Glucocorticoids
ATC code: H02AB06 (Prednisolone)
Binds intracellular glucocorticoid receptors, suppressing inflammatory and immune responses at multiple levels – inhibits transcription of pro-inflammatory cytokines, reduces leukocyte migration, and suppresses phospholipase A2 activity. Intermediate potency: 4 times more potent than hydrocortisone but weaker than dexamethasone. Duration of action 12-36 hours.
First line
A short course of systemic corticosteroids (5-7 days) is the standard of care for moderate-to-severe asthma exacerbations per . Prednisolone 40-50 mg daily in adults, 1-2 mg/kg in children. Start as early as possible during an exacerbation. Long-term systemic corticosteroid therapy for asthma is reserved for severe uncontrolled disease after all inhaled options are exhausted.
First line
Core drug for autoimmune disease flares – SLE, rheumatoid arthritis, vasculitis, autoimmune hepatitis. Acute situations require high doses (1 mg/kg daily) with subsequent gradual tapering. The goal is the lowest maintenance dose or full discontinuation to minimize cumulative toxicity.
First line
In anaphylaxis, epinephrine is first-line. Prednisolone is given as an adjunct to prevent biphasic reactions and suppress the late-phase allergic response. In severe drug reactions – Stevens-Johnson syndrome, serum sickness – it is used at high doses.
First line
In patients with COVID-19 and hypoxaemia or critical illness, corticosteroids reduce mortality. The RECOVERY trial (NEJM 2021, 6,425 participants) showed dexamethasone 6 mg daily for 10 days reduced mortality by 17 % on oxygen therapy and by 35 % on mechanical ventilation. Prednisolone 40–50 mg daily is used as the dexamethasone 6 mg equivalent (anti-inflammatory potency ratio 1:7). Living Guidelines and Russian Ministry of Health guidelines classify systemic corticosteroids as a strong recommendation for severe and critical disease. In outpatients without hypoxaemia, there is no benefit and potential harm: increased risk of secondary infections and delayed viral clearance.
Use is restricted to hospital setting and a specific group – patients with hypoxaemia (SpO2 below 94 %) or on mechanical ventilation. In outpatients with mild-to-moderate disease, glucocorticoids are not appropriate.
The drug is promoted for these uses outside international guidelines. Each entry below is analyzed against AEMPS, FDA, EMA, Cochrane and major RCTs.
Not recommended
Corticosteroids for "getting back on one's feet," chronic fatigue, subjective weakness, or asthenia are not supported by any international guideline. Short-term improvement on prednisolone is the drug's euphoric effect, not treatment of a cause. Upon discontinuation, state worsens below baseline due to withdrawal syndrome. Prolonged use produces cumulative complications: osteoporosis, steroid-induced diabetes, Cushing syndrome, adrenal insufficiency. Chronic fatigue requires differential workup: anaemia, B12 deficiency, hypothyroidism, depression, chronic infections – treat the cause.
Not recommended
Prednisolone and other systemic corticosteroids are not used for acute viral upper respiratory infections in any international guideline (, , , CDC, BMJ Best Practice). A viral infection without bacterial complication resolves in 5–10 days on its own. Systemic corticosteroids do not suppress the virus; they suppress the immune response and prolong viral shedding. Self-prescribed prednisolone «to recover faster» carries risks of secondary bacterial infections, hyperglycaemia, ulcer complications, and withdrawal syndrome on abrupt discontinuation.
Not recommended
Prednisolone for muscle gain reflects a fitness-community confusion between glucocorticoids and anabolic-androgenic steroids. These are entirely different drug classes. Glucocorticoids (prednisolone, dexamethasone, hydrocortisone) act on muscle catabolically: they break down muscle protein, induce steroid myopathy, and cause weakness predominantly in proximal groups. Anabolic muscle action belongs to testosterone, nandrolone, and other AAS – separate drugs with their own risks. Prednisolone for «bulking» produces the opposite: loss of muscle strength, fat mass gain, and Cushingoid fat redistribution.
14 pairs found. Sorted from critical to minor.
Mechanism
Prednisolone (a systemic glucocorticoid) modestly lowers the seizure threshold; bupropion also lowers it. The effect is clinically significant during prolonged high-dose prednisolone, especially with prior epilepsy.
Symptoms
Seizures (generalised tonic-clonic or focal). Agitation, anxiety, insomnia from both drugs are possible.
Management
Avoid the combination in patients with prior epilepsy. If unavoidable, do not increase bupropion dose and use prednisolone at the minimum effective dose. Alternative antidepressants without seizure threshold reduction: sertraline, escitalopram.
Mechanism
Additive tendon injury risk. Fluoroquinolones disrupt collagen synthesis in tendon fibres; glucocorticoids suppress repair. carries a boxed warning for tendinitis and Achilles tendon rupture.
Symptoms
Pain and swelling in the Achilles tendon (less often other large tendons). Sudden 'snap' and inability to bear weight indicates rupture. Symptoms typically appear within 1–4 weeks.
