Prednisolone: Drug Monograph & Prescribing Guide

Pharmacokinetic Profile

Plasma Half-Life

2–4 h (biological 18–36 h)

Metabolism

Hepatic (CYP3A4 6β-hydroxylation; 11β-HSD interconversion with prednisone; A-ring reduction)

Protein Binding

~70–95% (CBG saturable; albumin)

Bioavailability

~80–100% (oral)

Volume of Distribution

~0.4–1.5 L/kg (dose-dependent)

Clinical Information

Drug Class

Glucocorticoid corticosteroid

Available Forms

Tablet 1, 2.5, 5 mg · Solution 5 & 15 mg/5 mL · ODT 10, 15, 30 mg · IV/IM (sodium phosphate)

Route

PO · IV · IM · Intra-articular · Ophthalmic

Renal Adjustment

Generally none required

Hepatic Adjustment

Use with caution; preferred over prednisone in severe hepatic impairment

Pregnancy

Compatible at usual doses (limited fetal exposure via placental 11β-HSD2)

Lactation

Compatible; consider 4-h delay if dose >20 mg

Schedule / Legal

Prescription only · Not controlled

Generic Available

Yes (multiple manufacturers)

Indications

Prednisolone is a synthetic glucocorticoid used across virtually every medical specialty wherever physiologic replacement, anti-inflammatory, or immunosuppressive activity is needed. Because prednisolone is the active form (whereas prednisone requires hepatic conversion via 11β-HSD1), it is generally preferred over prednisone in significant hepatic impairment and in young infants whose hepatic conversion capacity may be incomplete.

Indication	Approved Population	Therapy Type	Status
Primary or secondary adrenocortical insufficiency	All ages	Replacement (alternative to hydrocortisone)	FDA Approved
Congenital adrenal hyperplasia	All ages	Replacement / suppression	FDA Approved
Rheumatoid arthritis & juvenile idiopathic arthritis	Adults & children	Adjunctive (low-dose bridging)	FDA Approved
Polymyalgia rheumatica & giant cell arteritis	Adults	Monotherapy or with steroid-sparing agent	FDA Approved
Systemic lupus erythematosus & vasculitides	Adults & children	Induction or flare therapy	FDA Approved
Acute gouty arthritis	Adults	Short-course monotherapy	FDA Approved
Severe allergic states & drug hypersensitivity	Adults & children	Adjunctive (with antihistamines / epinephrine if anaphylaxis)	FDA Approved
Symptomatic sarcoidosis, Löffler syndrome, aspiration pneumonitis	Adults & children	Monotherapy or adjunctive	FDA Approved
Idiopathic thrombocytopenic purpura, autoimmune haemolytic anaemia	Adults & children	First-line	FDA Approved
Idiopathic nephrotic syndrome	Adults & children	Induction	FDA Approved
Ulcerative colitis & Crohn disease (active flare)	Adults & children	Induction	FDA Approved
Acute exacerbations of multiple sclerosis	Adults	Short-course (where IV methylprednisolone is unavailable)	FDA Approved
Acute leukaemias & lymphomas	Adults & children	Adjunctive within combination protocols	FDA Approved

The label is broad because prednisolone has been in clinical use since the 1950s and predates the modern indication-by-indication FDA approval framework. In practice the agent is also used widely for conditions that fall outside the formally approved list but that are supported by strong contemporary evidence.

Common Off-Label & Guideline-Endorsed Uses

Acute asthma exacerbation (high evidence): 40–50 mg/day (adults) or 1–2 mg/kg/day (children) for 5–7 days — endorsed by GINA. No taper required if ≤7 days.

COPD exacerbation (high evidence): 40 mg/day for 5 days — GOLD-recommended. The REDUCE trial (which used prednisone 40 mg/day, considered therapeutically equivalent to prednisolone) demonstrated non-inferiority of 5-day vs 14-day courses.

Croup (high evidence): Prednisolone 1–2 mg/kg as a single oral dose is an alternative to dexamethasone 0.6 mg/kg, which remains first-line owing to its longer biological half-life and stronger trial evidence.

Bell palsy (high evidence): Prednisolone within 72 h of onset improves complete recovery; the Sullivan 2007 trial regimen was 25 mg twice daily for 10 days (no taper). The AAN 2012 update endorses oral steroids for new-onset disease.

Pneumocystis jirovecii pneumonia with hypoxaemia (high evidence): Adjunct to antimicrobial therapy when PaO₂ <70 mmHg on room air or A–a gradient ≥35 mmHg.

Dose

Dosing

Glucocorticoid dosing is best framed by clinical scenario rather than by tablet strength, because the same drug may be given as a 1 mg replacement dose or as 60 mg pulses for autoimmune induction. The tables below collect the regimens that account for the majority of prednisolone prescribing in adult practice.

