(hydrocortisone · DailyMed)
NETRACORT SKIN OINTMENT
HYDROCORTISONE
What it does
Hydrocortisone is a corticosteroid used to reduce inflammation and treat various conditions.
Commonly used for: Inflammation, Allergic reactions, Skin conditions, Adrenal insufficiency (Addison's disease)
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Source: Pharmacy and Poisons Board · fetched 2026-01-28 21:09:41 · updated 2026-07-26 13:52:07
Drug Interactions
41Pharmacodynamic Warnings
Hydrocortisone appears in TABLE 17: Drugs that reduce serum potassium
Severe (1)
Mifamurtide - decreases efficacy
Corticosteroidsarepredictedtodecreasetheefficacyof mifamurtide.Avoid.rTheoretical
Moderate (20)
Corticosteroids - increases exposure
Dronedarone is predicted to increase the exposure to corticosteroids (methylprednisolone). Monitor and adjust dose.
Corticosteroids - increases concentration
Miconazole is predicted to increase the concentration of corticosteroids (methylprednisolone). Monitor and adjust dose.
Corticosteroids - increases exposure
Antifungals, azoles (fluconazole, isavuconazole, posaconazole) are predicted to increase the exposure to corticosteroids (methylprednisolone). Monitor and adjust dose.
Corticosteroids - decreases exposure
Cenobamate is predicted to decrease the exposure to corticosteroids (fluticasone). Adjust dose.
Corticosteroids - decreases efficacy
Mifepristone is predicted to decrease the efficacy of corticosteroids. Use with caution and adjust dose.
Unknown (20)
Aspirin - decreases concentration
Corticosteroids are predicted to decrease the concentration of aspirin (high-dose) and aspirin (high-dose) increases the risk of gastrointestinal bleeding when given with corticosteroids.
Choline Salicylate - decreases concentration
Corticosteroids are predicted to decrease the concentration of cholinesalicylate. Ciclesonide → see corticosteroids Ciclosporin → see TABLE 2 p. 1517 (nephrotoxicity), TABLE 16 p. 1521 (increased seru
Corticosteroids - increases exposure
Cobicistat is predicted to increase the exposure to corticosteroids (beclometasone) (risk with beclometasone is likely to be lower than with other corticosteroids).
Corticosteroids - increases risk of gastrointestinal perforation
Erlotinib is predicted to increase the risk of gastrointestinal perforation when given with corticosteroids.
Corticosteroids - increases exposure
Idelalisib is predicted to increase the exposure to corticosteroids (betamethasone, budesonide, ciclesonide, deflazacort, dexamethasone, fludrocortisone, fluticasone, hydrocortisone, methylprednisolon
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: class
About this medicine
Hydrocortisone is a corticosteroid used to reduce inflammation and treat various conditions.
What it treats
- Inflammation
- Allergic reactions
- Skin conditions
- Adrenal insufficiency (Addison's disease)
How it works
It works by decreasing inflammation and suppressing the immune system.
Who it's for
Hydrocortisone is for people dealing with severe inflammation or conditions related to hormone deficiency.
Drug class
Corticosteroids
Cautions
- • Be cautious if you are taking medications that lower potassium levels in your blood.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
Clinical monograph: Hydrocortisone
BNF-referencedHydrocortisone is a corticosteroid that exhibits both glucocorticoid and mineralocorticoid activities, making it effective in managing various inflammatory and autoimmune conditions. It is commonly used as a replacement therapy in adrenal insufficiency and as an anti-inflammatory agent in a range of disorders.
Indications
- Adrenocortical insufficiency
- Inflammatory bowel disease
- Severe acute asthma
- Acute hypersensitivity reactions
- Congenital adrenal hyperplasia
- Replacement therapy in adrenal insufficiency
Dosage
Children: For children aged 1-5 months: Initially 25 mg 3 times a day, adjusted according to response. For children aged 6 months-5 years: Initially 50 mg 3 times a day, adjusted according to response. For children aged 6-11 years: Initially 100 mg 3 times a day, adjusted
Adults: 100-500 mg 3-4 times a day or when required. For replacement in adrenocortical insufficiency, 20-30 mg once daily, adjusted according to response.
