Formulary
Prednisolone: Uses, Dosing, Side Effects and Indian Brand Names
Prednisolone is the most widely used oral glucocorticoid, acting by suppressing NF-kB-mediated inflammation and immune responses. It is used across autoimmune, allergic, and oncological conditions but causes Cushing syndrome and HPA axis suppression with chronic use.
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Prednisolone: Uses, Dosing, Side Effects and Indian Brand Names
Prednisolone is the most widely used oral glucocorticoid, acting by suppressing NF-kB-mediated inflammation and immune responses. It is used across autoimmune, allergic, and oncological conditions but causes Cushing syndrome and HPA axis suppression with chronic use.
NEET PG High-Yield: Prednisolone is first-line for childhood nephrotic syndrome (ISKDC protocol). Key side effects for exams: Cushing syndrome, osteoporosis, steroid-induced diabetes, posterior subcapsular cataract, avascular necrosis of femoral head, and adrenal suppression. Never stop abruptly after >2-3 weeks (adrenal crisis). Prednisolone is preferred in hepatic impairment (prednisone needs hepatic activation).
Clinical overview
Prednisolone is the most commonly used oral glucocorticoid in India and is a cornerstone drug across virtually every medical specialty. It has intermediate duration of action (biological half-life 12-36 hours) and moderate mineralocorticoid activity. It is approximately 4 times more potent than hydrocortisone as an anti-inflammatory agent. Prednisolone is preferred over prednisone in patients with hepatic impairment because prednisone requires hepatic conversion to prednisolone (its active form). Clinical uses span an enormous range: autoimmune diseases (SLE, rheumatoid arthritis, inflammatory bowel disease, autoimmune hepatitis), allergic conditions (severe asthma, anaphylaxis adjunct), haematological malignancies (ALL, lymphomas), organ transplant rejection, nephrotic syndrome in children, and inflammatory eye diseases. The Cushing syndrome features of chronic glucocorticoid use -- moon face, central obesity, buffalo hump, striae, osteoporosis, diabetes, and adrenal suppression -- are the most important adverse consequences. The hypothalamic-pituitary-adrenal (HPA) axis is suppressed after more than 2-3 weeks of supraphysiological doses, and abrupt withdrawal can precipitate adrenal crisis. Tapering schedules are essential. In Indian paediatric practice, prednisolone is the first-line drug for nephrotic syndrome (ISKDC protocol: 2 mg/kg/day for 6 weeks, then alternate-day tapering).
Pharmacological class
Prednisolone belongs to the Glucocorticoid (synthetic corticosteroid) class. Prednisolone binds to intracellular glucocorticoid receptors (GRs), forming a hormone-receptor complex that translocates to the nucleus. It modulates gene transcription by two main mechanisms: transactivation (inducing anti-inflammatory proteins like lipocortin-1/annexin A1, which inhibits phospholipase A2) and transrepression (suppressing NF-kB and AP-1 transcription factors, reducing expression of pro-inflammatory cytokines, COX-2, iNOS, and adhesion molecules). The net effect is broad-spectrum suppression of inflammation and immunity.
Indian brand names and formulations
Available as: Omnacortil (Macleods Pharmaceuticals), Wysolone (Pfizer/Upjohn), Hostacortin (Sanofi India), Predsol (GlaxoSmithKline).
Tablets (5 mg, 10 mg, 20 mg, 40 mg), Oral solution (15 mg/5 mL), Eye drops (1%, 0.5%), Rectal foam/enemas (for ulcerative colitis), Injection (IV -- methylprednisolone is more commonly used for IV pulse therapy)
Regulatory status
Prednisolone is classified under Schedule H in India under the Drugs and Cosmetics Act, 1940. Schedule H prescription drug. NLEM 2022 listed. Chronic use requires monitoring for hyperglycaemia, osteoporosis, hypertension, and adrenal suppression. Steroid card/alert is recommended for chronic users.
Indications
- Autoimmune diseases (SLE, rheumatoid arthritis, vasculitis, autoimmune hepatitis)
- Nephrotic syndrome (first-line in children -- ISKDC protocol)
- Allergic conditions (severe asthma exacerbation, anaphylaxis adjunct)
- Inflammatory bowel disease (Crohn's disease, ulcerative colitis flares)
- Haematological malignancies (ALL, lymphomas -- part of chemotherapy protocols)
- Organ transplant rejection (acute)
- Adrenal insufficiency (physiological replacement -- hydrocortisone preferred)
- Cerebral oedema (dexamethasone preferred for tumours)
- Dermatological conditions (pemphigus, severe eczema)
- Eye inflammation (uveitis -- topical and systemic)
Dosing
Variable by indication. General: 0.5-2 mg/kg/day in divided doses for acute conditions, then taper. Nephrotic syndrome (children): 2 mg/kg/day (max 60 mg) for 6 weeks, then 1.5 mg/kg alternate days for 6 weeks (ISKDC protocol). Asthma exacerbation: 40-50 mg/day for 5-7 days. SLE: 0.5-1 mg/kg/day initially, taper to lowest effective dose. Physiological replacement: 5 mg/day (equivalent to hydrocortisone 20 mg). Tapering: reduce by 5-10 mg every 1-2 weeks when dose >20 mg/day; by 2.5 mg when <20 mg/day. NEVER stop abruptly after >2-3 weeks of use.
