Antiplatelet agents (low dose) / NSAIDs (analgesic dose)
ATC code: B01AC06 (Acetylsalicylic acid)
Irreversible inhibitor of cyclooxygenase-1 and -2 via acetylation of the active-site serine. In platelets it blocks COX-1 → thromboxane A2 → aggregation for the platelet lifespan (7–10 days). At cardiovascular doses (75–100 mg) it inhibits platelets while relatively sparing endothelial prostacyclin. At doses ≥ 500 mg it produces antiinflammatory, analgesic, and antipyretic effects. Dose-dependently increases the risk of hemorrhagic stroke and GI bleeding.
First line
Low-dose aspirin (75–100 mg daily) is the cornerstone of secondary prevention in established ASCVD. It reduces the risk of recurrent MI, stroke, and vascular death by 20–25 %. Prescribed lifelong if no absolute contraindications exist. After ACS or stenting, dual antiplatelet therapy (aspirin plus clopidogrel, , or prasugrel) is given for 6–12 months.
Individual decision
Routine aspirin for primary prevention is not recommended. ASPREE, ARRIVE, and ASCEND trials showed that in moderate-risk patients, the reduction in ischemic events is offset by increased bleeding. 2022 recommends against initiating aspirin in adults 60 and older for primary prevention. In adults 40–59 with a 10-year ASCVD risk of 10 % or more, the decision is individualized.
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
Low-dose aspirin (75-100 mg) is taken in anti-aging and longevity communities to suppress chronic inflammation of aging and to extend life. Primary-prevention trials ASCEND 2018 (patients with diabetes) and ASPREE 2018 (older adults over 70) showed: in healthy adults, aspirin for primary CV prevention is not justified – the small reduction in heart attack risk is offset by an increase in major bleeding, and in older adults ASPREE even showed increased all-cause mortality on aspirin. 2019 and 2021 do not recommend aspirin for primary CV prevention in people without confirmed coronary disease, stroke, or other high CV risk. The drug raises the risk of gastrointestinal bleeding, hemorrhagic stroke, and hypersensitivity reactions. If aspirin is being taken for longevity without confirmed high CV risk, consider seeking a second opinion.
39 pairs found. Sorted from critical to minor.
Mechanism
Ketorolac is the most potent oral and parenteral NSAID. Aspirin irreversibly blocks platelet cyclooxygenase. Co-administration of two NSAIDs adds up the risks: gastrointestinal bleeding, acute kidney injury, sodium and fluid retention. Toradol Section 4.3 specifically lists aspirin and 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. If aspirin is required for cardioprotection (75–100 mg/day), replace ketorolac with paracetamol, metamizole, or a short opioid course. Ketorolac courses are limited to 5 days under all circumstances.
Mechanism
Aspirin irreversibly blocks platelet cyclooxygenase and reduces platelet aggregation. Warfarin blocks vitamin K-dependent clotting factor synthesis. Two different antithrombotic mechanisms add up. Aspirin also damages the gastric mucosa, raising bleeding risk independently of coagulation parameters.
Symptoms
Gum bleeding, epistaxis, black or tarry stools (melena), vomiting blood or coffee-ground material. Severe cases include fatal intracranial haemorrhage. Risk multiplies in patients over 75 and with prior peptic ulcer disease.
Management
The combination is acceptable only for strict indications: after coronary stenting, mechanical heart valves, acute coronary syndrome. Limit triple/dual antithrombotic therapy to 1–6 months based on risk. Aspirin dose: 75–100 mg/day. PPI cover (pantoprazole) is mandatory. Check INR every 2–4 weeks.
Sources
Mechanism
Aspirin irreversibly blocks platelet cyclooxygenase; apixaban directly inhibits factor Xa. Dual antithrombotic action roughly doubles major bleeding risk versus apixaban alone.
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
Combine only for strict indications: after coronary stenting or in acute coronary syndrome. Limit aspirin to 75–100 mg/day, and dual therapy to 1–6 months. PPI cover with pantoprazole is mandatory.
