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Hydrocortisone; Uses, Side Effects, Interactions, Pregnancy

Hydrocortisone is the main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is a Corticosteroid. The mechanism of action of hydrocortisone is as a Corticosteroid Hormone Receptor Agonist.

Therapeutic Hydrocortisone is a synthetic or semisynthetic analog of natural hydrocortisone hormone produced by the adrenal glands with primary glucocorticoid and minor mineralocorticoid effects. As a glucocorticoid receptor agonist, hydrocortisone promotes protein catabolism, gluconeogenesis, capillary wall stability, renal excretion of calcium, and suppresses immune and inflammatory responses.

Hydrocortisone is the name for the hormone cortisol when supplied as a medication. Uses include conditions such as adrenocortical insufficiency, adrenogenital syndrome, high blood calcium, thyroiditis, rheumatoid arthritis, dermatitis, asthma, and COPD. It is the treatment of choice for adrenocortical insufficiency.T he main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions.

Mechanism of action of Hydrocortisone

Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.

Reactive oxygen species (ROS) generation by polymorphonuclear leukocytes (PMNL) and mononuclear cells (MNC) is inhibited following the intravenous administration of hydrocortisone. This is associated with a parallel decrease in intranuclear NFkappaB, known to modulate inflammatory responses including ROS generation. Plasma levels of interleukin-10 (IL-10), an anti-inflammatory and immunosuppressive cytokine produced by TH2 cells, are also increased after hydrocortisone administration. In this study, we have investigated the effect of hydrocortisone on p47(phox) subunit, a key component of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, in MNC and the pharmacodynamics of this effect with ROS generation and plasma IL-10 levels /were investigated/. p47(phox) subunit protein levels in MNC showed a progressive decrease after hydrocortisone administration. It reached a nadir at 4 hours and increased thereafter to a baseline level at 24 hours. ROS generation also decreased, reached a nadir between 2 and 4 hours, and returned to a baseline level at 24 hours. IL-10 concentrations increased, peaked at 4 hours, and reverted to the baseline levels at 24 hours. In conclusion, p47(phox) subunit suppression may contribute to the inhibition of ROS generation in MNC after hydrocortisone administration. This suppression occurs in parallel with the suppression of NF-kappaB and an increase in IL-10 plasma levels. Therefore, it would appear that the decrease in intranuclear NFkappaB and an increase in IL-10 may cause the inhibitory modulation on p47(phox) subunit and ROS generation by MNC following hydrocortisone and other glucocorticoids.

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Indications of Hydrocortisone

Asthma, acute
Inflammatory Conditions
Adrenocortical Insufficiency
Addison’s Disease
Inflammatory Bowel Disease
Shock
Ulcerative Colitis
Ulcerative Proctitis
Acute Gouty Arthritis
Allergic Rhinitis (AR)
Allergic corneal marginal ulcers
Ankylosing Spondylitis (AS)
Anterior Segment Inflammation
Aspiration Pneumonitis
Asthma Bronchial
Atopic Dermatitis (AD)
Berylliosis
Bullous dermatitis herpetiformis
Congenital Adrenal Hyperplasia (CAH)
Conjunctivitis, Seasonal Allergic
Corneal Inflammation
Crohn’s Disease (CD)
Dermatitis, Contact
Dermatomyositis
Dermatosis
Drug hypersensitivity reaction
Epicondylitis
Erythroblastopenia
Hypercalcemia of Malignancy
Idiopathic Thrombocytopenic Purpura (ITP)
Iridocyclitis
Iritis
Leukemia, Acute
Leukemias
Loeffler’s syndrome
Malignant Lymphomas
Mycosis Fungoides (MF)
Ophthalmia, Sympathetic
Optic Neuritis
Pemphigus
Primary adrenocortical insufficiency
Proteinuria
Psoriatic Arthritis
Rheumatic heart disease, unspecified
Rheumatoid Arthritis
Rheumatoid Arthritis, Juvenile
Secondary adrenocortical insufficiency
Secondary thrombocytopenia
Serum Sickness
Severe Seborrheic Dermatitis
Stevens-Johnson Syndrome
Synovitis
Systemic Lupus Erythematosus (SLE)
Trichinosis
Tuberculous Meningitis
Ulcerative Colitis (UC)
Acquired immune hemolytic anemia
Acute Bursitis
Acute Tenosynovitis
Diffuse posterior uveitis
Disseminated Pulmonary Tuberculosis
Exfoliative erythroderma
Fulminating Pulmonary Tuberculosis
Non-suppurative Thyroiditis
Severe Psoriasis
Subacute Bursitis
Symptomatic Sarcoidosis
Systemic Dermatomyositis
Varicella-zoster virus acute retinal necrosis

