taking your medication.
  • Brush your teeth at least twice a day and floss daily – or as often as your dentist recommends.
  • Check your dentures – Remove your dentures at night. Make sure dentures fit properly and don’t cause irritation. Clean your dentures daily. Ask your dentist for the best way to clean your type of dentures.
  • See your dentist regularly – especially if you have diabetes or wear dentures. Ask your dentist how often you need to be seen.
  • Watch what you eat – Try limiting the amount of sugar-containing foods you eat. These may encourage the growth of candida.
  • Maintain good blood sugar control if you have diabetes – Well-controlled blood sugar can reduce the amount of sugar in your saliva, discouraging the growth of candida.
  • Treat a vaginal yeast infection – as soon as possible.
  • Treat dry mouth – Ask your doctor about ways to avoid or treat your dry mouth.
  • Avoid douching
  • Do not use feminine deodorant or deodorant pads or tampons
  • Wear underwear made from cotton or other natural fibers
  • Wear loose fitting pants or skirts
  • Wash underwear at a high temperature
  • Avoid tight underwear and pantyhose
  • Eat a healthy, varied diet
  • Promptly change wet clothing, for example bathing suits
  • Avoid hot tubs and hot baths

Home Remedies

Some home remedies include

  • Gentian violet – This is a dye made from coal tar. A person can apply it directly by swabbing it over thrush in the mouth, but they should not swallow it.
  • Probiotic-rich foods – Foods that contain probiotics, such as yogurt or cottage cheese, may help the body recover. These foods contain healthful bacteria that may help prevent the growth of thrush.
  • Probiotic supplements – Similarly to probiotic-rich foods, these supplements can help the body maintain its healthy bacteria. This may prevent a future thrush infection.

References

Esophageal candidiasis

Irritant Contact Dermatitis, Causes, Symptoms, Treatment

Irritant Contact Dermatitis/Contact dermatitis is an inflammatory eczematous skin disease. Contact dermatitis is a type of inflammation of the skin. It results from either exposure to allergens (allergic contact dermatitis) or irritants (irritant contact dermatitis). Phototoxic dermatitis occurs when the allergen or irritant is activated by sunlight. Diagnosis of allergic contact dermatitis can often be supported by patch testing.[rx]It is caused by chemicals or metal ions that exert toxic effects without inducing a T-cell response (contact irritants) or by small reactive chemicals that modify proteins and induce innate and adaptive immune responses (contact allergens).

Pathophysiology of Contact Dermatitis

The pathophysiology of allergic contact dermatitis (ACD) begins with the contact of the allergen to the skin. The allergen penetrates that stratum corneum and is taken up by Langerhans cells. The antigens are subsequently processed by these cells and displayed on their surface. As part of the skin’s normal immunity, Langerhans cells migrate towards regional lymph nodes. The antigens taken up by the Langerhans cells come in contact with the adjacent T-lymphocytes. Because of the process of clonal expansion as well as cytokine-induced proliferation, antigen-specific T lymphocytes are created. These lymphocytes may then traverse through the blood and into the epidermis. This process collectively is known as the sensitization phase of allergic contact dermatitis. The elicitation phase is what occurs after reexposure to the antigen takes place. The Langerhans cells containing the antigen interacts with the antigen-specific T-lymphocytes for that antigen which triggers a cytokine-induced proliferation process. This, in turn, creates a localized inflammatory response.

Types of Contact Dermatitis

There are three types of contact dermatitis: irritant contact dermatitis; allergic contact dermatitis; and photocontact dermatitis. Photocontact dermatitis is divided into two categories: phototoxic and photoallergic.

Irritant contact dermatitis

Irritant contact dermatitis (ICD) can be divided into forms caused by chemical irritants, and those caused by physical irritants. Common chemical irritants implicated include:

  • Solvents(alcohol, xylene, turpentine, esters, acetone, ketones, and others) –  metalworking fluids (neat oils, water-based metalworking fluids with surfactants); latex; kerosene; ethylene oxide; surfactants in topical medications and cosmetics (sodium lauryl sulfate); and alkalis (drain cleaners, strong soap with lye residues).
  • Physical irritant contact dermatitis – may most commonly be caused by low humidity from air conditioning.[rx] Also, many plants directly irritate the skin.

Allergic contact dermatitis

Allergic contact dermatitis (ACD) is accepted to be the most prevalent form of immunotoxicity found in humans, and is a common occupational and environmental health problem.[rx]

  • By its allergic nature –  this form of contact dermatitis is a hypersensitive reaction that is atypical within the population. The mechanisms by which this reaction occurs are complex, with many levels of fine control. Their immunology centres on the interaction of immunoregulatory cytokines and discrete subpopulations of T lymphocytes.
  • Allergens include nickel – gold, Balsam of Peru (Myroxylon pereirae), chromium, and the oily coating from plants of the genus Toxicodendron, such as poison ivy, poison oak, and poison sumac.

Photocontact dermatitis

  • Sometimes termed “photoaggravated”,[rx] and divided into two categories, phototoxic and photoallergic, PCD is the eczematous condition which is triggered by an interaction between an otherwise unharmful or less harmful substance on the skin and ultraviolet light (320–400 nm UVA) (ESCD 2006), therefore manifesting itself only in regions where the sufferer has been exposed to such rays.

Both irritant contact dermatitis and allergic contact dermatitis can present with three morphological patterns.

  • Acute phase  erythema, edema, oozing,  crusting, tenderness, vesicles or pustules
  • Subacute phase  crusts, scales, and hyperpigmentation
  • Chronic phase  Lichenification.

Classification of Occupational Dermatoses

Type of Dermatosis Example or Cause
Contact dermatitis
 Irritant Solvents, detergents
 Allergic p-Phenylenediamine in hairdressers
Contact urticaria
 Immunologic Natural rubber latex, crabmeat
 Non-immunologic Ammonium persulfate (hairdressers)
Infections
 Bacterial Erysipelothrix in fishmongers
 Fungal Sporotrichosis in gardeners
 Viral Warts in butchers
 Parasitic Cheyletiellosis in veterinarians
Hair follicle disorders
 Folliculitis Motor oil in mechanics
 Chloracne Polychlorinated biphenyls
Pigmentation disorders
 Post-inflammatory hyperpigmentation Phytophotodermatitis
 Acquired leukoderma Hydroquinones in rubber/plastics
Neoplasms
 Granulomas Foreign bodies, beryllium
 Benign tumours or carcinomas Anthracene in soot or petroleum
Ionizing or ultraviolet radiation
Miscellaneous
 Scleroderma Vinyl chloride
 Raynaud phenomenon Vibrating tools
 Telangiectasias Aluminum smelter workers

Causes of Irritant Contact Dermatitis

Substances that commonly trigger contact allergies include the following:

  • Metals (e.g. nickel and cobalt)
  • Latex rubber
  • Adhesives (e.g. the sticky substances in plasters)
  • Plants (e.g. chamomile and arnica)
  • Scents (in cosmetics such as lipsticks, perfumes and soaps)
  • Cleaning agents and solvents
  • Essential oils
  • Common causes of allergic contact dermatitis include: nickel allergy, 14K or 18K gold, Balsam of Peru (Myroxylon pereirae), and chromium.
  • The alkyl resorcinols in Grevillea banksii and Grevillea ‘Robyn Gordon’ are responsible for contact dermatitis.[rx] Bilobol, another alkyl resorcinol found in Ginkgo biloba fruits, is also a strong skin irritant.[rx]
  • Paraphenylenediamine (PPD) present in hair dye; common cause of allergic contact dermatitis on the scalp, face, ears.
  • Neomycin and bacitracin applied to the areas of stasis dermatitis and leg ulcers may be the cause of allergic contact dermatitis on the legs and feet
  • Topical neomycin and corticosteroids can lead to allergic contact dermatitis in patients with otitis externa
  • In women with lichen sclerosus et atrophicus, benzocaine applied in pruritus ani and pruritus vulvae may develop allergic contact dermatitis
  • Nickel is the most common metal present in artificial jewelry which is the cause of allergic contact dermatitis.

Common allergens include

  • Nickel, which is used in jewelry, buckles and many other items
  • Medications, such as antibiotic creams and oral antihistamines
  • Balsam of Peru, which is used in many products, such as perfumes, cosmetics, mouth rinses and flavorings
  • Formaldehyde, which is in preservatives, disinfectants and clothing
  • Personal care products, such as deodorants, body washes, hair dyes, cosmetics and nail polish
  • Plants such as poison ivy and mango, which contain a highly allergenic substance called urushiol
  • Airborne substances, such as ragweed pollen and spray insecticides
  • Products that cause a reaction when you’re in the sun (photoallergic contact dermatitis), such as some sunscreens and oral medications

Symptoms of Irritant Contact Dermatitis

Symptoms of both forms include the following:

  • Red rash. This is the usual reaction. The rash appears immediately in irritant contact dermatitis; in allergic contact dermatitis, the rash sometimes does not appear until 24–72 hours after exposure to the allergen.
  • Blisters or wheals. Blisters, wheals (welts), and urticaria (hives) often form in a pattern where skin was directly exposed to the allergen or irritant.
  • Itchy, burning skin. Irritant contact dermatitis tends to be more painful than itchy, while allergic contact dermatitis often itches.
  • a red rash, often without clearly defined edges,
  • Itchy skin (often intense)
  • Rash (skin red, swollen, and hot)
  • Excessively dry skin
  • Burning
  • Stinging
  • Hives (round welts on the skin that itch intensely)
  • Fluid-filled blisters
  • Oozing blisters that leave crusts and scales
  • swelling,
  • itching, and
  • dry skin.

