Fever
First line
Ibuprofen is a first-line antipyretic alongside paracetamol. Adult single dose is 200–400 mg. In children the dose is 5–10 mg/kg. Antipyretic effect lasts 6–8 hours, longer than paracetamol.
Non-steroidal anti-inflammatory drugs (NSAIDs)
ATC code: M01AE01 (Ibuprofen)
Non-selectively inhibits cyclooxygenase COX-1 and COX-2, reducing prostaglandin synthesis responsible for pain, inflammation, and fever. Analgesic effect begins within 30–60 minutes. Anti-inflammatory effect builds over the first week of regular use.
First line
Ibuprofen is a first-line antipyretic alongside paracetamol. Adult single dose is 200–400 mg. In children the dose is 5–10 mg/kg. Antipyretic effect lasts 6–8 hours, longer than paracetamol.
First line
Ibuprofen 200–400 mg every 6–8 hours is one of the most studied NSAIDs for mild to moderate pain. Maximum OTC daily dose is 1200 mg, up to 2400 mg under medical supervision. Superior to paracetamol for inflammatory pain. Taking with food reduces dyspepsia risk.
First line
NSAIDs are first-line in osteoarthritis when paracetamol provides insufficient relief. Ibuprofen is prescribed at the lowest effective dose for the shortest duration. Patients with GI risk factors receive a concomitant PPI.
Second line
Ibuprofen 400 mg is an option for mild to moderate migraine attacks. Take as early as possible after headache onset. Less effective than triptans in severe attacks.
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
Ibuprofen is a nonsteroidal anti-inflammatory drug (NSAID). It is taken short-term for acute pain, fever, headache, and menstrual pain. In anti-aging regimens and sports, ibuprofen is widely taken as a universal prophylactic against low-grade aging-related inflammation and for post-exercise recovery. Regular use in healthy adults is not justified: systematic reviews (Trappe 2011, Schoenfeld 2012) show that regular NSAID use after exercise reduces muscle hypertrophy and training adaptation. Chronic NSAID use in healthy adults raises the risk of gastrointestinal bleeding, hypertension, myocardial infarction, stroke, and acute kidney injury. If ibuprofen is being taken daily for inflammation prophylaxis or recovery, consider seeking a second opinion.
17 pairs found. Sorted from critical to minor.
Mechanism
Ketorolac and ibuprofen are both NSAIDs. Additive risk of gastrointestinal bleeding, acute kidney injury, and blood pressure dysregulation. Toradol Section 4.3 specifically lists other NSAIDs as contraindications.
Symptoms
Black or tarry stools (melena), vomiting blood or coffee-ground material, epigastric pain. Acute kidney injury and a rise in blood pressure are also possible. Risk of bleeding multiplies in patients over 65 and with prior peptic ulcer disease.
Management
The combination is not prescribed. One NSAID at a time. Ketorolac courses are limited to 5 days. If analgesia from one NSAID is insufficient, add paracetamol or a short opioid – not a second NSAID.
Sources
Mechanism
Ibuprofen reversibly binds platelet cyclooxygenase-1 and transiently blocks aspirin access for acetylation. When taken together, aspirin's cardioprotective effect is lost; antiplatelet protection fails.
Symptoms
The patient feels no symptoms. Recurrent myocardial infarction and ischaemic stroke risk rises in patients on low-dose aspirin for cardiovascular indications. GI bleeding risk from two NSAIDs persists.
Management
If the patient takes aspirin for cardioprotection, give aspirin 30 minutes before or 8 hours after ibuprofen ( 2006 recommendation). Alternative analgesic without this issue: paracetamol or a selective COX-2 inhibitor (celecoxib).
Mechanism
Apixaban inhibits factor Xa; ibuprofen (NSAID) injures the gastric mucosa and transiently inhibits platelet aggregation. The GI bleeding risk is additive.
Symptoms
Gum bleeding, epistaxis, bruising without trauma, blood in urine or stool, menorrhagia. Severe cases include gastrointestinal or intracranial haemorrhage. Risk rises in patients over 65 and with prior peptic ulcer disease.
Management
Avoid where possible. If a short ibuprofen course is needed, use the minimum effective dose for no more than 5–7 days under pantoprazole cover. For chronic analgesia, choose paracetamol, a selective COX-2 inhibitor (celecoxib), or topical NSAIDs.
Mechanism
Ibuprofen (NSAID) suppresses prostaglandin synthesis maintaining glomerular perfusion at lower blood pressure. On enalapril, which dilates efferent arterioles, the combination raises acute kidney injury risk (the 'triple whammy' with a diuretic is more dangerous still).