Adult Dosing by Clinical Scenario

Clinical Scenario	Starting Dose	Maintenance Dose	Maximum Dose	Notes
Asthma exacerbation (adult)	40–50 mg PO once daily	40–50 mg/day × 5–7 days	60 mg/day	No taper required if ≤7 days GINA-endorsed regimen
COPD exacerbation	40 mg PO once daily	40 mg/day × 5 days	40 mg/day	5 days non-inferior to 14 days (REDUCE used prednisone) No taper required
Acute gout (when NSAIDs/colchicine contraindicated)	30–40 mg PO once daily	Same dose × 5 days	40 mg/day	ACR-endorsed alternative to colchicine/NSAIDs Brief taper optional
Polymyalgia rheumatica	12.5–25 mg PO once daily	Taper to 10 mg over 4–8 wk; then 1 mg/month	25 mg/day initial	Slow taper essential to avoid relapse Total course typically 1–2 years
Giant cell arteritis (uncomplicated)	40–60 mg PO once daily	Taper over 12–18 months	60 mg/day	IV methylprednisolone preferred if visual symptoms Add tocilizumab as steroid-sparing where available
Rheumatoid arthritis (low-dose bridging)	5–10 mg PO once daily	Lowest effective dose; aim ≤7.5 mg/day	10 mg/day (chronic)	Bridge to DMARD; taper as DMARD takes effect EULAR: limit chronic use to ≤6 months where possible
SLE flare (moderate)	0.5 mg/kg/day PO	Taper over weeks–months	1 mg/kg/day	For severe organ-threatening flare use IV methylprednisolone pulse Combine with hydroxychloroquine + immunosuppressant
IBD flare (mild–moderate, oral therapy appropriate)	40 mg PO once daily	40 mg × 1–2 wk → taper 5–10 mg/wk	60 mg/day	Not for maintenance — switch to steroid-sparing therapy Total course typically ~8 weeks
Idiopathic thrombocytopenic purpura	1 mg/kg/day PO	2–4 wk then taper	100 mg/day	Alternative: high-dose dexamethasone pulse Response within 1–4 wk
Bell palsy (within 72 h of onset)	25 mg PO BID (Sullivan trial)	50 mg/day × 10 days, no taper	60–80 mg/day (alternative regimens)	AAN-endorsed; some clinicians use 60 mg/day × 5–7 days then taper Earliest possible initiation maximises benefit
Primary adrenal insufficiency (replacement)	3–5 mg PO once daily	3–5 mg/day (lowest dose preventing symptoms)	7.5 mg/day	Hydrocortisone or cortisone acetate is the preferred replacement (Endocrine Society 2016); prednisolone is an alternative for once-daily dosing. Add fludrocortisone in primary disease Sick-day rules: double oral dose during minor illness
Adrenal crisis / major surgical stress	Hydrocortisone 100 mg IV is first-line	If only prednisolone available: 25 mg IV q6h × 24 h	Up to 100 mg/day prednisolone-equivalent	Hydrocortisone preferred because of mineralocorticoid activity at stress doses Switch to oral once stable
Pneumocystis pneumonia (PaO₂ <70 mmHg)	40 mg PO BID	40 mg BID × 5 days → 40 mg daily × 5 days → 20 mg daily × 11 days	80 mg/day initial	Started within 72 h of antimicrobial Total course 21 days

Pediatric Dosing

Clinical Scenario	Starting Dose	Maintenance Dose	Maximum Dose	Notes
Asthma exacerbation	1–2 mg/kg/day PO	Same dose × 3–5 days	60 mg/day	Often given as ODT or oral solution No taper if ≤7 days
Croup	1–2 mg/kg PO single dose	May repeat once at 24 h if symptoms persist	60 mg per dose	Dexamethasone 0.6 mg/kg is first-line; prednisolone is an alternative Use where dexamethasone is unavailable or palatability is an issue
Idiopathic nephrotic syndrome (induction)	60 mg/m²/day (or 2 mg/kg/day)	4–6 wk then 40 mg/m² alternate days × 4–6 wk	60 mg/day	Total induction course ~8–12 weeks per KDIGO/IPNA Bone-health monitoring from week 6
Juvenile idiopathic arthritis (bridging)	0.1–0.5 mg/kg/day	Lowest effective dose	10 mg/day	Used while DMARD takes effect Avoid chronic systemic therapy

Adjustment in Special Populations

Population	Starting Dose	Maintenance Dose	Maximum Dose	Notes
Severe hepatic impairment	Standard dose	Standard dose	Standard maximum	Prednisolone preferred over prednisone (no hepatic activation needed) Monitor for amplified glucocorticoid effects
Renal impairment (any stage)	Standard dose	Standard dose	Standard maximum	No empiric reduction required Monitor potassium & fluid status
Older adults (≥65 y)	Use lowest effective dose	Aim for <5 mg/day if chronic	As clinically required	Higher risk of fracture, infection, hyperglycaemia, delirium Initiate bone-protective therapy early
Pregnancy	Lowest effective dose	As required for maternal disease	Minimise above 20 mg/day in T1	Placental 11β-HSD2 inactivates much of the fetal exposure (Murphy 2007) Stress-dose during labour if chronic use ≥20 mg/day for >3 wk

Tapering Pearl

Patients who have received prednisolone >5 mg/day for more than 3 weeks should be assumed to have HPA-axis suppression. A typical taper from 40 mg is: reduce by 10 mg/week until 20 mg, then 5 mg/week to 10 mg, then 2.5 mg/week to 5 mg, then 1 mg every 2–4 weeks. The terminal phase below 5 mg is the slowest because endogenous cortisol production must recover.

Courses of ≤7 days at any dose can usually be stopped abruptly without taper, regardless of the indication.