Diagnosis of Irritant Contact Dermatitis

History and Physical

Symptoms of irritant contact dermatitis may include burning, itching, stinging, soreness, and pain, particularly at the beginning of the clinical course, while pruritus is more common in allergic contact dermatitis. Patients with a history are at increased risk for developing nonspecific hand dermatitis and irritant contact dermatitis.

Distinguishing Features of Irritant and Allergic Contact Dermatitis

Feature Irritant Contact Dermatitis Allergic Contact Dermatitis
Pathogenesis Direct cytotoxic effect T cell-mediated immune reaction
Affected individuals Everyone A minority of individuals
Onset Immediate (chemical burns) 12-48 h in previously sensitized individuals
After repeated exposure to weak irritants
Signs Subacute or chronic eczema with desquamation, fissures Acute to subacute eczema with vesiculation
Symptoms Pain or burning sensation Pruritus
Concentration of contactant High Low
Investigation None Patch or prick tests

Testing for allergens

  • The best way to test for a reaction to allergens is by patch testing. During a patch test, tiny amounts of known allergens are applied to your skin. The substances are attached to your back using a special kind of non-allergic tape. They may sometimes be attached to the upper arms. After two days, the patches are removed and your skin assessed to check if there has been any reaction.
  • Your skin will usually be examined again after a further two days, as most allergic contact dermatitis reactions take this long to develop.

Testing for irritants

  • It’s very difficult to test whether specific products irritate your skin, because testing for these is very unreliable.In some cases, a repeated open application test (ROAT) is useful, particularly to assess cosmetics. A ROAT involves reapplying the substance onto the same area of skin twice a day for 5 to 10 days, to see how your skin reacts.

Treatment of Irritant Contact Dermatitis

Self-care

  • If blistering develops – cold moist compresses[rx] applied for 30 minutes, 3 times a day can offer relief.
  • Calamine lotion  – may relieve itching.[rx]
  • Oral antihistamines – such as diphenhydramine (Benadryl, Ben-Allergin) can relieve itching.[rx]
  • For patients with oozing lesions – Burrow’s solution (aluminum triacetate), calamine, and/or oatmeal baths can also be utilized.
  • In hand dermatitis – avoiding excessive hand washing and using non-irritating moisturizers is recommended. Choose mild soaps, moisturizers, and detergents without dyes or perfumes. Wear gloves to protect your hands and other body parts from exposure if contact with these chemicals is unavoidable, however be aware that you can become allergic to chemicals in the gloves as well.
  • In foot dermatitis – the use of barrier socks may be helpful.
  • Wash skin immediately – after contact with an allergen to limit the spread and severity of the reaction such as after known contact with a plant allergen (poison ivy).
  • Immediately after exposure to a known allergen or irritant – wash with soap and cool water to remove or inactivate most of the offending substance.
  • For mild cases that cover a relatively small area –  hydrocortisone cream in nonprescription strength may be sufficient.
  • Weak acid solutions (lemon juice, vinegar) – can be used to counteract the effects of dermatitis contracted by exposure to basic irritants.
  • A barrier cream – such as those containing zinc oxide (e.g., Desitin, etc.), may help protect the skin and retain moisture.
  • Avoid scratching.[rx]
  • For acute symptoms cold compresses can help with the itch.
  • Apply covers over metal fasteners in clothing to avoid contact with nickel.

Medical care

If the rash does not improve or continues to spread after 2–3 of days of self-care, or if the itching and/or pain is severe, the patient should contact a dermatologist or other physician. Medical treatment usually consists of lotions, creams, or oral medications.

  • CorticosteroidsA corticosteroid medication like hydrocortisone may be prescribed to combat inflammation in a localized area. It may be applied to the skin as a cream or ointment. If the reaction covers a relatively large portion of the skin or is severe, a corticosteroid in pill or injection form may be prescribed.
  • In severe cases – a stronger medicine like halobetasol may be prescribed by a dermatologist.
  • Friction – should be avoided as well as the use of soaps, perfumes, and dyes. Emollients are used for hydrating the skin. Tacrolimus ointment and pimecrolimus cream are immunomodulating drugs that inhibit calcineurin and are helpful in allergic contact dermatitis.
  • Topical Immunomodulators – Topical calcineurin inhibitors (pimecrolimus, tacrolimus) are anti-inflammatory agents that may provide another option in patients with ACD or ICD. However, they are not FDA approved for CD. They do not cause skin thinning, which is beneficial for the treatment of patients with facial dermatitis and dermatitis in other sensitive areas (bending areas, genitals). The most common adverse effects encountered are burning and itch at the application site.
  • Topical Antibiotics – These creams or ointments are sometimes used if there are open fissures and evidence of a secondary bacterial infection. However over-the-counter topical antibiotics are frequent causes of CD and should be used under the recommendation of your allergist / immunologist.
  • Topical SteroidsTopical steroids are anti-inflammatory medications. They help to get the rash under control more quickly and are usually applied 1-2 times a day. Topical steroids come in different formulations and strengths. Milder topical steroids such as hydrocortisone can be purchased over the counter. If the rash is not improving after 7 days or getting worse, you should consult your physician. A more potent topical steroid may be required, but should be used sparingly in sensitive areas such as the face, underarms and groin as they can thin the skin and cause stretch marks.
  • Unfortunately –  recurrence is common and people with no identifiable cause have a poor quality of life. A nurse educator specializing in dermatology and dermatology should work together to assist in patient education, particularly for challenging cases.
  • Avoiding the noxa – Contact dermatitis is triggered by exogenous toxins in the vast majority of cases. The most important therapeutic approach, therefore, is to cease causal exposure — no form of symptomatic treatment can substitute for this approach. Attempts to induce tolerance to contact allergens by means of immunotherapy have been hitherto unsuccessful [rx, rx].
  • Calcineurin antagonists – In Germany, Austria, and Switzerland, calcineurin antagonists are only approved for the treatment of atopical dermatitis. They are less effective than strong corticosteroids in manifest contact dermatitis [rx, rx, rx]. However, if long-term use is indicated, topical calcineurin antagonists may be beneficial in contact dermatitis compared to corticosteroids, particularly in sensitive areas of the skin (e. g., face, intertriginous areas), since they carry no atrophy risk [rx]. With regard to safety, the reader is referred to the AWMF guidelines of the DDG on topical calcineurin antagonists and neurodermatitis [rx, rx].
  • Ultraviolet therapy – Short-wave ultraviolet light (UVB) and PUVA (psoralen plus UV-A) are effective in chronic dermatitis, most notably in hand dermatitis [rx, rx, rx, rx]. In some forms of hand dermatitis, topical application of psoralens is advisable in the context of PUVA therapy in order to intensify the therapeutic effect. It appears possible to achieve a certain degree of “protective hardening” using UVB [rx]. Positive data are also available on the use of UVA1 and narrow-band UVB, particularly in hand dermatitis [rx, rx, rx].
  • Other external agents – Due to its antiphlogistic and antiproliferative effects, the use of coal tar as a follow-up treatment is still reasonable today in cases where other external agents are ineffective or declined by the patient. There is no evidence to support the fear that local treatment with coal tar is carcinogenic [rx,rx, rx,rx].
  • Phototherapy – Your allergist / immunologist may refer you to a dermatologist for light therapy if the rash is not responding to the above therapy.

Basic therapy and skin protection

Follow-up treatment with basic moisturizing agents to promote skin barrier regeneration and protect against recurrence, combined with the use of skin protection creams, is beneficial when individually tailored to skin status and skin exposure [rx, rx, rx]. On the other hand, preparations containing unsuitable levels of water and fat or allergenic components may delay the resolution of dermatitis or even intensify the effect of substances harmful to the skin [rx]. Although skin protection training is beneficial in the case of hazardous occupational exposure [rx], the effectiveness of skin protection creams alone under working conditions has not be unequivocally proven [rx]. Complete restoration of barrier function is not expected until several weeks after the clinical resolution of contact dermatitis. However, the beneficial effect of moisturizers is measurable [rx].