Management
Avoid the combination, especially in patients over 60 and athletes. Alternative antibiotics: a cephalosporin or nitrofurantoin (no tendon effect). If ciprofloxacin is needed, limit physical activity for the whole course and 1 month after.
Mechanism
Similar to ibuprofen – additive GI bleeding risk. Diclofenac has a higher ulcerogenic potential among NSAIDs.
Symptoms
Black or tarry stools (melena), vomiting blood or coffee-ground material, epigastric pain. Risk multiplies in older patients and with prior peptic ulcer disease.
Management
Avoid prolonged combination. If diclofenac is needed, use the minimum effective dose for 5–7 days with mandatory pantoprazole cover. For chronic analgesia: paracetamol or celecoxib.
Mechanism
Additive gastroesophageal ulcer and bleeding risk. Glucocorticoids reduce GI mucosal repair; NSAIDs block protective prostaglandins.
Symptoms
Black or tarry stools (melena), vomiting blood or coffee-ground material, epigastric pain. Risk multiplies in older patients and with prior peptic ulcer disease.
Management
Avoid prolonged combination. If ibuprofen is needed for a short course on prednisolone, use the minimum effective dose for 5–7 days with mandatory pantoprazole cover. For chronic analgesia: paracetamol or celecoxib.
Mechanism
Prednisolone (a systemic glucocorticoid) suppresses muscle glucose uptake and stimulates hepatic gluconeogenesis – steroid-induced diabetes develops or existing type 2 diabetes decompensates. Metformin offsets part of the effect but not all.
Symptoms
Hyperglycaemia: thirst, polyuria, fatigue, rising fasting glucose and . With high prednisolone doses: decompensation risk with ketoacidosis in type 1 diabetes.
Mechanism
Prednisolone (a systemic glucocorticoid) raises fibrinogen and clotting factors but can also alter warfarin metabolism through liver enzymes. The effect is unpredictable: INR may either drop or rise.
Symptoms
If INR drops: thromboembolic risk (deep vein thrombosis, stroke in atrial fibrillation). If INR rises: gum bleeding, epistaxis, bruising, GI bleeding (amplified by glucocorticoid-induced gastric mucosa injury).
Management
When prednisolone starts, is escalated, or is withdrawn, check INR at 1 week, then every 2 weeks until stable. Titrate warfarin to INR. PPI cover with pantoprazole is mandatory.
Mechanism
Similar to ASA + methylprednisolone. Prednisolone + antiplatelet – additive risk of GI ulcer and bleeding.
Symptoms
Epigastric pain, nausea, heartburn. With prolonged therapy: peptic ulcer and GI bleeding risk (black stools, vomiting blood). Older patients and prior peptic ulcer disease: higher risk.
Management
For short prednisolone courses, cardioprotective aspirin is acceptable with pantoprazole cover. For prolonged systemic therapy, watch dyspepsia symptoms carefully.
Mechanism
Prednisolone causes sodium and water retention via mineralocorticoid effect, antagonising amlodipine's antihypertensive action.
Symptoms
Gradual blood pressure rise 2–4 weeks after starting the glucocorticoid. In heart failure: oedema, weight gain.
Management
For short prednisolone courses, no adjustment. For prolonged systemic therapy, increase amlodipine or add a diuretic (hydrochlorothiazide, indapamide) with blood pressure monitoring.
Mechanism
Prednisolone causes sodium and water retention via mineralocorticoid effect, reducing bisoprolol's antihypertensive effect.
Symptoms
Gradual blood pressure rise 2–4 weeks after starting the glucocorticoid. In heart failure: oedema, weight gain.
Management
For short prednisolone courses (up to 7 days), no adjustment. For prolonged systemic therapy, increase bisoprolol or add a diuretic with blood pressure monitoring every 2 weeks.
Mechanism
Glucocorticoids retain sodium and water via mineralocorticoid effect, blunting the ACE inhibitor's antihypertensive effect. Both can also cause hyperkalaemia (prednisolone via muscle catabolism, ACE inhibitor via aldosterone suppression).
Symptoms
Return or rise of blood pressure, leg oedema. Hyperkalaemia symptoms in CKD: Weakness, fatigue, paraesthesias, arrhythmia. Symptoms develop at potassium above 5.5 mmol/L; life-threatening above 6.5 mmol/L.
Management
For short prednisolone pulses (3–7 days), no specific adjustment needed. For long-term therapy, check BP weekly in the first month; if it rises, increase enalapril or add a diuretic. Potassium and creatinine every 2 weeks in the first month.
Sources
Mechanism
Prednisolone is ulcerogenic; escitalopram reduces platelet aggregation via serotonin uptake. Additive GI bleeding risk.
Symptoms
Epigastric pain, heartburn, black or tarry stools, blood in vomit, bruising. Higher risk in older patients and prior peptic ulcer.
Management
On long-term prednisolone (over 2 weeks) or in patients over 65, add pantoprazole 20 mg/day. Escitalopram also prolongs QT, so cap older patients at 10 mg/day.