Pharmacology

Mechanism of Action

Prednisolone acts through the cytoplasmic glucocorticoid receptor (GR-α). Once bound, the steroid–receptor complex translocates into the nucleus and modifies gene transcription by two complementary routes: transactivation, in which it binds glucocorticoid-response elements to upregulate anti-inflammatory genes such as annexin A1, MAPK phosphatase-1, and IκB; and transrepression, in which it tethers and silences pro-inflammatory transcription factors NF-κB and AP-1, suppressing the synthesis of cytokines (IL-1, IL-2, IL-6, TNF-α), prostaglandins, leukotrienes, COX-2, and adhesion molecules. The net result is broad inhibition of leukocyte migration, capillary permeability, T-cell proliferation, and antibody production. Many of the metabolic and growth-suppressing adverse effects appear to arise from transactivation, while most therapeutic benefit comes from transrepression — a separation that has driven the search for selective glucocorticoid receptor agonists.

ADME Profile

Parameter	Value	Clinical Implication
Absorption	Oral bioavailability ~80–100%; T_max 1–2 h; food may delay but does not reduce absorption	Rapid clinical onset; can be taken with food to reduce gastric irritation without loss of efficacy
Distribution	V_d ~0.4–1.5 L/kg (dose-dependent); protein binding 70–95% (corticosteroid-binding globulin saturable above ~30 mg dose, then albumin)	At doses above ~20–30 mg the unbound fraction rises sharply, producing non-linear pharmacokinetics and disproportionately greater tissue exposure
Metabolism	Hepatic 6β-hydroxylation by CYP3A4; reversible interconversion with prednisone via 11β-hydroxysteroid dehydrogenase (11β-HSD); A-ring reduction by 5α/5β-reductase	Strong CYP3A4 inhibitors and inducers significantly alter exposure; severe hepatic disease favours prednisolone over prednisone because no activation step is required
Elimination	Plasma t½ 2–4 h (Pickup 1979); biological t½ 18–36 h; metabolites excreted predominantly in urine as glucuronide/sulfate conjugates	Allows once-daily morning dosing in most indications; renal impairment does not require dose adjustment

Relative potency in equivalents: 5 mg prednisolone = 5 mg prednisone = 4 mg methylprednisolone = 0.75 mg dexamethasone = 20 mg hydrocortisone. Prednisolone retains modest mineralocorticoid activity (~0.8 relative to hydrocortisone), which becomes clinically meaningful at doses above ~20 mg/day.

Side Effects

Side-effect frequency depends heavily on cumulative dose and duration. The figures below reflect long-term oral therapy at >5 mg/day prednisolone-equivalent unless otherwise stated, drawn predominantly from cohort and pharmacovigilance data on systemic glucocorticoids (Curtis 2006; Fardet 2007 Drug Safety; Bloechliger 2018). Short courses (<14 days) at ≤40 mg/day produce a much lower frequency of metabolic and bone-related events.

≥10% Very Common Adverse Effects (long-term use)

Adverse Effect	Incidence	Clinical Note
Weight gain	~70% (chronic users; Curtis 2006)	Most prominent in the first 3 months; counsel about portion control before initiation
Insomnia & sleep disturbance	~30–50%	Reduced by morning-only dosing; can be severely disruptive at doses ≥20 mg/day
Mood disturbance (irritability, lability, anxiety)	~20–30%	Frank psychosis or mania is rare; most often presents as agitation or insomnia-driven anxiety
Cushingoid changes (moon facies, central adiposity, buffalo hump)	~13% at 60 days; rises with prolonged exposure	Dose- and duration-dependent; partial reversal with dose reduction
Skin thinning & easy bruising	~15–20% within 3 months at ≥10 mg/day	Often the first visible sign of long-term exposure; partially reversible after withdrawal
Cataracts (chronic users)	~15% at long-term follow-up (Curtis 2006)	Posterior subcapsular; not reversible — annual ophthalmology review for chronic use

1–10% Common Adverse Effects

Adverse Effect	Incidence	Clinical Note
New-onset hyperglycaemia / steroid-induced diabetes	~5–10% (higher with risk factors)	Risk highest with family history of diabetes, BMI ≥30, prednisolone ≥20 mg/day. Check fasting glucose at week 1–2
Acne & folliculitis	~5–10%	More frequent in adolescents; topical therapy usually sufficient
Dyspepsia / heartburn	~5–10%	Take with food; PPI not routinely required unless concomitant NSAID or prior peptic disease
Fluid retention & mild hypertension	~3–10% (dose-dependent)	Most pronounced at >20 mg/day owing to mineralocorticoid activity; consider sodium restriction
Menstrual irregularity	~4–8%	Typically oligomenorrhoea; resolves after taper
Hypokalaemia (mild)	~5%	Higher risk with concomitant loop or thiazide diuretics
Glaucoma / raised intra-ocular pressure	~3–5%	Higher risk if family history of glaucoma; check IOP if symptoms develop
Increased non-serious infection	~5–10% at ≥20 mg/day	Risk approximately doubles at >10 mg/day; counsel about prompt evaluation of fever or new symptoms

Serious Serious Adverse Effects (any frequency)