Prevention of Irritant Contact Dermatitis

General prevention steps include the following

  • Avoid irritants and allergens. Try to identify and avoid substances that irritate your skin or cause an allergic reaction.
  • Wash your skin. You might be able to remove most of the rash-causing substance if you wash your skin right away after coming into contact with it. Use a mild, fragrance-free soap and warm water. Rinse completely. Also wash any clothing or other items that may have come into contact with a plant allergen, such as poison ivy.
  • Cleaning your skin – if you come into contact with an allergen or irritant, rinse the affected skin with warm water and an emollient as soon as possible
  • Using gloves to protect your hands – but take them off every now and again, as sweating can make any symptoms worse; you may find it useful to wear cotton gloves underneath rubber gloves if the rubber also irritates you
  • Changing products that irritate your skin – check the ingredients on make-up or soap to make sure it does not contain any irritants or allergens; in some cases, you may need to contact the manufacturer or check online to get this information
  • Applying emollients frequently and in large amounts – these keep your skin hydrated and help protect it from allergens and irritants; you could also use emollient soap substitutes rather than regular bar or liquid soaps, which can dry out your skin
  • Wear protective clothing or gloves. Face masks, goggles, gloves and other protective items can shield you from irritating substances, including household cleansers.
  • Apply an iron-on patch to cover metal fasteners next to your skin. This can help you avoid a reaction to jean snaps, for example.
  • Apply a barrier cream or gel. These products can provide a protective layer for your skin. For example, an over-the-counter skin cream containing bentoquatam (IvyBlock) may prevent or lessen your skin’s reaction to poison ivy.
  • Use moisturizer. Regularly applying moisturizing lotions can help restore your skin’s outermost layer and keep your skin supple.
  • Take care around pets – Allergens from plants, such as poison ivy, can cling to pets and then be spread to people.

References

Irritant Contact Dermatitis

Folacin Health Benefit, Food Source, Deficiency Symptoms

Folacin Health Benefit/Vitamin B9 is one of the B vitamins. Folic acid is a form of vitamin B-9 that can dissolve in water. It is a key ingredient in the making of the nucleic acid that forms part of all genetic material.The recommended daily intake of folate in the US is 400 micrograms from foods or dietary supplements. Folate in the form of folic acid is used to treat anemia caused by folic acid deficiency. Folic acid is also used as a supplement by women during pregnancy to prevent neural tube defects(NTD) in the baby. Low levels in early pregnancy are believed to be the cause of more than half of babies born with neural tube defects. More than 50 countries use fortification of certain foods with folic acid as a measure to decrease the rate of NTDs in the population. Long term supplementation is also associated with small reductions in the risk of stroke and cardiovascular disease.It may be taken by mouth or by injection.

Folate, distinct forms of which are known as folic acidfolacin, and vitamin B9,[rx] is one of the B vitamins.[rx] It may be taken by mouth or by injection.[rx] The recommended adult daily intake of folate in the U.S. is 400 micrograms from foods or dietary supplements.[rx] Folate in the form of folic acid is used to treat anemia caused by folic acid deficiency.[4] Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in the baby.[4][9] Low levels in early pregnancy are believed to be the cause of more than half of babies born with NTDs.[rx] More than 80 countries use fortification of certain foods with folic acid as a measure to decrease the rate of NTDs

Symptoms of Vitamin B9 Deficiency

Folic acid deficiency occurs when the newborn baby does not receive enough of this vitamin in the womb. A fetus that has received insufficient quantities of folic acid has strong possibilities of being born with spina bifida and may also suffer from serious defects of the nervous system.

Deficiency of folic acid may also lead to the following

  • occurrence of acne
  • cracked lips
  • Loss of appetite
  • weight loss can occur
  • weakness,
  • sore tongue,
  • headaches,
  • heart palpitations
  • irritability, and
  • behavioral disorders
  • anemia(macrocytic, megaloblastic anemia) can be a sign of advanced folate deficiency.
  • Women with folate deficiency who become pregnant are more likely to give birth to low birth weight premature infants, and infants with neural tube defects.
  • In infants and children, folate deficiency can lead to failure to thrive or slow growth rate,
  • diarrhea
  • oral ulcers
  • megaloblastic anemia,
  • neurological deterioration.
  • Microcephaly
  • seizures
  • blindness and cerebellar ataxia can also be observed.
  • cracking on the corners of the mouth
  • sore tongue
  • feeling of tiredness
  • nausea
  • osteoporosis
  • anemia
  • chronic fatigue syndrome
  • high blood pressure
  • Alzheimer’s disease
  • cancer of the cervix, rectum and bowel

Folic acid has many roles to play in the development of bones and iron uptake by the cells. Hence its deficiency may lead to malfunctioning of the vital systems.

Recommended Intakes of Vitamin B9

Intake recommendations for folate and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by the Food and Nutrition Board (FNB) at the Institute of Medicine (IOM) of the National Academies (formerly National Academy of Sciences) . DRI is the general term for a set of reference values used for planning and assessing nutrient intakes of healthy people. These values, which vary by age and gender, include:

  • Recommended Dietary Allowance (RDA) – Average daily level of intake sufficient to meet the nutrient requirements of nearly all (97%–98%) healthy individuals; often used to plan nutritionally adequate diets for individuals.
  • Adequate Intake (AI) – Intake at this level is assumed to ensure nutritional adequacy; established when evidence is insufficient to develop an RDA.
  • Estimated Average Requirement (EAR) – Average daily level of intake estimated to meet the requirements of 50% of healthy individuals; usually used to assess the nutrient intakes of groups of people and to plan nutritionally adequate diets for them; can also be used to assess the nutrient intakes of individuals.
  • Tolerable Upper Intake Level (UL) – Maximum daily intake unlikely to cause adverse health effects.

Table 1 lists the current RDAs for folate as micrograms (mcg) of dietary folate equivalents (DFEs). The FNB developed DFEs to reflect the higher bioavailability of folic acid than that of food folate. At least 85% of folic acid is estimated to be bioavailable when taken with food, whereas only about 50% of folate naturally present in food is bioavailable . Based on these values, the FNB defined DFE as follows:

  • 1 mcg DFE = 1 mcg food folate
  • 1 mcg DFE = 0.6 mcg folic acid from fortified foods or dietary supplements consumed with foods
  • 1 mcg DFE = 0.5 mcg folic acid from dietary supplements taken on an empty stomach

For infants from birth to 12 months, the FNB established an AI for folate that is equivalent to the mean intake of folate in healthy, breastfed infants in the United States.

 Recommended Dietary Allowances (RDAs) for Folate 
Age Male Female Pregnant Lactating
Birth to 6 months* 65 mcg DFE* 65 mcg DFE*
7–12 months* 80 mcg DFE* 80 mcg DFE*
1–3 years 150 mcg DFE 150 mcg DFE
4–8 years 200 mcg DFE 200 mcg DFE
9–13 years 300 mcg DFE 300 mcg DFE
14–18 years 400 mcg DFE 400 mcg DFE 600 mcg DFE 500 mcg DFE
19+ years 400 mcg DFE 400 mcg DFE 600 mcg DFE 500 mcg DFE

* Adequate Intake (AI)

Food Source of Vitamin B9

Selected Food Sources of Folate and Folic Acid 
Food mcg DFE
per serving
Percent DV*
Beef liver, braised, 3 ounces 215 54
Spinach, boiled, ½ cup 131 33
Black-eyed peas (cowpeas), boiled, ½ cup 105 26
Breakfast cereals, fortified with 25% of the DV† 100 25
Rice, white, medium-grain, cooked, ½ cup† 90 23
Asparagus, boiled, 4 spears 89 22
Spaghetti, cooked, enriched, ½ cup† 83 21
Brussels sprouts, frozen, boiled, ½ cup 78 20
Lettuce, romaine, shredded, 1 cup 64 16
Avocado, raw, sliced, ½ cup 59 15
Spinach, raw, 1 cup 58 15
Broccoli, chopped, frozen, cooked, ½ cup 52 13
Mustard greens, chopped, frozen, boiled, ½ cup 52 13
Green peas, frozen, boiled, ½ cup 47 12
Kidney beans, canned, ½ cup 46 12
Bread, white, 1 slice† 43 11
Peanuts, dry roasted, 1 ounce 41 10
Wheat germ, 2 tablespoons 40 10
Tomato juice, canned, ¾ cup 36 9
Crab, Dungeness, 3 ounces 36 9
Orange juice, ¾ cup 35 9
Turnip greens, frozen, boiled, ½ cup 32 8
Orange, fresh, 1 small 29 7
Papaya, raw, cubed, ½ cup 27 7
Banana, 1 medium 24 6
Yeast, baker’s, ¼ teaspoon 23 6
Egg, whole, hard-boiled, 1 large 22 6
Vegetarian baked beans, canned, ½ cup 15 4
Cantaloupe, raw, 1 wedge 14 4
Fish, halibut, cooked, 3 ounces 12 3
Milk, 1% fat, 1 cup 12 3
Ground beef, 85% lean, cooked, 3 ounces 7 2
Chicken breast, roasted, ½ breast 3 1

* DV = Daily Value. The FDA developed DVs to help consumers compare the nutrient contents of products within the context of a total diet. The DV for folate is 400 mcg for adults and children aged 4 and older. However, the FDA does not require food labels to list folate content unless a food has been fortified with this nutrient. Foods providing 20% or more of the DV are considered to be high sources of a nutrient.

† Fortified with folic acid as part of the folate fortification program.

The U.S. Department of Agriculture’s Nutrient Database Web site  lists the nutrient content of many foods and provides a comprehensive list of foods containing folate arranged by nutrient content and by food name.