Sources
Mechanism
Diclofenac competitively inhibits platelet cyclooxygenase-1 and blocks aspirin's access for COX-1 acetylation. Co-administration loses aspirin's cardioprotective effect. Additive ulcerogenic effect of two 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
If the patient takes aspirin for cardioprotection, give aspirin 30 minutes before or 8 hours after diclofenac. Alternative analgesic without this issue: paracetamol or a selective COX-2 inhibitor (celecoxib).
Mechanism
Escitalopram (SSRI) depletes the platelet serotonin pool, impairing primary haemostasis. Aspirin irreversibly blocks platelet cyclooxygenase. Combined, GI bleeding risk roughly doubles.
Symptoms
Gum bleeding, epistaxis, bruising without trauma, black tarry stools, blood in urine. Severe cases include gastrointestinal or intracranial haemorrhage.
Management
The combination is acceptable at low aspirin doses (75–100 mg as cardioprotection). Mandatory PPI cover with pantoprazole. Alternative antidepressants with minimal platelet effect: mirtazapine or agomelatine.
Sources
Mechanism
Fluoxetine (SSRI) depletes the platelet serotonin pool, impairing primary haemostasis. Aspirin irreversibly blocks platelet cyclooxygenase. Combined, GI bleeding risk roughly doubles.
Symptoms
Gum bleeding, epistaxis, bruising without trauma, black stools, blood in urine. Severe cases include gastrointestinal or intracranial haemorrhage.
Management
The combination is acceptable at low aspirin doses (75–100 mg as cardioprotection). PPI cover with pantoprazole is mandatory. Alternative antidepressants with minimal platelet effect: mirtazapine or agomelatine.
Sources
Mechanism
Dual mechanism: aspirin competes with furosemide for organic anion tubular secretion in the renal tubules (so furosemide does not reach its target in the loop of Henle lumen), and concurrently suppresses renal prostaglandin synthesis supporting glomerular perfusion.
Symptoms
Reduced urine output, worsening oedema, weight gain. In heart failure: dyspnoea, orthopnoea. Blood pressure and creatinine may rise.
Management
At low aspirin doses (75–100 mg for cardioprotection), the clinical effect is minimal. At full anti-inflammatory doses, furosemide-induced diuresis drops markedly – titrate furosemide clinically or temporarily withhold aspirin during decompensation.
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
Aspirin suppresses tubular secretion of methotrexate and displaces it from albumin binding. Methotrexate plasma levels rise – particularly dangerous at oncologic doses.
Symptoms
Mouth ulcers (mucositis), nausea, diarrhoea, hair loss. Blood counts fall: leukocytes, platelets, erythrocytes. Severe cases include fatal pancytopenia, nephrotoxicity, and hepatotoxicity.
Management
At oncologic methotrexate doses, the combination is not prescribed. At low rheumatologic doses (5–25 mg/week), cardioprotective aspirin (75–100 mg/day) is acceptable when renal function is preserved, with full blood count and creatinine every 1–3 months.
Mechanism
Aspirin irreversibly blocks platelet cyclooxygenase; rivaroxaban directly inhibits factor Xa. Dual antithrombotic action raises major bleeding risk roughly 1.5- to 2-fold versus rivaroxaban alone.
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
Combine only for strict indications. Limit aspirin to 75–100 mg/day and dual therapy to 1–6 months. PPI cover with pantoprazole is mandatory.
Mechanism
Sertraline (SSRI) depletes the platelet serotonin pool, weakening platelet aggregation. Aspirin irreversibly blocks platelet cyclooxygenase. Combined, GI bleeding risk roughly doubles.
Symptoms
Gum bleeding, epistaxis, bruising without trauma, black stools, blood in urine. Severe cases include gastrointestinal or intracranial haemorrhage.
Management
The combination is acceptable at low aspirin doses (75–100 mg as cardioprotection). PPI cover with pantoprazole is mandatory. Alternative antidepressants with minimal platelet effect: mirtazapine or agomelatine.