Contraindications
- Systemic fungal infections
- Live vaccine administration (immunosuppressive doses)
- Ocular herpes simplex (risk of corneal perforation)
- Untreated infections (masks symptoms, worsens sepsis)
- Psychotic tendencies (relative -- steroids can worsen psychosis)
Adverse effects
- Cushing syndrome (moon face, buffalo hump, central obesity, striae, thin skin)
- Adrenal suppression and adrenal crisis on abrupt withdrawal
- Osteoporosis (inhibits osteoblasts, promotes osteoclast activity)
- Steroid-induced diabetes mellitus (hepatic gluconeogenesis, peripheral insulin resistance)
- Peptic ulcer disease (especially with concomitant NSAIDs)
- Immunosuppression and increased infection risk (including opportunistic -- tuberculosis reactivation in India)
- Posterior subcapsular cataract
- Growth retardation in children
- Myopathy (proximal muscle weakness)
- Psychiatric effects (euphoria, insomnia, psychosis -- 'steroid psychosis')
- Hypertension and sodium/water retention
- Avascular necrosis of femoral head
Drug interactions
- NSAIDs -- additive GI ulceration risk
- CYP3A4 inducers (rifampicin, phenytoin) -- reduce prednisolone levels (may need dose increase with concurrent anti-TB therapy)
- Live vaccines -- contraindicated during immunosuppressive doses
- Oral anticoagulants (warfarin) -- variable effect on INR; monitor closely
- Antidiabetic drugs -- prednisolone antagonises their effect; dose adjustment needed
- Diuretics (thiazide, loop) -- additive hypokalaemia
Pregnancy and lactation
Category C. Prednisolone crosses the placenta poorly (inactivated by placental 11-beta-hydroxysteroid dehydrogenase), making it preferred over dexamethasone/betamethasone when treating maternal conditions. High doses in the first trimester carry a small increased risk of cleft palate. Used for many maternal conditions where benefit outweighs risk (SLE flares, asthma, etc.). For fetal lung maturation, betamethasone or dexamethasone (which DO cross the placenta effectively) are used instead.
Exam-style clinical scenario
A 4-year-old boy presents with generalised oedema (periorbital puffiness worse in the morning, scrotal oedema, ascites), massive proteinuria (40 mg/m2/hour), serum albumin 1.8 g/dL, and normal renal function. What is the first-line treatment? Answer: This is nephrotic syndrome (most likely minimal change disease in this age group). First-line treatment is oral prednisolone per the ISKDC protocol: 2 mg/kg/day (max 60 mg/day) for 6 weeks, followed by 1.5 mg/kg on alternate days for 6 weeks, then gradual taper. About 85-90% of children with minimal change disease respond to steroids (steroid-sensitive nephrotic syndrome). Renal biopsy is NOT indicated first-line in children 1-8 years with typical presentation.
Cost in India
INR 15-40 per strip of 10 tablets (5 mg); INR 20-50 per strip (10 mg); INR 30-70 per strip (20 mg)
Clinical governance
Author: MedNext Editorial Team. Clinical reviewer: Awaiting clinical review. Jurisdiction: India (Drugs and Cosmetics Act, 1940). Sources: CIMS India, Indian Pharmacopoeia. Publication state: Awaiting clinical review. Correction: Report errors at support@mednext.academy.
Frequently Asked Questions
Why must prednisolone be tapered and not stopped abruptly?
Chronic supraphysiological glucocorticoid administration suppresses the hypothalamic-pituitary-adrenal (HPA) axis through negative feedback. The adrenal glands atrophy from disuse, and abrupt withdrawal leaves the patient with inadequate endogenous cortisol production, precipitating acute adrenal crisis (hypotension, shock, hypoglycaemia, electrolyte disturbances, potentially fatal). Gradual tapering allows the HPA axis to recover over weeks to months.
Why is prednisolone preferred over prednisone in liver disease?
Prednisone is a prodrug that requires hepatic 11-beta-hydroxysteroid dehydrogenase type 1 to convert it to the active form, prednisolone. In severe hepatic impairment, this conversion is impaired, leading to subtherapeutic drug levels. Prednisolone is already in its active form and does not require hepatic activation, making it the preferred choice in patients with significant liver disease.
How do corticosteroids cause osteoporosis?
Glucocorticoids cause osteoporosis through multiple mechanisms: (1) Direct inhibition of osteoblast function and promotion of osteoblast apoptosis, (2) Promotion of osteoclastogenesis via RANKL upregulation and OPG downregulation, (3) Reduced intestinal calcium absorption and increased renal calcium excretion, (4) Decreased gonadal hormone production (secondary hypogonadism), (5) Reduced muscle mass (sarcopenia reduces mechanical loading on bone). Bone loss is most rapid in the first 6-12 months. Calcium, vitamin D, and bisphosphonate prophylaxis should be considered for patients on long-term steroids.
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