Folacin Health Benefits

  • Folate deficiency – Taking folic acid improves folate deficiency.
  • Serious kidney disease – About 85% of people with serious kidney disease have high levels of homocysteine. High levels of homocysteine have been linked to heart disease and stroke. Taking folic acid lowers homocysteine levels in people with serious kidney disease. However, folic acid supplementation does not appear to reduce the risk of heart disease-related events.
  • High amounts of homocysteine in the blood (hyperhomocysteinemia) – High levels of homocysteine have been linked to heart disease and stroke. Taking folic acid lowers homocysteine levels by 20% to 30% in people with normal to slightly elevated homocysteine levels. It is recommended that people with homocysteine levels greater than 11 micromoles/L supplement with folic acid and vitamin B12.
  • Reducing harmful effects of a medicine called methotrexate – Taking folic acid seems to reduce nausea and vomiting, which are possible side effects of methotrexate treatment.
  • Birth defects (neural tube defects) – Folic acid during pregnancy reduces the risk of neural tube birth defects. It is recommended that pregnant women get 600-800 mcg of folic acid per day from their diet or supplements starting 1 month before pregnancy and during pregnancy. Pregnant women with a history of neural tube birth defects are advised to get 4000 mcg of folic acid per day.

Possibly Effective for

  • Age-related vision loss (age-related macular degeneration) – Research shows that taking folic acid with other vitamins including vitamin B6 and vitamin B12 reduces the risk of developing age-related vision loss.
  • Depression – Limited research shows that taking folic acid along with antidepressants seems to improve symptoms in people with depression.
  • High blood pressure –  Research shows that taking folic acid daily for at least 6 weeks reduces blood pressure in people with high blood pressure. But Taking folic acid with blood pressure medication does not seem to lower blood pressure more than taking only blood pressure medicine
  • Gum problems due to a drug called phenytoin – Applying folic acid to the gums seems to prevent gum problems caused by phenytoin. However, taking folic acid by mouth does not seem to improve symptoms of this condition.
  • Gum disease during pregnancy – Applying folic acid to the gums seems to improve gum disease during pregnancy.
  • Stroke – Taking folic acid can reduce the risk of stroke by 10% to 25% in people who live in countries that don’t fortify grain products with folic acid. But folic acid doesn’t seem to prevent strokes in most people who live in countries that do fortify grain products with folic acid.
  • A skin discoloration disorder called vitiligo – Taking folic acid by mouth seems to improve symptoms of vitiligo.
  • Cancer of the white blood cells (acute lymphoblastic leukemia) – Taking folate during pregnancy does not reduce the risk of childhood cancer of the white blood cells.
  • Iron deficiency – Taking folic acid with iron supplements is not more effective than taking the iron supplements without folic acid for treating and preventing iron deficiency and anemia caused by too little iron in the body.
  • Memory and thinking skills in older people – Most research shows that taking folic acid does not prevent decline in memory and thinking skills in the elderly.
  • Preventing re-blockage of blood vessels after angioplasty – There is inconsistent evidence on the benefits of taking folic acid after a procedure to widen the blood vessels. But taking folic acid plus vitamin B6 and vitamin B12 might actually interfere with healing in cases where a device (stent) is inserted in the blood vessel to keep it open.
  • Breast cancer – Consuming folate in the diet might lower the risk of developing breast cancer in women who also eat high amounts of methionine, vitamin B12 (cyanocobalamin), or vitamin B6 (pyridoxine), but research is not consistent. Other research suggests that taking folic acid supplements alone does not lower the risk of breast cancer.
  • Heart disease – Most research shows that taking folic acid alone or with other B vitamins does not reduce the risk of death or heart disease-related events in people with heart disease.
  • Cataracts – Research shows that taking folic acid with other vitamins including vitamin B6 and vitamin B12 does not prevent cataracts. In fact, it might increase the chance of needing to have cataracts removed.
  • Chronic fatigue syndrome – Daily injections of folic acid appear to have no effect on symptoms of chronic fatigue syndrome.
  • Diarrhea – Taking a specific nutritional supplement with added folic acid and possibly vitamin B12 does not seem to prevent diarrhea in children at risk of malnutrition. Taking this product may increase the risk of having diarrhea last more than a few days.
  • Preventing falls –  Taking folic acid with vitamin B-12 does not seem to prevent falls in older people who are also taking vitamin D.
  • Fetal and early infant death – Taking folic acid during pregnancy does not seem to reduce the risk of having a baby die just before or after birth.
  • Toxicity from the drug lometrexol – Daily injections of folic acid appear to have no effect on symptoms of chronic fatigue syndrome.
  • Lower respiratory tract infections – Taking a specific nutritional supplement with added folic acid and possibly vitamin B12 does not seem to prevent infections in the lungs in children at risk of malnutrition.
  • Weak bones (osteoporosis) – In elderly individuals with osteoporosis, taking folic acid with vitamin B12 and possibly vitamin B6 (pyridoxine) does not seem to prevent broken bones.
  • Performance in older people – Taking folic acid with vitamin B-12 doesn’t seem to help older people walk better or have stronger hands.
  • Growths in the large intestine and rectum (colorectal adenoma) – Taking folic acid supplements does not seem to prevent growths in the large intestine or rectum.
  • Inherited disease called Fragile-X syndrome – Taking folic acid by mouth does not improve symptoms of fragile-X-syndrome.
  • Premature infants – Taking folic acid during pregnancy does not decrease the risk of having a premature baby.

Insufficient Evidence for

  • Acne – Limited evidence suggests that taking a specific nutritional supplement, containing vitamin B3 (nicotinamide), a compound isolated from grains (azelaic acid), zinc, vitamin B6 (pyridoxine), copper, and folic acid (NicAzel, Elorac Inc., Vernon Hills, IL) appears to reduce inflammation associated with pimples on the face.
  • Alzheimer’s disease – Limited evidence suggests that elderly people who consume more folic acid than the recommended dietary allowance (RDA) appear to have a lower risk of developing Alzheimer’s disease than people who consume less folic acid.
  • Autism – Limited research suggests taking folic acid during pregnancy might reduce the risk of autism in the child.
  • Beta-thalassemia – Beta-thalassemia is a disorder of the blood that results in the production of less hemoglobin, the protein that carries oxygen in the blood. Patients with beta-thalassemia usually have bone and muscle pain and have less strength. In children with this disorder, limited research suggests taking folic acid by itself, or with L-carnitine a compound similar to an amino acid from protein, might reduce bone pain and help increase strength.
  • Bipolar disorder – Taking folic acid does not appear to improve the antidepressant effects of lithium in people with bipolar disorder. However, taking folate with the medication valproate improves the effects of valproate.
  • Cervical cancer – There is some evidence that increasing folic acid and folate intake from dietary and supplement sources, along with thiamine, riboflavin, and vitamin B12, might help to prevent cervical cancer.
  • Long-term kidney disease (chronic kidney disease, CKD) – Taking folic acid might help slow kidney function decline in people with CKD. But it is not beneficial when used along with vitamin B12 (cyanocobalamin). In fact, the combination might make kidney disease worse.
  • Colon cancer, rectal cancer – Research suggests that taking folic acid or eating folate in the diet can reduce the risk of developing colon or rectal cancer. However, there is some research that does not suggest that taking folic acid or folate in the diet offers the same benefit. It is possible that folic acid may be more helpful for preventing colon cancer than rectal cancer or it may be more helpful for specific kinds of colon cancer.
  • Diabetes – Taking folic acid supplements does not seem to benefit people with diabetes.
  • Epilepsy – Taking folic acid does not reduce seizures in people with epilepsy.
  • Esophageal cancer – Research suggests that consuming more folate in the diet lowers the risk for developing esophageal cancer.
  • High amounts of homocysteine in the blood caused by the drug fenofibrat – Taking folic acid every other day might lower levels of homocysteine in the blood caused by the drug fenofibrate.
  • Stomach cancer – Research suggests that taking folic acid reduces the risk of developing some types of stomach cancer.
  • Gout – Early research suggests that folate might reduce the risk of gout.
  • Head and neck cancer – Getting more folic acid from the diet has been linked to a lower risk of head and neck cancer.
  • Hearing loss – Low levels of folate in the blood seem to be related to the risk for sudden hearing loss in adults. Some evidence suggests that taking folic acid daily for 3 years slows the decline of hearing loss in older people who have low folate levels. It is not clear if folic acid supplementation reduces hearing loss in people with normal folate levels.
  • Male infertility – Some research suggests that taking folic acid plus zinc sulfate daily can increase sperm count in men with low sperm counts.
  • Low birth weight – Taking folic acid during pregnancy does not prevent some babies from being born at a low birth weight but it does seem to increase the overall average of birth weights. However, some early research suggests that taking folic acid before getting pregnant might reduce the risk of having a baby that is too small even when born full term. Although this risk is not reduced in mothers that start supplementation after the baby is conceived.
  • Lung cancer – There does not appear to be a relationship between low levels of folic acid and lung cancer in most people.
  • A type of skin cancer called melanoma – Early research shows that taking folic acid might reduce the risk of melanoma.
  • Helping medicines used for chest pain work longer – Some evidence suggests that taking folic acid does not help medications for chest pain (nitrates) work longer.
  • Cleft lip – Some research suggests that taking folic acid during pregnancy lowers the risk of left lip. However, other research shows no effect.
  • Pancreatic cancer – Eating more than 280 mcg of folate in the diet daily is linked to a lower risk of developing pancreatic cancer. However, other research suggests that folate intake is not linked to pancreatic cancer risk.
  • Nerve pain (peripheral neuropathy) – There is conflicting evidence about the role of folic acid in nerve pain for people with diabetes (diabetic neuropathy). Some research suggests that taking folic acid with vitamin B6 (pyridoxine) and vitamin B12 improves some symptoms of nerve pain so that people feel happier. However, the nerves do not seem to function any better.
  • Cancer of the throat – Limited research suggests folic acid and folate from dietary and sources and supplements may protect against oropharyngeal cancer, a specific type of throat cancer.
  • Pre-eclampsia – Pre-eclampsia is marked by high blood pressure and protein in the urine during pregnancy. Limited research suggests taking folic acid supplements during pregnancy does not reduce the risk of pre-eclampsia.
  • Pregnancy-induced high blood pressure – Limited research suggests that taking folic acid during pregnancy does not reduce the risk of high blood pressure (gestational hypertension).
  • A disorder that causes a strong urge to move ones legs (restless legs syndrome; RLS) – Taking folic acid seems to reduce symptoms of restless legs syndrome. Researchers are studying whether folic acid deficiency causes restless legs syndrome.
  • Schizophrenia – Taking a combination of folic acid and vitamin B12 may reduce some of the negative symptoms associated with schizophrenia, but only in some patients with a specific genetic make-up. In most people, folic acid does not help with these symptoms.
  • Sickle-cell disease. Taking folic acid might lower homocysteine levels. However, it is not known if this will benefit people with sickle-cell disease.
  • Alcoholism
  • Liver disease

