Prednisolone
Synthetic glucocorticoid for anti-inflammatory and immunomodulatory therapy
Prednisolone is a synthetic glucocorticoid derived from cortisol that has approximately five times the anti-inflammatory potency of its precursor. It is one of the most widely used corticosteroids in clinical practice and is employed in a broad range of inflammatory, allergic, and immunological conditions. Prednisolone is the biologically active metabolite of prednisone and exerts its effects directly after absorption without requiring hepatic activation.
The drug is available as tablets, injection solutions, eye drops, and topical preparations. Numerous generics as well as original products such as Decortin H are available on the market. Prednisolone has been a cornerstone of treatment guidelines for conditions such as rheumatoid arthritis, asthma, inflammatory bowel disease, and organ transplantation for decades.
Mechanism of Action
Prednisolone binds intracellularly to the glucocorticoid receptor (GR) located in the cytoplasm. After binding, the receptor complex translocates into the cell nucleus and influences the transcription of numerous genes. Via glucocorticoid-responsive elements (GRE), anti-inflammatory genes are upregulated while pro-inflammatory cytokines such as interleukin-1 (IL-1), IL-2, IL-6, tumour necrosis factor alpha (TNF-alpha), and interferon-gamma are suppressed.
In addition, prednisolone inhibits phospholipase A2 via lipocortin-1, reducing the synthesis of arachidonic acid metabolites including prostaglandins and leukotrienes. The migration of inflammatory cells into tissue is reduced, vascular permeability decreases, and the release of histamine from mast cells is inhibited. These mechanisms explain the pronounced effects in allergic and inflammatory conditions.
Beyond its anti-inflammatory effects, prednisolone also influences metabolism: it stimulates gluconeogenesis, promotes protein and fat catabolism, and inhibits peripheral insulin action. This explains the risk of steroid-induced diabetes mellitus with prolonged use.
Indications
- Rheumatic diseases: Rheumatoid arthritis, systemic lupus erythematosus, polymyalgia rheumatica, vasculitides
- Respiratory diseases: Severe bronchial asthma, acute COPD exacerbation, croup syndrome
- Allergic reactions: Anaphylaxis (adjunctive), severe urticaria, angioedema
- Inflammatory bowel disease: Crohn's disease and ulcerative colitis in acute flares
- Dermatological conditions: Pemphigus vulgaris, severe atopic dermatitis, erythema multiforme
- Neurological conditions: Multiple sclerosis (relapse therapy), myasthenia gravis, CIDP
- Transplant medicine: Rejection prophylaxis in combination with other immunosuppressants
- Oncology: Component of various chemotherapy regimens (e.g. CHOP in lymphomas)
Dosage and Administration
Low-dose therapy (antirheumatic): 5 to 10 mg daily, preferably in the morning with food to reduce gastrointestinal discomfort and align with the circadian cortisol rhythm. Medium dose: 20 to 40 mg daily, often used in acute flares of inflammatory conditions. High-dose pulse therapy: 1 mg/kg body weight per day up to 2 mg/kg per day, for example in severe allergic reactions or MS relapses. Intravenous high-dose pulse therapy up to 500 to 1000 mg daily (methylprednisolone) is common in MS and severe autoimmune reactions.
The dose is generally reduced stepwise (tapering) to avoid adrenocortical suppression. After long-term therapy exceeding three weeks, prednisolone must not be stopped abruptly as the body's own cortisol production is suppressed and an acute adrenal insufficiency (Addisonian crisis) may occur. The lowest still effective dose should always be the therapeutic goal.
Side Effects
Common with short-term therapy: Blood glucose elevation (especially in diabetic patients), mood swings including euphoria or depression, sleep disturbances, fluid retention with weight gain, increased susceptibility to infections.
With long-term therapy (weeks to months): Cushing's syndrome (moon face, truncal obesity, buffalo hump), osteoporosis with fracture risk, muscle weakness (steroid myopathy), cataract and glaucoma, skin atrophy and striae, delayed wound healing, gastrointestinal ulcers (especially in combination with NSAIDs), atherosclerosis through hyperglycaemia and dyslipidaemia, growth retardation in children.