Mechanism
Both cause hypokalaemia: glucocorticoids via mineralocorticoid effect and muscle catabolism; furosemide via direct urinary potassium loss. Additive risk, especially on long-term prednisolone.
Symptoms
Weakness, muscle cramps, fatigue, palpitations, arrhythmia (particularly dangerous with digoxin). Symptoms appear at potassium below 3.5 mmol/L.
Management
For short prednisolone courses (3–7 days), no specific adjustment needed. For long-term therapy, check potassium at 1, 2, and 4 weeks, then monthly. If it falls below 3.5 mmol/L, add potassium supplements (10–20 mmol/day) or a potassium-sparing diuretic. On digoxin, hypokalaemia is dangerous — arrhythmia risk.
Mechanism
Prednisolone retains sodium and water via mineralocorticoid effect, blunting the ARB's antihypertensive effect. Both also contribute to hyperkalaemia in CKD.
Symptoms
Return or rise of blood pressure, leg oedema. Weakness, fatigue, paraesthesias, arrhythmia. Symptoms develop at potassium above 5.5 mmol/L; life-threatening above 6.5 mmol/L.
Management
For short prednisolone courses (3–7 days), no specific adjustment needed. For long-term therapy, check BP weekly in the first month. If BP rises, increase losartan or add a thiazide. Potassium and creatinine every 2 weeks.
Mechanism
Prednisolone is ulcerogenic — suppresses prostaglandin synthesis and gastric mucosal turnover. Sertraline reduces platelet aggregation via serotonin uptake. Additive GI bleeding risk.
Symptoms
Epigastric pain, heartburn, black or tarry stools, blood in vomit, bruising. Higher risk in older patients and prior peptic ulcer disease.
Management
On the combination, in patients over 65, with prior peptic ulcer, or on long-term prednisolone (over 2 weeks), add pantoprazole 20 mg/day. For short courses (3–7 days), additional gastroprotection is not mandatory.
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FDA category C (prednisone/prednisolone). Use in pregnancy when benefit outweighs risk. Prednisolone is partially inactivated by placental 11-beta-HSD, so less reaches the fetus compared to dexamethasone. Prolonged high-dose use carries risk of cleft palate and neonatal adrenal insufficiency.
Passes into breast milk. At doses up to 20 mg daily, the amount reaching the infant is minimal. A 4-hour gap between dosing and nursing is recommended at higher doses.
Reference information, not a clinical decision. Discuss feeding pauses or changes with your physician or an IBCLC.
Prednisolone is evaluated for the following indications with varying evidence strength: Autoimmune conditions (evidence tier A), Asthma (evidence tier A), Severe allergic reactions (evidence tier A). See the full indication matrix with dosing and citations above on this page.
Common side effects of Prednisolone (≥ 1 in 100): Increased appetite and weight gain, Insomnia, irritability, mood swings, Fluid retention, edema, Hyperglycemia, Dyspepsia, increased gastric acidity. See the Safety section for uncommon and serious reactions.
FDA category C. FDA category C (prednisone/prednisolone). Use in pregnancy when benefit outweighs risk. Prednisolone is partially inactivated by placental 11-beta-HSD, so less reaches the fetus compared to dexamethasone. Prolonged high-dose use carries risk of cleft palate and neonatal adrenal insufficiency.
Passes into breast milk. At doses up to 20 mg daily, the amount reaching the infant is minimal. A 4-hour gap between dosing and nursing is recommended at higher doses.
Prednisolone is contraindicated in: Systemic fungal infections; Hypersensitivity to prednisolone; Live vaccine administration at immunosuppressive doses. Full list in the Safety section.
no international guideline supports corticosteroids for uncomplicated viral infection. Prednisolone suppresses the immune response, prolongs viral shedding, and raises the risk of secondary bacterial infection. A cold resolves in 5–10 days on its own.
corticosteroids do lower temperature through anti-inflammatory action. But this masks a symptom, not its cause. In viral infection, fever is part of the immune response; treat it with paracetamol or ibuprofen as needed, not with systemic corticosteroids. Frequent use for fever is a gateway to steroid dependence.
this reflects confusion between glucocorticoids (prednisolone, dexamethasone) and anabolic steroids (testosterone, nandrolone). Glucocorticoids are catabolic for muscle – they break down protein, cause myopathy, and weakness. Prednisolone for «bulking» produces the opposite effect.
the euphoric effect of corticosteroids gives subjective improvement in the first days but does not treat fatigue's cause. On withdrawal, symptoms worsen – a direct path to steroid dependence on repeated courses.
corticosteroids for severe allergic reactions are used as short, one-time therapy. Chronic self-administration for itch, allergic rhinitis, or urticaria leads to steroid dermatitis, tachyphylaxis, and rebound flares on discontinuation.
the opposite extreme. In autoimmune flares, anaphylaxis, severe COVID-19 with hypoxia, or asthma exacerbation, corticosteroids save lives – high-evidence indications. Principled refusal is as dangerous as self-prescribing without indication.