The European Food Safety Authority (EFSA), which provides scientific advice to assist policy makers, has confirmed that clear health benefits have been established for the dietary intake of folate (vitamin B9) in contributing to:

  • normal blood formation;
  • normal homocysteine;
  • a normal metabolism of the immune system;
  • normal cell division;
  • normal maternal tissue growth during pregnancy;
  • normal amino acid synthesis;
  • normal psychological functions;
  • the reduction of tiredness and fatigue;
  • maintanance of normal vision;
  • In addition, the EFSA has confirmed that supplemental folate intake increases maternal folate status, which contributes to the reduction of the risk of neural tube defects (NTD).

References

Folacin Health Benefit

Appendicitis Early Signs Symptoms, Causes, Surgery

Appendicitis Early Signs Symptoms, Causes, Surgery/Appendicitis is an inflammation of the appendix that may lead to an abscess, ileus, peritonitis, or death if untreated. Appendicitis is the most common abdominal surgical emergency. The current standard treatment of uncomplicated appendicitis is usually surgery, but there has been increasing evidence published on the use of antibiotics.

Appendicitis is inflammation of the vermiform appendix. This is a hollow organ located at the tip of the cecum, usually in the right lower quadrant of the abdomen. The appendix develops embryonically at the fifth week. During this time there is a movement of the midgut to the external umbilical cord with the eventual return to the abdomen and rotation of the cecum. This results in the usual retrocecal location of the appendix. It is most often a disease of acute presentation, usually within 24 hours, but it can also present as a more chronic condition. If there has been a perforation with a contained abscess, then the presenting symptoms can be more indolent. The exact function of the appendix has been a debated topic. Today it is accepted that this organ may have an immunoprotective function and acts as a lymphoid organ especially in the younger person. Other theories contend that the appendix acts as a storage vessel for “good” colonic bacteria. Still, others argue that it is a mear developmental remnant and has no real function.

Anatomy of Appendicitis

The vermiform appendix is a tubular structure attached to the base of the caecum at the confluence of the taeniae coli. It is approximately 8-10 cm long in adults and represents the underdeveloped distal end of the large caecum seen in other animals. In humans it is regarded as a vestigial organ, and acute inflammation of this structure is called acute appendicitis

  • Retrocaecal/retrocolic (75%)—Right loin pain is often present, with tenderness on examination. Muscular rigidity and tenderness to deep palpation are often absent because of protection from the overlying caecum. The psoas muscle may be irritated in this position, leading to hip flexion and exacerbation of the pain on hip extension (psoas stretch sign)
  • Subcaecal and pelvis (20%)—Suprapubic pain and urinary frequency may predominate. Diarrhea may be present as a result of irritation of the rectum. Abdominal tenderness may be lacking, but rectal or vaginal tenderness may be present on the right. Microscopic haematuria and leucocytes may be present on urine analysis
  • Pre-ileal and post-ileal (5%)—Signs and symptoms may be lacking. Vomiting may be more prominent, and diarrhea may result from irritation of the distal ileum

Direct and indirect (secondary) signs of acute appendicitis in graded-compression, real-time US, colour Doppler and contrast-enhanced US (CEUS; adopted according to references 7, 9, 20 and 21)

Appendicitis Early Signs Symptoms

A blockage in the lining of the appendix that results in infection is the likely cause of appendicitis. The bacteria multiply rapidly, causing the appendix to become inflamed, swollen and filled with pus. If not treated promptly, the appendix can rupture.

There are numerous issues that can cause appendix luminal blockage, including:

  • Appendicoliths or fecaliths, which are calcified fecal deposits, also known as “appendix stones” (this is more common in children than adults) (rx)
  • Intestinal worms or parasites, including pinworm (Enterobius vermicularis)
  • Irritation and ulcers in the gastrointestinal (GI) tract resulting from long-lasting disorders, such as Crohn’s disease or ulcerative colitis
  • Abdominal injury or trauma
  • Enlarged lymph tissue of the wall of the appendix, which is typically the result of infections in the GI tract
  • Benign or malignant tumors
  • Various foreign objects, such as stones, bullets, air gun pellets, and pins (rx)
  • Sometimes appendicitis is due to a viral, bacterial, or fungal infection that has spread to the appendix. (rx) Possible causes of infection include, but are not limited to:
  • E. coli, which are bacteria found in the environment, foods, and intestines of animals. Most strains of E. coli are harmless, but others can cause illness. (rx)
  • Pseudomonas bacteria, which are found in soil and water and moist areas such as sinks and toilets (rx)
  • Bacteroides, bacteria that already inhabit the digestive tract of humans (rx)
  • Adenovirus, a very common virus spread through contact or through the air that can cause cold-like symptoms as well as bladder and other infections. (rx)
  • Salmonella, a foodborne bacteria that typically causes gastrointestinal upset (diarrhea, nausea, and vomiting) but can have serious complications
  • Shigella bacteria, germs that are very contagious and typically result in diarrheal illness that usually lasts no more than a week. (rx)
  • Measles, a highly contagious virus spread through the air and contact. Vaccination protects most of the population, but there are outbreaks in which unvaccinated people are susceptible (rx)
  • The fungal infections mucormycosis (a rare but serious mold infection caused by environmental molds) (rx) and histoplasmosis; most people who breathe in these spores won’t get sick or will have mild symptoms, but infection can become severe in people with weakened immune systems (11

Appendicitis can have more than one cause, and in many cases, the cause is not clear. Possible causes include

  • Blockage of the opening inside the appendix
  • enlarged tissue in the wall of your appendix, caused by an infection in the gastrointestinal (GI) tract or elsewhere in your body
  • inflammatory bowel disease
  • stool, parasites, or growths that can clog your appendiceal lumen
  • trauma to your abdomen

Appendicitis can cause serious complications, such as:

  • A ruptured appendix. A rupture spreads infection throughout your abdomen (peritonitis). Possibly life-threatening, this condition requires immediate surgery to remove the appendix and clean your abdominal cavity.
  • A pocket of pus that forms in the abdomen. If your appendix bursts, you may develop a pocket of infection (abscess). In most cases, a surgeon drains the abscess by placing a tube through your abdominal wall into the abscess. The tube is left in place for two weeks, and you’re given antibiotics to clear the infection.

Symptoms of Appendicitis

Classically, appendicitis presents as an initial generalized or periumbilical abdominal pain that then localizes to the right lower quadrant. Initially, as the visceral afferent nerve fibers at T8 through T10 are stimulated, and this leads to vague centralized pain. As the appendix becomes more inflamed and the adjacent parietal peritoneum is irritated, the pain becomes more localized to the right lower quadrant. Pain may or may not be accompanied by any of the following symptoms:

  • Sudden pain that begins on the right side of the lower abdomen
  • Sudden pain that begins around your navel and often shifts to your lower right abdomen
  • Pain that worsens if you cough, walk or make other jarring movements
  • Nausea and vomiting
  • Loss of appetite
  • Low-grade fever that may worsen as the illness progresses
  • Constipation or diarrhea
  • Abdominal bloating
  • Anorexia
  • Nausea/vomiting
  • Fever (40% of patients)
  • Diarrhea
  • Generalize malaise
  • Urinary frequency or urgency
  • begins near your belly button and then moves lower and to your right
  • Gets worse in a matter of hours
  • Gets worse when you move around, take deep breaths, cough, or sneeze
  • Is severe and often described as different from any pain you’ve felt before
  • Occurs suddenly and may even wake you up if you’re sleeping
  • An inability to pass gas
  • A low-grade fever
  • Swelling in your abdomen
  • The feeling that having a bowel movement will relieve discomfort

Symptoms can be different for each person and can seem like the following conditions that also cause pain in the abdomen:

  • Abdominal adhesions
  • Constipation
  • Inflammatory bowel disease, which includes Crohn’s disease and ulcerative colitis, long-lasting disorders that cause irritation and ulcers in the GI tract
  • Intestinal obstruction
  • Pelvic inflammatory disease

As inflammation progresses, signs of peritoneal inflammation develop. Signs include:

  • Right lower quadrant guarding and rebound tenderness over McBurney’s point (1.5 to 2 inches from the anterior superior iliac spine on a straight line from the ASIS to the umbilicus)
  • Rovsing’s sign (right lower quadrant pain elicited by palpation of the left lower quadrant)
  • Dunphy’s sign (increased abdominal pain with coughing)

Other associated signs such as psoas sign (pain on external rotation or passive extension of the right hip suggesting retrocecal appendicitis) or obturator sign (pain on internal rotation of the right hip suggesting pelvic appendicitis) are rare.