Adverse Effect	Estimated Frequency	Typical Onset	Required Action
HPA-axis suppression / iatrogenic adrenal insufficiency	Common above 5 mg/day for >3 weeks	Onset by 3 weeks; recovery may take 6–12 months after withdrawal	Mandatory taper; stress-dose cover for surgery, sepsis, or significant illness; medical-alert identification
Glucocorticoid-induced osteoporosis & fragility fracture	Bone loss most rapid in first 6 months; ~12% fracture rate in long-term users (Curtis 2006)	Bone loss begins within weeks; fracture rate climbs from month 3 onward	Calcium 1000–1200 mg/day + vitamin D 600–800 IU/day; bisphosphonate at start of any course expected to last ≥3 months at ≥7.5 mg/day; baseline DEXA (ACR 2017 / 2022)
Avascular necrosis (commonly femoral head)	~1–3% with chronic high-dose use	Median onset 6–12 months; can occur after a single high-dose pulse	MRI for any new persistent hip, shoulder, or knee pain; orthopaedic referral
Serious infection (bacterial, viral, opportunistic)	Rate rises with dose; severe-infection rate ~78/1000 patient-years in oral-prednisolone asthma cohort (Bloechliger 2018)	Anytime during therapy; risk persists after withdrawal of high-dose courses	Low threshold for evaluation of fever; PJP prophylaxis if ≥20 mg/day for ≥4 weeks; screen for latent TB, HBV, strongyloidiasis before chronic therapy
Steroid psychosis / mania	~1.3% at <40 mg/day; ~4.6% at 41–80 mg/day; ~18% at >80 mg/day (Boston Collaborative Drug Surveillance)	First 1–2 weeks of high-dose therapy	Reduce dose if possible; antipsychotic if severe; usually resolves on taper
Peptic ulcer disease & GI bleeding	Modest increase with steroids alone; markedly higher with concurrent NSAIDs (RR ~4)	Anytime; perforation risk peaks in first weeks of high-dose therapy	PPI cover if concomitant NSAID, anticoagulant, or prior ulcer; urgent imaging for acute abdomen
Posterior reversible encephalopathy syndrome (PRES)	Very rare	Days–weeks after high-dose therapy	Discontinue, control BP, neuro-imaging; usually reversible
Anaphylaxis	Very rare	Minutes–hours of administration	Emergency epinephrine; permanent discontinuation; document allergy
Steroid myopathy	~5–10% with chronic high-dose use	Weeks to months	Resistance exercise; reduce dose where possible; CK characteristically normal

Discontinuation Discontinuation Patterns

Prednisolone is rarely stopped in clinical trials because of intolerance — patients are usually titrated rather than withdrawn. The figures below come from long-term cohort and survey data of chronic glucocorticoid users in rheumatic disease and should be interpreted as approximate.

Adults (chronic use)

~10–15% of long-term users discontinue or switch for adverse effects

Top reasons: weight gain & cushingoid appearance, intolerable mood disturbance, uncontrolled hyperglycaemia, infection

Pediatric (chronic use)

~5–10% discontinue or switch chronic therapy for adverse effects

Top reasons: growth suppression, behavioural disturbance, weight gain, cushingoid features

Reason for Discontinuation	Approximate Rate	Context
Cushingoid features & weight gain	~3–5%	Most common cosmetic reason; often drives the patient request
Severe mood disturbance / steroid psychosis	~2–3%	Usually requires dose reduction rather than abrupt withdrawal
Uncontrolled hyperglycaemia	~1–2%	More common with pre-existing diabetes or family history
Serious infection	~1–2%	Often necessitates pause or steroid-sparing switch
Fragility fracture	~1%	Usually triggers dose minimisation rather than full stop

Management Priority — HPA-Axis Suppression

The single most clinically dangerous adverse effect of chronic prednisolone is unrecognised adrenal insufficiency at the moment of physiological stress (surgery, sepsis, trauma, severe gastroenteritis). Any patient who has received >5 mg/day for more than 3 weeks should be issued a steroid-emergency card, instructed in sick-day rules (double the oral dose during minor illness), and counselled never to stop the drug abruptly. Parenteral hydrocortisone 100 mg should be available where access to medical care may be delayed.

Int

Drug Interactions

Prednisolone is metabolised principally via hepatic CYP3A4-mediated 6β-hydroxylation, so the most clinically relevant pharmacokinetic interactions involve strong CYP3A4 modulators. Pharmacodynamic interactions (additive immunosuppression, additive hypokalaemia, antagonism of antidiabetics) are equally important but easier to anticipate.

Major Live attenuated vaccines (MMR, varicella, yellow fever, BCG, oral typhoid, intranasal influenza)

MechanismGlucocorticoid-mediated immunosuppression permits replication of vaccine organism

EffectRisk of disseminated vaccine-strain infection

ManagementAvoid during therapy and for ≥1 month (preferably 3 months) after stopping doses ≥20 mg/day used for ≥14 days. Inactivated vaccines remain safe but immune response may be reduced

CDC ACIP

Major Strong CYP3A4 inducers (rifampin, phenytoin, carbamazepine, phenobarbital, St John’s wort)

MechanismAccelerated CYP3A4-mediated clearance reduces plasma exposure

EffectLoss of glucocorticoid efficacy; risk of disease flare or adrenal crisis if used for replacement

ManagementIncrease prednisolone dose (commonly by 50–100%); consider parenteral steroid in adrenal insufficiency. Monitor disease activity closely

FDA PI / Lexicomp

Major Strong CYP3A4 inhibitors (clarithromycin, ritonavir, cobicistat, itraconazole, ketoconazole)