Symptoms
Reduced urine output, rising creatinine and potassium. Blood pressure rise and oedema. Symptoms appear earlier in older patients and chronic kidney disease.
Management
Avoid chronic ibuprofen on enalapril. If a short course is needed, use the minimum effective dose for 5–7 days with pantoprazole cover. For chronic analgesia: paracetamol, celecoxib, or topical NSAIDs.
Sources
Mechanism
Ibuprofen reduces lithium renal clearance by inhibiting prostaglandin synthesis in the proximal tubule. Lithium plasma concentration rises 25–60%, leading to intoxication. Lithium has a narrow therapeutic index (target 0.6–1.0 mmol/L, toxic above 1.5).
Symptoms
Within 5–10 days: nausea, vomiting, diarrhea, tremor, confusion, drowsiness. Severe toxicity: seizures, coma, renal injury, arrhythmia.
Management
In bipolar disorder, paracetamol is the first-line analgesic. If an NSAID is needed, use a short course (up to 5 days); check lithium level 4–7 days after NSAID start and 4–7 days after stop. Reduce lithium by 50% and titrate to level.
Sources
Mechanism
NSAIDs reduce renal blood flow via prostaglandin blockade. The ARB (losartan) lowers glomerular pressure. The combination causes acute kidney injury, especially in older patients, chronic kidney disease, and dehydration.
Symptoms
Reduced urine output, rising creatinine and potassium, oedema. Symptoms appear earlier in older patients and in chronic kidney disease.
Management
Avoid prolonged combination. If ibuprofen is needed for a short course, use the minimum effective dose for 5–7 days with pantoprazole cover and creatinine monitoring. For chronic analgesia: paracetamol or celecoxib.
Mechanism
Ibuprofen reduces methotrexate renal elimination by inhibiting proximal tubular secretion. With high-dose methotrexate (oncology, high-dose psoriasis) concentration rises 2–3 fold causing severe myelosuppression and mucositis. With low-dose weekly methotrexate (rheumatoid arthritis 7.5–25 mg/week) risk is lower but not absent.
Symptoms
Within 7–14 days: mouth ulcers, fever, infections, bruising, gum bleeding. CBC: leukopenia, thrombocytopenia; rising creatinine.
Management
With high-dose methotrexate, contraindicated: stop NSAID 48 h before infusion, resume no sooner than 2–3 days after. With low-dose weekly methotrexate, choose paracetamol as first-line analgesic. If an NSAID is needed, check CBC, creatinine and transaminases every 2 weeks for the first 2 months.
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
Additive GI bleeding risk: anticoagulant (rivaroxaban) + ulcerogenic NSAID with antiplatelet effect (ibuprofen).
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, use the minimum effective dose for 5–7 days under pantoprazole cover. For chronic analgesia: paracetamol, celecoxib, or topical NSAIDs.
Mechanism
Ibuprofen reduces renal blood flow via PGE2 inhibition. Tacrolimus is nephrotoxic in its own right. Additive acute kidney injury risk in transplant patients.
Symptoms
Reduced urine output, rising creatinine and potassium, oedema. Symptoms appear earlier in older patients and in chronic kidney disease.
Management
Avoid prolonged combination. For analgesia post-transplant, use paracetamol (up to 2 g/day) or a short opioid course. For neuropathic pain: gabapentin or pregabalin.
Mechanism
Similar to losartan + ibuprofen. NSAIDs reduce renal blood flow; the ARB (telmisartan) lowers glomerular pressure. The combination causes acute kidney injury.
Symptoms
Reduced urine output, rising creatinine and potassium, oedema. Symptoms appear earlier in older patients and in chronic kidney disease.
Management
Avoid prolonged combination. If ibuprofen is needed for a short course, use the minimum effective dose for 5–7 days with pantoprazole cover and creatinine monitoring. For chronic analgesia: paracetamol or celecoxib.
Mechanism
Ibuprofen and warfarin compete for plasma protein (albumin) binding. The free warfarin fraction rises and its anticoagulant effect intensifies. In parallel, ibuprofen reversibly inhibits platelet aggregation and damages the gastric mucosa – two additional bleeding mechanisms. INR may rise modestly, but gastrointestinal bleeding risk increases independently of INR.
Symptoms
Black or tarry stools (melena), vomiting blood or coffee-ground material, epigastric pain. Less severe presentations: gum bleeding, epistaxis, bruising. Risk multiplies in patients with a history of peptic ulcer disease.
Management
For analgesia in a warfarinised patient, paracetamol is preferred (up to 2 g/day, short courses). If chronic NSAID therapy is needed, switch to a selective COX-2 inhibitor (celecoxib) with proton pump inhibitor cover and frequent INR monitoring. Topical NSAIDs (gels, creams) deliver minimal systemic absorption and are acceptable.