Adrenocortical suppression: Even after a few weeks of daily dosing above the physiological cortisol level (approximately 7.5 mg prednisolone equivalent), prednisolone suppresses endogenous cortisol production via the HPA axis. Stress situations such as surgery, infection, or trauma can then trigger acute adrenal insufficiency.
Interactions
- NSAIDs (ibuprofen, diclofenac, aspirin): Markedly increased risk of gastrointestinal bleeding and ulcers; combination only with gastric protection (PPI)
- Antidiabetic drugs and insulin: Prednisolone raises blood glucose; dose adjustment of antidiabetic therapy required
- Antihypertensives and diuretics: Enhanced potassium excretion (hypokalaemia risk); blood pressure increase possible
- CYP3A4 inducers (rifampicin, carbamazepine, phenytoin): Accelerated metabolism of prednisolone; loss of efficacy possible
- CYP3A4 inhibitors (ketoconazole, clarithromycin): Slowed metabolism; increased prednisolone exposure
- Live vaccines: Contraindicated at immunosuppressive doses (risk of vaccine-induced disease)
- Cardiac glycosides (digoxin): Hypokalaemia caused by prednisolone enhances digitalis toxicity
Special Notes
Osteoporosis prophylaxis: For anticipated long-term therapy exceeding three months, early osteoporosis prophylaxis with calcium (1000 to 1500 mg per day) and vitamin D (800 to 2000 IU per day) should be initiated. In high-risk patients (postmenopausal women, older men, pre-existing osteoporosis) a bisphosphonate should additionally be considered.
Steroid card: Patients on prolonged corticosteroid therapy should carry a steroid treatment card that enables adequate care in emergencies such as unconsciousness or surgery.
Pregnancy and breastfeeding: Prednisolone is considered one of the safer corticosteroids in pregnancy as it is largely inactivated in the placenta. Repeated high-dose use in the first trimester carries a slightly increased risk of cleft palate. During breastfeeding, prednisolone is acceptable at therapeutic doses below 25 mg per day.
Infection monitoring: Under immunosuppressive prednisolone therapy, signs of infection should be carefully watched as prednisolone can mask signs of inflammation. Tuberculosis reactivation is possible in patients with a relevant history.
Related Topics
- Dexamethasone — Potent glucocorticoid used especially in oncology and intensive care
- Methotrexate — Disease-modifying drug in rheumatoid arthritis and psoriasis
- Azathioprine — Immunosuppressant for steroid-sparing therapy
- All active ingredients overview
Frequently Asked Questions
Why must prednisolone not be stopped suddenly?
With prolonged use, prednisolone suppresses endogenous cortisol production via the HPA axis. If the medication is abruptly stopped, the adrenal cortex cannot respond quickly enough. Acute adrenal insufficiency with circulatory failure may occur. Therefore the dose must be reduced stepwise, always under medical guidance.
What is the difference between prednisolone and prednisone?
Prednisone is a prodrug that is activated to prednisolone in the liver. Prednisolone is the biologically active form and therefore acts directly. In cases of impaired hepatic function, prednisolone is more reliable as the activation capacity for prednisone may be reduced. In terms of potency and dosing, both substances are considered equivalent.
Can prednisolone raise blood glucose?
Yes. Prednisolone stimulates gluconeogenesis in the liver and inhibits insulin action in peripheral tissues. In patients with existing diabetes this can lead to poor control; even in non-diabetic patients temporarily elevated blood glucose values are possible. Postprandial values in particular rise. Close glucose monitoring is important during long-term therapy.
Why should prednisolone be taken in the morning?
Morning administration (between 6:00 and 8:00 a.m.) is aligned with the natural circadian rhythm of cortisol secretion, which peaks in the early morning hours. This minimises suppression of the adrenal cortex. Taking the dose with breakfast also reduces the risk of gastrointestinal side effects.