MechanismInhibition of hepatic CYP3A4 reduces clearance

EffectIncreased prednisolone exposure; iatrogenic Cushing syndrome reported, especially with ritonavir-boosted regimens

ManagementUse lowest effective steroid dose; substitute azithromycin or fluconazole where appropriate; monitor for cushingoid features

FDA PI

Major NSAIDs (including COX-2 selective)

MechanismAdditive injury to gastric mucosa & impaired prostaglandin protection

EffectApproximately 4-fold increase in upper GI bleeding/perforation when combined

ManagementAvoid combination where possible; if essential, add a PPI for the duration of co-administration

Cohort meta-analysis / Lexicomp

Major Fluoroquinolones (ciprofloxacin, levofloxacin)

MechanismSynergistic tendinopathy (mechanism incompletely understood)

EffectMarkedly elevated risk of tendon rupture, especially Achilles, in adults >60 y

ManagementAvoid combination in older patients; counsel about new tendon pain; prefer non-fluoroquinolone alternatives

FDA Safety Communication

Moderate Insulin & oral antidiabetics

MechanismGlucocorticoid-induced insulin resistance and hepatic gluconeogenesis

EffectReduced glycaemic control; post-prandial hyperglycaemia is the dominant pattern

ManagementPre-emptively raise insulin needs by 20–50% at steroid doses ≥20 mg/day; intensify monitoring during taper

Lexicomp

Moderate Loop & thiazide diuretics

MechanismAdditive renal potassium wasting

EffectHypokalaemia, particularly at prednisolone >20 mg/day

ManagementCheck potassium at baseline and every 1–2 weeks during high-dose therapy; supplement as needed

FDA PI

Moderate Warfarin & other VKAs

MechanismVariable effect on clotting factor synthesis and GI mucosal integrity

EffectINR may rise or fall unpredictably; bleeding risk increases regardless

ManagementCheck INR within 3–5 days of starting or stopping prednisolone, then weekly until stable

Lexicomp

Moderate Aspirin (high-dose)

MechanismAdditive GI mucosal injury; glucocorticoid-induced increase in salicylate clearance

EffectIncreased GI bleeding; salicylate concentrations may fall during steroid therapy and rise on withdrawal

ManagementAdd PPI; monitor salicylate levels at high anti-inflammatory doses; expect upward shift on prednisolone taper

Lexicomp

Moderate Other immunosuppressants (azathioprine, cyclophosphamide, mycophenolate, biologics)

MechanismAdditive immunosuppression (intentional in many regimens but raises infection risk)

EffectIncreased risk of opportunistic infection, including PJP and reactivation of latent TB or HBV

ManagementScreen for latent TB, HBV, and strongyloides before starting; consider PJP prophylaxis where prednisolone ≥20 mg/day for ≥4 weeks alongside another immunosuppressant

EULAR / ACR

Moderate Estrogen-containing contraceptives

MechanismEstrogen increases corticosteroid-binding globulin, raising total but not necessarily free prednisolone

EffectModest potentiation of glucocorticoid effect

ManagementNo routine adjustment; observe for cushingoid features at usual doses

Lexicomp

Minor Antacids (high-dose, simultaneous administration)

MechanismReduced absorption of prednisolone tablet

EffectMild reduction in steroid AUC

ManagementSeparate administration by ≥2 h

Lexicomp

Mon

Monitoring

Monitoring intensity scales with cumulative dose. A 5-day burst for asthma needs no laboratory follow-up; a planned 6-month course for vasculitis needs a structured surveillance plan from day one. The grid below sets out the routine programme for any patient expected to receive prednisolone for more than 3 months.

Blood pressure Baseline, then every 1–3 months
Routine Sodium retention can produce or worsen hypertension within weeks. Set a treatment threshold of 140/90 mmHg and treat with an agent that does not worsen hypokalaemia (consider a calcium channel blocker before adding a thiazide).
Fasting glucose & HbA1c Baseline, week 2, then every 3 months
Routine Steroid-induced hyperglycaemia is most often post-prandial. In patients with risk factors check 2-hour post-prandial glucose if fasting values are normal. HbA1c may underestimate glycaemia in the first weeks.
Weight & cushingoid features Every visit
Routine Track weight, waist circumference, and visible cushingoid features. Rapid weight gain (>5% in a month) prompts review of dose and consideration of steroid-sparing therapy.
Bone density (DEXA) Baseline if course expected ≥3 months at ≥7.5 mg/day; repeat every 1–3 years
Routine Most rapid bone loss occurs in the first 6 months. Start calcium, vitamin D, and a bisphosphonate at baseline rather than waiting for the follow-up scan (ACR 2017 / 2022 GIOP guideline).
Serum potassium Baseline, then with each dose change >20 mg/day
Routine Hypokalaemia is more common with concurrent diuretics and at doses ≥40 mg/day owing to mineralocorticoid activity at this range.
Lipid panel Baseline, then annually
Routine Triglycerides and LDL rise modestly during chronic therapy. Combine with cardiovascular risk reassessment for any patient on ≥6 months of treatment.
Mood & sleep Each visit during the first 3 months
Routine Ask specifically about insomnia, irritability, racing thoughts, and depressive symptoms. Patients with prior steroid psychosis or bipolar disorder need closer surveillance.
Ophthalmology review Annually if course ≥3 months
Routine Posterior subcapsular cataract and steroid-induced glaucoma are dose-cumulative. Earlier review for any new visual symptoms or family history of glaucoma.
Latent TB / HBV / strongyloides screen Once before chronic therapy
Trigger-based Required before any course expected ≥1 month at ≥20 mg/day, particularly with concurrent immunosuppressant. Treat latent TB before starting where possible.
Morning cortisol / ACTH stimulation If unexplained fatigue, hypotension, or hyponatraemia during taper
Trigger-based Confirms iatrogenic adrenal insufficiency. Consider before withdrawing the final 5 mg/day if therapy has lasted >6 months.
Linear growth (children) Every 3–6 months
Routine Glucocorticoid-induced growth suppression is the leading cause of paediatric discontinuation. Plot height velocity and consider alternate-day dosing to mitigate.
MRI of hip / shoulder / knee For new persistent joint pain
Trigger-based Avascular necrosis can occur after even brief high-dose pulses. MRI is more sensitive than plain radiography in early disease.