Real-time US signs of acute appendicitis
Direct signs Indirect signs
  • Non-compressibility of the appendix ,Perforation: appendix might be compressible
  • Free fluid surrounding appendix
  • The diameter of the appendix > 6 mm
  • Local abscess formation
  • Single wall thickness ≥ 3 mm
  • Increased echogenicity of local mesenteric fat
Target sign:

  • Hypoechoic fluid-filled lumen
  • Hyperechoic mucosa/submucosa
  • Hypoechoic muscular layer
  • Enlarged local mesenteric lymph nodes
Appendicolith: hyperechoic with posterior shadowing
  • Thickening of the peritoneum
  • Colour Doppler and the contrast-enhanced US:
  • Hypervascularity in the early stages of AA
  • Hypo- to avascularity in abscess and necrosis
  • Signs of secondary small bowel obstruction

Diagnosis of Appendicitis

Clinical

  • Aure-Rozanova’s sign – Increased pain on palpation with finger in right Petit triangle (can be a positive Shchetkin-Bloomberg’s).[rx]
  • Bartomier-Michelson’s sign – Increased pain on palpation at the right iliac region as the person being examined lies on his or her left side compared to when he/she lies on the back.[rx]
  • Dunphy’s sign – Increased pain in the right lower quadrant with coughing.[rx]
  • Hamburger sign -The patient refuses to eat (anorexia is 80% specific for appendicitis)[rx]
  • Kocher’s (Kosher’s) sign – From the person’s medical history, the start of pain in the umbilical region with a subsequent shift to the right iliac region.[rx]
  • Massouh sign – Developed in and popular in southwest England, the examiner performs a firm swish with his or her index and middle finger across the abdomen from the xiphoid process to the left and the right iliac fossa. A positive Massouh sign is a grimace of the person being examined upon a right sided (and not left) sweep.[rx]
  • Obturator sign – The person being evaluated lies on her or his back with the hip and knee both flexed at ninety degrees. The examiner holds the person’s ankle with one hand and knee with the other hand. The examiner rotates the hip by moving the person’s ankle away from his or her body while allowing the knee to move only inward. A positive test is pain with internal rotation of the hip.[rx]
  • Psoas sign, also known as Obraztsova’s sign –  is right lower-quadrant pain that is produced with either the passive extension of the right hip or by the active flexion of the person’s right hip while supine. The pain that is elicited is due to inflammation of the peritoneum overlying the iliopsoas muscles and inflammation of the psoas muscles themselves. Straightening out the leg causes pain because it stretches these muscles while flexing the hip activates the iliopsoas and causes pain.[rx]
  • Rovsing’s sign – Pain in the lower right abdominal quadrant with continuous deep palpation starting from the left iliac fossa upwards (counterclockwise along the colon). The thought is there will be increased pressure around the appendix by pushing bowel contents and air toward the ileocaecal valve provoking right-sided abdominal pain.[rx]
  • Sitkovskiy (Rosenstein)’s sign – Increased pain in the right iliac region as the person is being examined lies on his/her left side.[rx]

Investigation of acute appendicitis

  • Urine analysis—up to 40% can have abnormalities
  • Pregnancy test—to exclude pregnancy
  • Full blood count—neutrophil (> 75%) predominant leucocytosis is present in 80-90%
  • C reactive protein—raised concentration may be present, but its absence should not exclude a diagnosis of appendicitis
  • White Blood Cell Count (WBC) –Although an increase in peripheral WBC with a left shift may be the earliest marker of inflammation, its presence or absence is not significant enough to diagnose or exclude acute appendicitis. Many patients with gastroenteritis, mesenteric adenitis, pelvic inflammatory disease, and many other conditions have an elevated WBC. A normal WBC is also not uncommon in patients with appendicitis.
  • Urinalysis – Urinalysis is usually normal but may not be due to the inflamed appendix sitting on the ureter or bladder.

Differential diagnosis of acute appendicitis

Surgical

  • Intestinal obstruction
  • Intussusception
  • Acute cholecystitis
  • Perforated peptic ulcer
  • Mesenteric adenitis
  • Meckel’s diverticulitis
  • Colonic/appendicular diverticulitis
  • Pancreatitis
  • Rectus sheath haematoma

Urological

  • Right ureteric colic
  • Right pyelonephritis
  • Urinary tract infection

Gynaecological

  • Ectopic pregnancy
  • Ruptured ovarian follicle
  • Torted ovarian cyst
  • Salpingitis/pelvic inflammatory disease

Medical

  • Gastroenteritis
  • Terminal ileitis
  • Diabetic ketoacidosis
  • Preherpetic pain on the right 10th and 11th dorsal nerves
  • Porphyria

Imaging and diagnosis of acute appendicitis

Investigation Diagnostic criteria Evidence
Plain radiography None No role in diagnosis of acute appendicitis,w6although in some cases a faecolith may be shown
Ultrasonography Aperistaltic and non-compressible structure with diameter >6 mmw8 Sensitivity of 86%; specificity of 81%
Computed tomography scanning Abnormal appendix identified or calcified appendicolith seen in association with periappendiceal inflammation or diameter >6 mmw8 Sensitivity of 94% and specificity of 95% in diagnosis of acute appendicitis
Magnetic resonance imaging Not confirmed Restricted to cases in which radiation and diagnostic difficulties preclude use of other modalities (for example, pregnancy)

Ultrasound (US)

Use of ultrasound is increasing, particularly in children in whom the risks of ionizing radiation are greatest. The advantages include decreased cost relative to other imaging modalities and lack of ionizing radiation exposure. However, it is operator-dependent.

The visualization of a thickened, non-compressible appendix greater than 6 mm in diameter is diagnostic. If the US is non-diagnostic, further imaging with CT or MRI, particularly in pregnancy, is required. In practice, a positive ultrasound can be used to reduce CT scan utilization. However, a negative or non-diagnostic result is not sufficient to rule out appendicitis. During childbearing age, it can be helpful to exclude a tubo-ovarian abscess.

CT Scan

CT of the abdomen and pelvis is considered the modality of choice for definitive assessment of patients being evaluated for possible appendicitis. However, a major concern with CT scan is radiation exposure, particularly in children. Practitioners should, therefore, use these scans judiciously. Limited-range CT scans have been proposed in children to reduce the radiation dose. The following findings may be seen:

  • Dilated appendix greater than 6 mm with a thickened wall (greater than 2 mm)
  • Peri-appendiceal inflammation (peri-appendiceal fat stranding)
  • Appendicolith
  • Appendiceal or abscess
  • Free fluid

If the practitioner does not visualize the appendix, appendicitis is not ruled out.

MRI

MRI is a reliable modality which is particularly useful for pregnant women and children when ultrasound is inconclusive. Since intravenous (IV) gadolinium can cross the placenta, it should not be used during pregnancy. Also, patients with renal insufficiency should not receive IV gadolinium.

The following factors limit MRI use:

  • Higher cost
  • More time required to acquire images
  • Skilled radiologist required to interpret MRI
  • Not widely available

Also, MRI is not a test of choice for unstable patients and young children in whom sedation may be required. In recent years, the utility of rapid MRI without contrast agents or sedation has been assessed for a diagnosis of pediatric appendicitis.

Treatment of Appendicitis

If practitioners are evaluating the patient for appendicitis, they should also obtain an early surgical consultation.Intravenously administer isotonic crystalloid fluid.

  • Antibiotic prophylaxis, which is coverage for gram-negative and gram-positive aerobic and anaerobic bacteria, and anaerobes (Bacteroides fragilis and Escherichia coli), is recommended. However, its administration should be timed in consultation with the surgical service to ensure that high antibiotic levels coincide with the operative procedure. Treat nonperforated appendicitis with cefoxitin or cefotetan.