Dosage of Hydrocortisone

Strengths: 10 mg; 20 mg; acetate 50 mg/mL; sodium phosphate 50 mg/mL;

Adrenocortical Insufficiency

Acute Adrenal Crisis

100 mg IV followed by IV infusion of 200 mg over 24 hours OR 50 mg IV every 6 hours; then 100 mg IV the following day

Management of Primary Adrenal Insufficiency (PAI)

15 mg to 25 mg orally in 2 or 3 divided doses per day
Highest dose should be given in the morning, then 2 hours after lunch (2-dose/day regimen) or at lunch and afternoon (3-dose/day regimen)

Prevention of Acute Adrenal Crisis

Adjust dose according to the severity of illness or magnitude of the stressor

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Anti-inflammatory

Dosing should be individualized on the basis of disease and patient response

Oral

Initial dose: 20 mg to 240 mg orally per day

Parenteral

Initial dose: 100 mg to 500 mg IV or IM; may repeat doses at intervals of 2, 4, or 6 hours as indicated by the response and clinical indication
Maintenance dose: After a favorable initial response, the dose should be decreased in small amounts to the lowest dose that maintains an adequate clinical response; if a positive response is not achieved after a reasonable period of time, alternative therapy should be sought.

Asthma

100 mg IV every 8 hours during the surgical period; dose should be rapidly reduced within 24 hours after surgery

Ulcerative Colitis

100 mg rectally (retention enema) nightly for 21 days or until both clinical and pathological remission occurs
Difficult cases may require 2 or 3 months of treatment

Multiple Sclerosis

Acute exacerbation: 800 mg oral/IV/IM once a day for 1 week followed by 320 mg oral/IV/IM every other day for 1 month

Pediatric Adrenocortical Insufficiency

Acute Adrenal Crisis

Initial dose: 2 to 3 mg/kg IV or intraosseous (IO) over 3 to 5 minutes; Maximum dose: 100 mg

Follow with

Infants: 1 to 5 mg/kg IV/IO every 6 hours
Children: 12.5 mg/m2 IV/IO every 6 hours OR 50 mg/m2 IV followed by 50 to 100 mg/m2 IV in divided doses every 6 hours or via 24-hour continuous IV infusion

Management of Primary Adrenal Insufficiency (PAI)

8 mg/m2 orally in 3 or 4 divided doses per day
Highest dose should be administered in the morning

Prevention of Acute Adrenal Crisis

Adjust dose according to the severity of illness or magnitude of the stressor

Side Effects of Hydrocortisone

The most common

Constipation
Burning or stinging
itching at the application site
Blistering, burning, crusting, dryness, or flaking of the skin
cracking or tightening of the skin
Euphoria
Adrenal suppression
Hypertension
Groupings of fine blood vessels becoming prominent under the skin,
dizziness
drowsiness
dry mouth
chest pain
a headache
joint painPain
dizziness
nausea and vomiting
Severe stomach ache
epigastric pain,
diarrhea,
anorexia,
flatulence,
a headache,
fainting, fast or pounding heartbeats.

More common

Fast or irregular heartbeat
fever
Back pain
dizziness
a headache
increased cough
Acid or sour stomach
decreased appetite
Agitation
chest congestion
chest pain
cold sweats
confusion
decreased sexual ability or desire
diarrhea or loose stools
heartburn
sleepiness or unusual drowsiness
stomach or abdominal cramps, gas, or pain
trouble sleeping

Less common

Abnormal dreams
change in sense of taste
congestion
discouragement, feeling sad, or empty
Suicide attempts
Acting on dangerous impulses
Aggressive or violent behavior
Thoughts about suicide or dying
New or worse depression
New or worse anxiety or panic attacks
Agitation, restlessness, anger, or irritability
Trouble sleeping

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Drug Interactions of Hydrocortisone

Hydrocortisone may interact with following drugs, supplements & may decrease the efficacy of the drug

chlorpromazine, clozapine, haloperidol, olanzapine, quetiapine, risperidone)
“azole” antifungals (e.g., itraconazole, ketoconazole, voriconazole)
itraconazole
medications applied to the skin that has irritating effects
other topical medications that contain corticosteroids
natalizumab
pimecrolimus
ritonavir
tacrolimus

Pregnancy & Lactation

FDA Pregnancy Category C

Pregnancy

The safety of using this medication during pregnancy has not been established. This medication should not be used during pregnancy unless the benefits outweigh the risks. If you become pregnant while taking this medication, contact your doctor immediately.

Lactation

It is not known if clioquinol – hydrocortisone passes into breast milk. If you are a breastfeeding mother and are using this medication, it may affect your baby. Talk to your doctor about whether you should continue breastfeeding.