Contraindications & Cautions

Absolute Contraindications

Documented hypersensitivity to prednisolone or any excipient (anaphylaxis or angio-oedema reported, although rare).
Untreated systemic fungal infection. Glucocorticoid-induced immunosuppression can permit rapid dissemination.
Administration of live attenuated vaccines during high-dose therapy (≥20 mg/day for ≥14 days).
Premature neonates for products containing benzyl alcohol — risk of gasping syndrome.

Relative Contraindications (Specialist Input Recommended)

Active or latent tuberculosis without concurrent antitubercular therapy. Screen and treat before starting where possible.
Active herpes simplex keratitis — risk of corneal perforation with topical or systemic glucocorticoids.
Severe psychiatric disease (history of steroid psychosis, mania, or unstable bipolar disorder). Use lowest dose for shortest duration with mental health input.
Recent intestinal anastomosis or active diverticulitis — increased risk of perforation; involve surgical colleagues in shared decision-making.
Active peptic ulcer disease — particularly when concomitant NSAID, anticoagulant, or aspirin is necessary; co-prescribe a PPI.
Uncontrolled congestive heart failure at doses >20 mg/day owing to mineralocorticoid-mediated fluid retention.

Use with Caution

Diabetes mellitus — anticipate hyperglycaemia and intensify monitoring.
Hypertension — escalate antihypertensive therapy proactively at doses >20 mg/day.
Established osteoporosis or fracture risk factors — co-initiate calcium, vitamin D, and bisphosphonate.
Glaucoma or strong family history — baseline IOP and ophthalmology review.
Pregnancy — usual doses appear safe, but minimise systemic exposure in the first trimester (a small association with oral cleft remains debated).
Children — monitor growth velocity; prefer alternate-day dosing for chronic indications.
Older adults — heightened risk of fracture, infection, hyperglycaemia, and delirium.
Concurrent immunosuppressant therapy — screen for latent infections and consider PJP prophylaxis.

FDA Class-Wide Regulatory Warning HPA-Axis Suppression with Systemic Corticosteroids

Systemic glucocorticoids may induce reversible hypothalamic–pituitary–adrenal axis suppression with the potential for adrenal crisis after stress, surgery, or abrupt withdrawal. Risk increases with daily dose, treatment duration, and route. Withdrawal should be gradual whenever therapy has continued for more than three weeks, and stress-dose cover is required for surgery, severe infection, or trauma. Patients should carry a medical-alert card identifying steroid dependence.

Additional class-level warnings include increased susceptibility to infection (with masking of signs), risk of GI perforation (particularly with active inflammatory bowel disease, recent anastomosis, or NSAID co-therapy), risk of cardiovascular events at high doses, and rare reports of Kaposi sarcoma after prolonged use.

Patient Counselling

Purpose of Therapy

Explain that prednisolone is a synthetic copy of the body’s own stress hormone, used to dampen overactive inflammation or replace adrenal hormones the body cannot produce. Set expectations: the medicine usually starts working within hours for inflammation, but full effect on conditions such as asthma or arthritis may take 24–48 hours. Make the planned duration explicit at the outset — short courses (a few days) are very different from long courses (months), in both expected benefit and the surveillance required.

How to Take

Take the dose once daily in the morning with food and a full glass of water. Morning dosing aligns with the body’s natural cortisol rhythm and reduces insomnia. If a dose is missed and remembered the same day, take it as soon as possible; if it is already evening, skip and resume the next morning rather than doubling up. Never stop the medicine suddenly without speaking to the prescriber if it has been taken every day for more than 3 weeks.

Increased Appetite, Weight Gain & Mood Changes

Tell patient Most people feel hungrier and notice some weight gain in the first month — this is expected and lessens at lower doses. Many also feel more energetic, irritable, or have trouble sleeping. Try to keep meal patterns regular, choose protein and fibre over sugar and salt, and take the dose before 9 am to protect sleep.

Call prescriber Severe insomnia despite morning dosing, racing thoughts, panic, suicidal ideas, or new confusion. These are urgent — call rather than waiting for the next clinic appointment.

Never Stop Suddenly & Sick-Day Rules

Tell patient If the medicine has been taken for more than 3 weeks the body slows its own natural cortisol production. Stopping abruptly, or being unable to take a dose during a serious illness, can cause low blood pressure and collapse. Carry a steroid-emergency card. During minor illness with fever or vomiting, double the usual oral dose for 2–3 days, and seek urgent care if vomiting prevents tablets being kept down.