In perforated appendicitis consider the following choices:

  • Carbapenem
  • Ticarcillin-clavulanate
  • Piperacillin-tazobactam
  • Ampicillin-sulbactam
  • Provide adequate analgesia
  • The primary treatment for appendicitis is surgery. Doctors should make operative decisions in con
  • Antibiotics are less effective if an appendicolith is present.[rx] Surgery is the standard management approach for acute appendicitis.[rx] The cost-effectiveness of surgery versus antibiotics is unclear.[rx]
  • Using antibiotics to prevent potential postoperative complications in emergency appendectomy procedures is recommended, and the antibiotics are effective when given to a person before, during, or after surgery.[rx]
  • Pain medications (such as morphine) do not appear to affect the accuracy of the clinical diagnosis of appendicitis and therefore should be given early in the patient’s care.[rx] Historically there were concerns among some general surgeons that analgesics would affect the clinical exam in children, and some recommended that they not be given until the surgeon was able to examine the person.[rx]

Surgery of Appendicitis

Health care professionals call the surgery to remove the appendix an appendectomy. A surgeon performs the surgery using one of the following methods:

  • Laparoscopic surgery – During laparoscopic surgery, surgeons use several smaller incisions and special surgical tools that they feed through the incisions to remove your appendix. Laparoscopic surgery leads to fewer complications, such as hospital-related infections, and has a shorter recovery time.
  • Laparotomy – Surgeons use laparotomy to remove the appendix through a single incision in the lower right area of your abdomen.

Surgery versus antibiotics

We found three systematic reviews (each with a search date of 2011). The three reviews reported many of the same RCTs, but in different combinations (see Further information on studies). Each review reported a synthesis of different outcome measures and came to different conclusions; therefore, we have reported all three reviews here to cover the full spectrum of evidence.

Treatment success

Surgery compared with antibiotics Appendicectomy may be more effective than antibiotics at reducing treatment failure including recurrence at up to 1 year, but may be less effective at reducing some complications in adults with uncomplicated acute appendicitis. However, the evidence is weak and results varied by outcome measured (very low-quality evidence).

Ref (type) Population Outcome, Interventions Results and statistical analysis Effect size Favours
Treatment success
Systematic review Adults with acute uncomplicated appendicitis (no abscess or phlegmon)
5 RCTs in this analysis
Initial treatment failure (antibiotic: failure to achieve definite improvement without the need for surgery and hospital discharge without an operation; appendicectomy: failure to achieve pathologically confirmed appendicitis after surgery or another surgical indication for operation)
40/470 (9%) with appendicectomy
137/510 (27%) with antibiotics
OR 2.43
95% CI 0.94 to 6.33
P = 0.07
Significant heterogeneity: I² = 69%, P = 0.01
Heterogeneity not further explained
Not significant
Systematic review Adults with suspected acute uncomplicated appendicitis (no abscess or phlegmon)
5 RCTs in this analysis
Overall treatment failure (initial treatment failure plus anyone in the antibiotic group requiring appendicectomy because of recurrence) up to 1 year
40/470 (9%) with appendicectomy
205/510 (40%) with antibiotics
OR 6.72
95% CI 3.48 to 12.99
P <0.00001
Moderate effect size appendicectomy
Systematic review Adults with acute uncomplicated appendicitis (no abscess or phlegmon)
5 RCTs in this analysis
Overall complications (e.g., surgical site infection, organ space infection, small bowel obstruction, other)
60/510 (12%) with antibiotics
83/470 (18%) with appendicectomy
OR 0.54
95% CI 0.37 to 0.78
P = 0.001
Small effect size antibiotics
Systematic review Mainly adults, mean age 28.2 years (range 13–75 years), suspected acute appendicitis based on disease history, clinical status, and laboratory findings
5 RCTs in this analysis
Mean cure (within 2 weeks [free of symptoms such as abdominal pain, fever, inflammatory parameters] and without major complication [including recurrence] within 1 year)
97% with appendicectomy
73% with antibiotics
Absolute numbers not reported
The review pooled data for each group and calculated 95% CI
Appendicectomy: 97% (95% CI 94% to 99%)
Antibiotics: 73% (95% CI 63% to 82%)
Mean cure rates were higher with appendicectomy, but the review did not report a between-group P value
Systematic review Mainly adults, mean age 28.2 years (range 13–75 years), suspected acute appendicitis based on disease history, clinical status, and laboratory findings
5 RCTs in this analysis
No major complications (including the need for further [invasive] treatment or prolonged admission [e.g., abscesses, ileus, deep wound infection, recurrence, re-operation, secondary perforation])
97% with appendicectomy
83% with antibiotics
Absolute numbers not reported
The review pooled data for each group and calculated 95% CI
Appendicectomy: 97% (95% CI 93% to 99%)
Antibiotics: 83% (95% CI 72% to 91%)
Proportion of people with no major complications was higher with appendicectomy, but the review did not report a between-group P value
Systematic review Mainly adults, mean age 28.2 years (range 13–75 years), suspected acute appendicitis based on disease history, clinical status, and laboratory findings
5 RCTs in this analysis
No minor complications (e.g., superficial wound infections, negative appendix at histology [no appendicitis], diarrhoea, urinary tract infection)
91% with appendicectomy
96% with antibiotics
Absolute numbers not reported
The review pooled data for each group and calculated 95% CI
Appendicectomy: 91% (95% CI 83% to 96%)
Antibiotics: 96% (95% CI 93% to 97%)
Proportion of people with no minor complications was higher with antibiotics, but the review did not report a between-group P value
Systematic review Adults with a diagnosis of uncomplicated acute appendicitis Complications (antibiotics: perforated or gangrenous appendix, peritonitis, or wound infection [in people who failed antibiotics and had appendicectomy subsequently]; appendicectomy: perforated appendicitis, peritonitis, or wound infection)
84/470 (18%) with antibiotics
108/430 (25%) with appendicectomy
RR 0.69
95% CI 0.54 to 0.89
P = 0.004
Small effect size antibiotics
Systematic review Adults with a diagnosis of uncomplicated acute appendicitis Risk of complicated appendiciti
54/470 (11%) with antibiotics
131/430 (31%) with appendicectomy
RR 0.46
95% CI 0.19 to 1.12
P = 0.09
Significant heterogeneity: I² = 82%, P <0.001
A sensitivity analysis removing 1 RCT with high crossover found a similar result, but there was still significant heterogeneity among groups (RR 0.58, 95% CI 0.18 to 1.90; I² = 74%)
Not significant

Mortality (from appendicitis)

Surgery compared with antibiotics We don’t know whether appendicectomy and antibiotics differ in effectiveness at reducing mortality from appendicitis in adults with uncomplicated acute appendicitis (very low-quality evidence).

Ref (type) Population Outcome, Interventions Results and statistical analysis Effect size Favours
Mortality
Systematic review Adults with acute uncomplicated appendicitis(no abscess or phlegmonrx)
5 RCTs in this analysis
Mortality 
with antibiotics
with appendicectomy

No data from the following reference on this outcome.

Length of hospital stay

Surgery compared with antibiotics We don’t know whether appendicectomy and antibiotics differ in effectiveness at reducing length of hospital stay in adults with uncomplicated acute appendicitis (rx).

Ref (type) Population Outcome, Interventions Results and statistical analysis Effect size Favours
Length of hospital stay
Systematic review Mainly adults, mean age 28.2 years (range 13–75 years), suspected acute appendicitis based on disease history, clinical status, and laboratory findings
4 RCTs in this analysis
Duration of hospital stay days 
with antibiotics
with appendicectomy
Mean difference 0.66 days
95% CI 0.44 days to 0.87 days
P <0.0001
1 RCT in the review was not included in the analysis; the review reported this was based on visual inspection, but did not report any further reason for its exclusion
Effect size not calculated appendicectomy
Systematic review Adults with a diagnosis of uncomplicated acute appendicitis Length of primary hospital stay, days (antibiotics: days of admission for people treated with antibiotics and discharged with antibiotics; appendicectomy: days of admission for people treated with appendicectomy and discharged with further follow-up)
with antibiotics
with appendicectomy
Mean difference +0.20 days
95% CI –0.16 days to +0.87 days
P = 0.29
Not significant
Systematic review Adults with acute uncomplicated appendicitis[rx] (no abscess or phlegmon)
5 RCTs in this analysis
Length of hospital stay days 
with antibiotics
with appendicectomy
Mean difference +0.34 days
95% CI –0.06 days to +0.73 days
P = 0.09
Not significant

Return to normal activities

Surgery compared with antibiotics Antibiotics may be more effective than appendicectomy at reducing the duration of sick leave or disability in adults with uncomplicated acute appendicitis. However, results vary based on the analysis performed (rx).

Ref (type) Population Outcome, Interventions Results and statistical analysis Effect size Favours
Sick leave days
Systematic review Mainly adults, mean age 28.2 years (range 13–75 years), suspected acute appendicitis based on disease history, clinical status, and laboratory findings
2 RCTs in this analysis
Duration of sick leave days 
with antibiotics
with appendicectomy
Mean difference –0.69 days
95% CI –1.65 days to +0.27 days
Not significant
Systematic review Adults with acute uncomplicated appendicitis[rx] (no abscess or phlegmon)
3 RCTs in this analysis
Duration of sick leave or disability 
with antibiotics
with appendicectomy
Standard mean difference –0.19
95% CI –0.06 to –0.33
P = 0.005
Effect size not calculated antibiotics

Quality of life

No data from the following reference on this outcome.