Sources
Mechanism
NSAIDs weaken amlodipine's antihypertensive effect via renal prostaglandin suppression. Additive acute kidney injury risk in dehydration.
Symptoms
Gradual blood pressure rise 1–2 weeks after starting the NSAID. In chronic kidney disease: risk of fluid retention and oedema.
Management
For short ibuprofen courses (5–7 days), monitor blood pressure. For chronic analgesia: switch to paracetamol, celecoxib (with PPI cover), or topical NSAIDs.
Mechanism
Similar to bisoprolol + ketorolac. Ibuprofen weakens the antihypertensive effect of the beta-blocker via renal prostaglandin blockade.
Symptoms
Gradual blood pressure rise 1–2 weeks after starting the NSAID. In chronic kidney disease: risk of fluid retention and oedema.
Management
For short ibuprofen courses (5–7 days), monitor blood pressure. For chronic analgesia: switch to paracetamol, celecoxib (with PPI cover), or topical NSAIDs.
Mechanism
Additive GI ulcer and bleeding risk with systemic budesonide. Inhaled budesonide does not clinically affect risk.
Symptoms
Epigastric pain, heartburn, black or tarry stools, blood in vomit, bruising. Higher risk in older patients, prior peptic ulcer, and concurrent anticoagulants.
Management
On systemic budesonide, limit ibuprofen to short courses (no more than 5–7 days) with pantoprazole 20 mg/day. For long-term analgesia: paracetamol up to 2 g/day. Inhaled budesonide with ibuprofen is safe. In older patients and prior peptic ulcer, risk outweighs benefit — consider paracetamol or topical NSAIDs.
Mechanism
Ibuprofen blocks platelet aggregation via COX-1 inhibition, additively with clopidogrel. NSAIDs also injure gastric mucosa, raising GI bleeding risk 2–3-fold.
Symptoms
Gum bleeding, epistaxis, bruising without trauma, black or tarry stools, haematuria. Higher risk in older patients, prior peptic ulcer disease, and chronic kidney disease.
Management
For analgesia on clopidogrel, use paracetamol. If NSAIDs are needed (arthritis, pain flare), choose a short course of no more than 5 days with gastroprotection (pantoprazole 20 mg/day). For osteoarthritis, alternatives include topical NSAIDs and physiotherapy. Ibuprofen can also competitively displace aspirin from the COX-1 active site, which matters for dual antiplatelet therapy.
Mechanism
Additive nephrotoxicity. NSAIDs reduce renal blood flow by suppressing vasodilatory prostaglandin synthesis; contrast adds tubular osmotic load. Contrast-induced AKI risk rises.
Symptoms
Decreased urine output, rising creatinine, oedema, nausea. Symptoms develop 24–72 hours after contrast.
Management
Stop ibuprofen 24–48 hours before elective contrast imaging; restart 48 hours after the study once creatinine normalises. With creatinine clearance below 60 mL/min, give IV isotonic hydration 6–12 hours before and after imaging. Alternative: paracetamol up to 3 g/day.
Sources
Opens the checker prefilled with this drug. Pick the second one from your regimen.
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FDA category C in the first and second trimesters. Contraindicated in the third trimester (category D) due to premature ductus arteriosus closure and oligohydramnios. Avoid after 20 weeks.
Excreted in breast milk in minimal amounts. Short-term use at standard doses is acceptable during breastfeeding.
Reference information, not a clinical decision. Discuss feeding pauses or changes with your physician or an IBCLC.
Ibuprofen is evaluated for the following indications with varying evidence strength: Fever (evidence tier A), Mild to moderate pain in adults (evidence tier A), Osteoarthritis (evidence tier A). See the full indication matrix with dosing and citations above on this page.
Common side effects of Ibuprofen (≥ 1 in 100): Dyspepsia, nausea, epigastric pain, Headache, dizziness, Fluid retention, peripheral edema. See the Safety section for uncommon and serious reactions.
FDA category C. FDA category C in the first and second trimesters. Contraindicated in the third trimester (category D) due to premature ductus arteriosus closure and oligohydramnios. Avoid after 20 weeks.
Excreted in breast milk in minimal amounts. Short-term use at standard doses is acceptable during breastfeeding.
Ibuprofen is contraindicated in: Active peptic ulcer disease or GI bleeding; Severe renal impairment (eGFR below 30); Severe heart failure (NYHA III–IV); Third trimester of pregnancy; Aspirin-exacerbated respiratory disease (aspirin triad). Full list in the Safety section.