Call prescriber Vomiting that prevents tablets being absorbed, planned surgery, severe injury, or before taking any new long-term medicine. Severe weakness, dizziness on standing, or confusion needs emergency assessment.

Infections & Vaccines

Tell patient The medicine can mask the early signs of infection and make some infections more severe, including chickenpox, shingles, and tuberculosis. Avoid live vaccines (such as MMR, yellow fever, BCG, and live nasal influenza) while on doses ≥20 mg/day for more than 14 days; the standard inactivated influenza and pneumococcal vaccines are encouraged. Tell every healthcare professional that the medicine is being taken.

Call prescriber New fever, sore throat, productive cough, painful skin rash, or contact with chickenpox or shingles in someone without a history of either. Do not wait — early antiviral therapy can prevent severe disease.

Bone Health & Falls

Tell patient Long courses can weaken the skeleton. Take the calcium and vitamin D supplement that has been prescribed, do regular weight-bearing or resistance exercise, stop smoking, and limit alcohol. A bone-protecting tablet may also be prescribed alongside the steroid — take it as directed.

Call prescriber Sudden severe back pain after a minor strain (possible vertebral fracture), or persistent groin or hip pain (possible avascular necrosis). Both need imaging.

Blood Sugar & Blood Pressure

Tell patient The medicine can raise blood sugar and blood pressure. People who already have diabetes will usually need more insulin or tablets while on the steroid; the prescriber will guide adjustments. Avoid added salt, monitor home blood pressure if a cuff is available, and report headaches or visual disturbance.

Call prescriber Blood glucose readings persistently above 11 mmol/L (200 mg/dL), unusual thirst, frequent urination, or blood pressure consistently above 160/100 mmHg.

Vision Changes

Tell patient Cataracts and raised eye pressure can develop with long courses. An annual eye check is recommended for anyone on steroids for 3 months or more.

Call prescriber New blurred vision, halos around lights, eye pain, or sudden loss of vision. Urgent ophthalmology assessment is needed.

Stomach Symptoms

Tell patient Mild heartburn or indigestion is common and improves when the medicine is taken with food. Avoid ibuprofen, naproxen, diclofenac, or other anti-inflammatory painkillers unless specifically advised — the combination significantly raises the risk of stomach bleeding.

Call prescriber Black, tarry stools, vomiting that looks like coffee grounds, severe abdominal pain, or persistent indigestion despite treatment.

Ref

Sources

Regulatory (PI / SmPC)

U.S. Food and Drug Administration / DailyMed. Prednisolone tablets, oral solution, and orally disintegrating tablets — current full prescribing information. https://dailymed.nlm.nih.gov/dailymed/search.cfm?query=prednisolone Authoritative source for FDA-approved indications, dosing, contraindications, and adverse-reaction tables across all marketed prednisolone products.
Electronic Medicines Compendium (eMC). Prednisolone — Summary of Product Characteristics. https://www.medicines.org.uk/emc/search?q=prednisolone UK regulatory equivalent of the FDA label, useful for paediatric dosing detail and EU-approved indications.
U.S. FDA. Drug Safety Communications — Fluoroquinolone antibiotics, tendon injury risk. https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communications Source for the major-severity tendon-rupture interaction with fluoroquinolones in older adults.

Key Clinical Trials & Cohort Studies

Leuppi JD, Schuetz P, Bingisser R, et al. Short-term vs conventional glucocorticoid therapy in acute exacerbations of chronic obstructive pulmonary disease (REDUCE). JAMA. 2013;309(21):2223–2231. doi:10.1001/jama.2013.5023. PMID 23695200. https://pubmed.ncbi.nlm.nih.gov/23695200/ RCT establishing 5-day systemic glucocorticoid (prednisone 40 mg/day; therapeutically equivalent to prednisolone) as non-inferior to 14-day courses for COPD exacerbations.
Sullivan FM, Swan IRC, Donnan PT, et al. Early treatment with prednisolone or acyclovir in Bell’s palsy. N Engl J Med. 2007;357(16):1598–1607. doi:10.1056/NEJMoa072006. PMID 17942873. https://pubmed.ncbi.nlm.nih.gov/17942873/ Pivotal RCT (prednisolone 25 mg twice daily for 10 days) demonstrating that early steroid therapy drives recovery in Bell palsy when started within 72 hours.
Curtis JR, Westfall AO, Allison J, et al. Population-based assessment of adverse events associated with long-term glucocorticoid use. Arthritis Rheum. 2006;55(3):420–426. doi:10.1002/art.21984. PMID 16739208. https://pubmed.ncbi.nlm.nih.gov/16739208/ Survey-based source for the dose- and duration-dependent prevalence of weight gain (~70%), cataracts (~15%), and fractures (~12%) in chronic users.
Fardet L, Kassar A, Cabane J, Flahault A. Corticosteroid-induced adverse events in adults: frequency, screening and prevention. Drug Saf. 2007;30(10):861–881. doi:10.2165/00002018-200730100-00005. PMID 17867724. https://pubmed.ncbi.nlm.nih.gov/17867724/ Comprehensive review of corticosteroid adverse-event frequencies used as the basis for cushingoid, mood, and metabolic incidence figures.
Bloechliger M, Reinau D, Spoendlin J, et al. Adverse events profile of oral corticosteroids among asthma patients in the UK: cohort study with a nested case-control analysis. Respir Res. 2018;19(1):75. doi:10.1186/s12931-018-0742-y. https://pubmed.ncbi.nlm.nih.gov/29683475/ UK Clinical Practice Research Datalink cohort quantifying incidence rates per 1,000 person-years for severe infection, fracture, hypertension, and other glucocorticoid-related events.
Yao TC, Huang YW, Chang SM, et al. Association between oral corticosteroid bursts and severe adverse events: a nationwide population-based cohort study. Ann Intern Med. 2020;173(5):325–330. doi:10.7326/M20-0432. https://www.acpjournals.org/doi/10.7326/M20-0432 Self-controlled case series quantifying short-burst (≤14 day) glucocorticoid risks for GI bleeding, sepsis, and heart failure.