Adverse effects

Ref (type) Population Outcome, Interventions Results and statistical analysis Effect size Favours
Adverse effects
Systematic review Mainly adults, mean age 28.2 years (range 13–75 years), suspected acute appendicitis based on disease history, clinical status, and laboratory findings Adverse effects 
with antibiotics
with appendicectomy
Systematic review Adults with a diagnosis of uncomplicated acute appendicitis Re-admissions with recurrence of symptoms 
with antibiotics
with appendicectomy
Significance not reported
Systematic review Adults with acute uncomplicated appendicitis (no abscess or phlegmon)
5 RCTs in this analysis
Recurrence of symptoms 
with antibiotics
with appendicectomy

References

Appendicitis Early Signs Symptoms,

Hair, Skin Care; The Best Health Tips for Hair and Skin

Hair, Skin Care The Best Health Tips for Hair and Skin. Hair is a protein filament that grows from follicles found in the dermis. Hair is one of the defining characteristics of mammals. The human body, apart from areas of glabrous skin, is covered in follicles which produce thick terminal and fine vellus hair. The most common interest in hair is focused on hair growth, hair types, and hair care, but hair is also an important biomaterial primarily composed of protein, notably alpha-keratin.

Attitudes towards different hair, such as hairstyles and hair removal, vary widely across different cultures and historical periods, but it is often used to indicate a person’s personal beliefs or social position, such as their age, sex, or religion.

How you wash your hair and the products you use can go a long way toward maintaining smooth, shiny hair. Follow these simple tips from dermatologists to maintain healthy hair.

  1. Wash oily hair more frequently. How often you wash your hair should be based on how much oil your scalp produces.
    • If your scalp is oily, you may need to wash it as often as once a day.
    • If you have chemically treated hair, your hair may be drier, so you may want to wash it less frequently.
    • As you get older, your scalp makes less oil, so you may not need to shampoo as often. But if you see flakes in your hair, you may not be shampooing enough. This can lead to dandruff and other scalp diseases.
  • Concentrate shampoo on the scalp. When washing your hair, concentrate on cleaning primarily the scalp, rather than washing the entire length of hair. Washing only your hair can create flyaway hair that is dull and coarse.
  • Use conditioner- after every shampoo unless you use a “2-in-1” shampoo, which cleans and conditions hair. Using a conditioner can significantly improve the look of damaged or weathered hair by increasing shine, decreasing static electricity, improving strength and offering some protection from harmful UV rays.
  • Concentrate conditioner on the tips of the hair. Because conditioners can make fine hair look limp, they only should be used on the tips of the hair and not on the scalp or length of the hair.
  • Choose a shampoo and conditioner formulated specifically for your hair type. For example, if you color your hair, use a shampoo designed for color-treated hair. If your hair is damaged or chemically treated, consider a “2-in-1” shampoo. Regardless of cost, many shampoos and conditioner brands provide the same benefits.
  • Protect hair when swimming – Protect your hair from the damaging effects of chlorine by wetting and conditioning your hair before swimming. Wear a tight-fitting swim cap and use a specially formulated swimmers shampoo and deep conditioner after swimming to replace lost moisture.
  • Choose your face wash smartly – an appropriate face wash meant for your skin type and wash twice a day. Go for cleansers. Use cleansers at night to remove make-up and dirt before using a face wash.
  • Hold onto sunscreens – Use sunscreen every day even if you are indoors – the sun’s UVA rays come through windows too and contribute to aging, pigmenting and tanning. Ideally, sunscreen should be applied every three hours.
  • But not just any Sunscreen should have an SPF of 30 or more. SPF is the degree of protection against UVB rays, hence sunscreen must have UVA protection as well. The usual UVA protection ingredients are Avobenzone, Titanium dioxide, Zinc oxide, Mexoryl and Tinosorb.
  • Protect your skin from the sun Make-up products like foundations, mineral powders and compacts do not have adequate sun protection.
  • Tanning is not equal to pigmentation – Indian skin tends to tan and pigment easily and patchily. There is a very thin line between tanning and pigmentation. If your tan hasn’t gone in 4-6 weeks, see a dermatologist.It is advisable to use mild skin lightening creams as prevention. Look for botanical ingredients like Arbutin, Bearberry, Licorice, Mulberry, Ginseng, Gingko, Emblica, Turmeric – Curcuma, Grapeseed and vitamins like C and A, and Niacinamide.
  • Delay your aging -aging can be intrinsic, i.e. genetic, and can be delayed by exercise and, to a lesser extent, through diet. Extrinsic factors include increased UV intensity, increased pollution as well as stress. All these factors tend to dry the skin and make it more prone to pigmentation and aging. Hence it is important to start caring for your skin in your teens.
  • Go for antioxidants –Extrinsic factors produce Reactive Oxygen Species (ROS), which are naughty oxygen molecules that damage the cells and make them age faster. Anti-oxidants neutralize these ROS.
  • Night care – At night, use a moisturizer with an age-protecting agent to complete your ‘skin tips’ list.
  • Antioxidants – For younger skin, look for ingredients with antioxidants like vitamins C, E or a whole range of botanicals like green tea, grapeseed or pomegranate extract, curcumin, etc. You might also like to look out for the following: Genistein, ECGC, Resveratrol, Idebenone and Coenzyme Q10 or CoQ10.
  • Skin care for older skin –For older skin, you cannot just follow any skin tips. Look for the following ingredients: peptides, vitamin A and derivatives like retinol and other retinoids, Alpha, beta and polyhydroxy acids.

The most important beauty foods

Deficiency in any nutrient will cause changes in the skin, hair, and nails, as well as in blood circulation, which supplies nutrients to the skin and removes toxic waste products, Somer explains. Here are the most important things we need and what happens when we don’t get enough

  • Antioxidants: This help protect the skin from free-radical damage (which can cause rough texture, wrinkles and sunspots), but frequent sun exposure and smog deplete them. Since it takes up to three months to accumulate antioxidants in the skin, load up on colorful fruits and vegetables every day.
  • Zinc: This trace mineral helps maintain collagen and elastin fibers that give skin its firmness and help prevent sagging and wrinkles. Zinc is important in healing cuts and scrapes, while a deficiency causes dry, rough skin.
  • B vitamins: Poor intake of almost any B vitamin can cause dry or scaly skin, itching and a burning sensation. Vitamins B2 and B6 also are important in maintaining the oil-producing glands, which keep skin moist and smooth.
  • Vitamin A: This fat-soluble vitamin is essential for maintaining epithelial tissues, and skin is the largest epithelial tissue you have. Skimp on this vitamin and your skin might be dry, scaly and rough.

Why vegetables are so crucial

According to popular registered dietitians and personal trainers, The Nutrition Twins, veggies are naturally rich in water, so they create moisture within your skin, plumping the cells and filling the crevices. “Think of them as your body’s natural lotion, plus a whole lot more.”

Here’s what else they’ve got

Vitamin C – Keeps skin youthful and elastic by aiding in collagen formation. Think tomatoes, cucumbers, bell peppers, broccoli, and potatoes.

Beta-carotene – Helps give a healthy glow and hue, while protecting skin from sun damage. Go for: carrots, spinach, sweet potatoes, butternut squash, and other orange and green-colored produce.

Antioxidants  –  Guard against premature aging by helping to prevent cell damage. They mop up free radicals, including those caused by pollution and other environmental toxins, stress and the sun. Eat up: most veggies.

Omega-3s – Contain powerful anti-inflammatory compounds that give skin a smoother appearance. Great source: cabbage.

Water and potassium-rich: Keeps skin hydrated and restores fluid balance so it doesn’t look wrinkled and withered. Indulge in: most veggies.

Improve Your Diet

Step 1

Remove refined sugar from your diet to prevent yeast infections on your skin and nails. Choose whole grains such as brown rice and oats over processed white flour to improve the health of your skin.

Step 2

Limit the amount of fats you get from animal sources such as red meat and dairy. Saturated fat can cause inflammation of the skin. Instead, add healthy fats from pumpkin seeds and fish to your diet to moisturize your hair, skin and nails and prevent dryness and flaky skin.

Step 3

Get your protein from lean sources, such as white-meat poultry, fish and beans. Beans are an especially good source of fiber, a substance that promotes intestinal health, leading to healthy, glowing skin.

Step 4

Drink plenty of water. The Food Doctor website recommends drinking 8 cups of plain water per day. Drinking extra water promotes kidney health and flushes toxins from the body, resulting in healthy skin, hair and nails.

Make Lifestyle Changes

Step 1

Relieve anxiety and minimize stress. Reducing stress in your life can help your skin appear healthier, according to the Food Doctor website. Consider doing some meditation and deep breathing promote health skin.

Step 2

Engage in moderate exercise. Aerobic exercise increases blood flow throughout your body, bringing better circulation to your scalp, fingers and skin.

Step 3

Avoid toxins whenever possible. Choose organic foods when you can to improve your overall health.

Step 4

Stop smoking. If you are a smoker, quitting can greatly improve the health of your hair, skin and fingernails. Exposure to smoke prematurely ages your skin, makes your hair dull and destroys your fingernails.

Step 5

Protect your hair, skin and nails to keep them healthy. Apply moisturizer daily to combat dryness. The Science Daily website recommends using sunblock when you go outside to prevent wrinkles.

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