Mechanism of action
Hydrocortisone binds to the glucocorticoid receptor, leading to decreased vasodilation and permeability of capillaries, inhibition of leukocyte migration to inflammation sites, and changes in gene expression that promote anti-inflammatory pathways. It inhibits phospholipase A2, NF-kappa B, and other inflammatory transcription factors, stabilizing leukocyte lysosomal membranes and reducing the release of destructive enzymes. High doses can raise sodium levels and decrease potassium levels through mineralocorticoid receptor activity.
Pharmacodynamics
Hydrocortisone's pharmacodynamic profile includes the inhibition of various inflammatory mediators and the promotion of anti-inflammatory cytokines. Its effects are dose-dependent, with lower doses providing anti-inflammatory benefits, while higher doses exhibit immunosuppressive effects. It has a wide therapeutic index and moderate duration of action.
Pharmacokinetics
Hydrocortisone is metabolized primarily in the liver, with its effects lasting for several hours to days. The onset of action varies with the route of administration, being more rapid when given intravenously. Its half-life is influenced by factors such as dose and administration route, and it is excreted through urine as metabolites.
Contra-indications
- Systemic fungal infections
- Hypersensitivity to hydrocortisone or any excipients
Adverse effects
- Increased risk of infections
- Hyperglycemia
- Hypertension
- Fluid retention and edema
- Gastrointestinal disturbances
- Mood changes
- Osteoporosis
- Peptic ulcer disease
- Cushing's syndrome with long-term use
Interactions
- Mitotane: Moderate decrease in hydrocortisone exposure
- Rifampicin: Moderate decrease in hydrocortisone exposure
- Cobicistat: Unknown effect, potential increase in hydrocortisone exposure
- Idelalisib: Unknown effect, potential increase in hydrocortisone exposure
- Clarithromycin: Unknown effect, potential increase in hydrocortisone exposure
Precautions
- Use with caution in patients with diabetes
- Monitor for signs of infection during therapy
- Consider dose adjustment in patients with hepatic impairment
- Gradual withdrawal is recommended to avoid adrenal insufficiency after prolonged therapy
Pregnancy
Hydrocortisone is categorized as category C. Use only if the potential benefit justifies the potential risk to the fetus.
Breast-feeding
Hydrocortisone is excreted in breast milk. Caution is advised when administering to nursing mothers.
Storage
Store at room temperature, away from moisture and heat. Protect from light.
Formulations
- Injectable form (sodium succinate)
- Modified-release tablets
- Immediate-release tablets
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Molecular reference: Hydrocortisone
PubChem CID 5754Molecular formula: C21H30O5
Mechanism of action
The short-term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days. Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10. Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive. High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels. Following topical application, corticosteroids produce anti-inflammatory, antipruritic, and vasoconstrictor actions. The activity of the drugs is thought to result at least in part from binding with a steroid receptor. Corticosteroids decrease inflammation by stabilizing leukocyte lysosomal membranes, preventing release of destructive acid hydrolases from leukocytes; inhibiting macrophage accumulation in inflamed areas; reducing leukocyte adhesion to capillary endothelium; reducing capillary wall permeability and edema formation; decreasing complement components; antagonizing histamine activity and release of kinin from substrates; reducing fibroblast proliferation, collagen deposition, and subsequent scar tissue formation; and possibly by other mechanisms as yet unknown. Corticosteroids, especially the fluorinated corticosteroids, have antimitotic activity on cutaneous fibroblasts and the epidermis. /Corticosteroids/ 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 NFkappaB 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.
Pharmacodynamics
Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes. Hydrocortisone has a wide therapeutic index and a moderate duration of action. Patients should stop taking the medication if irritation or sensitization occurs.
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
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