Guidelines

Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention — current report. https://ginasthma.org/ Source for adult and paediatric prednisolone dosing in acute asthma exacerbations.
Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for Prevention, Diagnosis, and Management of COPD — current report. https://goldcopd.org/ Endorses 40 mg/day for 5 days for COPD exacerbations and outlines criteria for systemic steroid use.
Bornstein SR, Allolio B, Arlt W, et al. Diagnosis and treatment of primary adrenal insufficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2016;101(2):364–389. doi:10.1210/jc.2015-1710. PMID 26760044. https://pubmed.ncbi.nlm.nih.gov/26760044/ Reference for replacement-dose strategy. The guideline recommends hydrocortisone or cortisone acetate as preferred agents, with prednisolone as an alternative for once-daily dosing.
Buckley L, Guyatt G, Fink HA, et al. 2017 American College of Rheumatology guideline for the prevention and treatment of glucocorticoid-induced osteoporosis. Arthritis Rheumatol. 2017;69(8):1521–1537. doi:10.1002/art.40137. PMID 28585373. https://pubmed.ncbi.nlm.nih.gov/28585373/ Anchor reference for bone-protection thresholds and choice of agent during chronic glucocorticoid therapy.
Humphrey MB, Russell L, Danila MI, et al. 2022 American College of Rheumatology guideline for the prevention and treatment of glucocorticoid-induced osteoporosis. Arthritis Rheumatol. 2023;75(12):2088–2102. doi:10.1002/art.42646. https://acrjournals.onlinelibrary.wiley.com/doi/full/10.1002/art.42646 2022 update to the ACR GIOP guideline; refines the role of bisphosphonates, denosumab, and anabolic agents in glucocorticoid users.
Gronseth GS, Paduga R; American Academy of Neurology. Evidence-based guideline update: steroids and antivirals for Bell palsy. Neurology. 2012;79(22):2209–2213. doi:10.1212/WNL.0b013e318275978c. PMID 23136264. https://pubmed.ncbi.nlm.nih.gov/23136264/ AAN endorsement of oral steroids for new-onset Bell palsy; basis for the 72-hour treatment window.
Centers for Disease Control and Prevention. ACIP General Best Practice Guidelines for Immunization — altered immunocompetence. https://www.cdc.gov/vaccines/hcp/acip-recs/general-recs/immunocompetence.html Defines the dose and duration thresholds for clinically significant glucocorticoid-induced immunosuppression and live vaccine avoidance (≥20 mg/day prednisone-equivalent for ≥14 days).

Mechanistic / Basic Science

Rhen T, Cidlowski JA. Antiinflammatory action of glucocorticoids — new mechanisms for old drugs. N Engl J Med. 2005;353(16):1711–1723. doi:10.1056/NEJMra050541. PMID 16236742. https://pubmed.ncbi.nlm.nih.gov/16236742/ Definitive review of the transactivation/transrepression model that informs the mechanism-of-action narrative.
Cain DW, Cidlowski JA. Immune regulation by glucocorticoids. Nat Rev Immunol. 2017;17(4):233–247. doi:10.1038/nri.2017.1. PMID 28192415. https://pubmed.ncbi.nlm.nih.gov/28192415/ Updated review of glucocorticoid effects on innate and adaptive immunity, supporting the infection-risk and immunosuppression sections.

Pharmacokinetics / Special Populations

Pickup ME. Clinical pharmacokinetics of prednisone and prednisolone. Clin Pharmacokinet. 1979;4(2):111–128. doi:10.2165/00003088-197904020-00004. PMID 378499. https://pubmed.ncbi.nlm.nih.gov/378499/ Foundational PK source for half-life (2.1–3.5 h plasma), protein binding, and the concentration-dependent nonlinearity of prednisolone.
Murphy VE, Fittock RJ, Zarzycki PK, Delahunty MM, Smith R, Clifton VL. Metabolism of synthetic steroids by the human placenta. Placenta. 2007;28(1):39–46. doi:10.1016/j.placenta.2005.12.010. PMID 16549198. https://pubmed.ncbi.nlm.nih.gov/16549198/ Underpins the relative pregnancy safety of prednisolone via 11β-HSD2-mediated placental inactivation.
U.S. National Library of Medicine. LactMed — Prednisolone. https://www.ncbi.nlm.nih.gov/books/NBK501077/ Contemporary lactation-safety reference, including the suggestion to delay breastfeeding 4 hours after doses >20 mg.