Sources
Mechanism
Aspirin suppresses renal prostaglandin synthesis that maintains glomerular perfusion. Diuretic and natriuretic effects of spironolactone diminish and potassium accumulates.
Symptoms
Oedema, weight gain, rising blood pressure. Weakness, paraesthesia, and arrhythmias from hyperkalaemia. Reduced diuretic effect emerges within 1–2 weeks of starting aspirin.
Management
At low aspirin doses (75–100 mg for cardioprotection), the clinical effect is minimal; co-prescription is acceptable with potassium and creatinine monitoring. At full anti-inflammatory doses, the diuretic response drops markedly – titrate spironolactone clinically.
Mechanism
Aspirin irreversibly blocks platelet cyclooxygenase and reduces aggregation. Warfarin blocks vitamin K-dependent clotting factor synthesis. Two different antithrombotic mechanisms add up. Aspirin also injures the gastric mucosa.
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
Combine only for strict indications: after coronary stenting, mechanical heart valves, acute coronary syndrome. Limit triple/dual antithrombotic therapy to 1–6 months based on risk. Aspirin 75–100 mg/day. Mandatory pantoprazole cover; check INR every 2–4 weeks.
Mechanism
At high aspirin doses (above 1 g/day), vasodilator prostaglandins are suppressed, weakening amlodipine's antihypertensive effect. At cardioprotective doses (75–100 mg/day), the effect is minimal.
Symptoms
Gradual blood pressure rise 1–2 weeks after starting the NSAID. In chronic kidney disease: risk of fluid retention and oedema.
Management
Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At anti-inflammatory aspirin doses, monitor blood pressure and increase amlodipine if needed.
Mechanism
Additive ulcerogenic effect with oral budesonide (used in inflammatory bowel disease). Inhaled forms have minimal systemic effect.
Symptoms
Epigastric pain, nausea, heartburn. With prolonged therapy: peptic ulcer and GI bleeding risk (black stools, vomiting blood or coffee-ground material). Older patients and prior peptic ulcer disease: higher risk.
Management
Inhaled budesonide for asthma or COPD requires no special measures. For oral therapy (Crohn's disease, ulcerative colitis): PPI cover with pantoprazole, cardioprotective aspirin no more than 100 mg/day.
Mechanism
At analgesic doses (above 1 g/day), aspirin suppresses vasodilator prostaglandins and weakens the ACE-I's hypotensive effect. At cardioprotective doses (75–100 mg), the effect is minimal.
Symptoms
Gradual blood pressure rise at high aspirin doses. At cardioprotective doses, no significant changes.
Management
Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high doses, monitor blood pressure and increase captopril if needed. Alternative analgesic: paracetamol.
Mechanism
Celecoxib is a selective COX-2 inhibitor and does not displace aspirin from COX-1 (unlike ibuprofen/naproxen). Aspirin's antiplatelet effect is preserved. Additive GI bleeding risk persists.
Symptoms
Gum bleeding, epistaxis, bruising without trauma, black or tarry stools. Severe cases: GI bleeding.
Management
The combination is acceptable. Aspirin's cardioprotective effect is preserved. PPI cover with pantoprazole is mandatory in chronic celecoxib therapy. Check blood pressure and creatinine every 3 months.
Mechanism
Old experimental data suggested NSAIDs combined with fluoroquinolones increase CNS excitability and seizure risk (via GABAergic suppression). Clinical data are very limited.
Symptoms
Mostly asymptomatic. In patients with prior epilepsy or head injury: rare seizure cases.
Management
The combination is acceptable in patients without prior epilepsy. In epilepsy or eating disorders: alternative antibiotics (a cephalosporin, nitrofurantoin) and paracetamol for analgesia.
Sources
Mechanism
Similar to ASA + fluvoxamine. SSRI-induced platelet dysfunction plus aspirin's antiplatelet effect – bleeding risk.
Symptoms
Gum bleeding, epistaxis, bruising without trauma. Severe cases: GI bleeding.
Management
The combination is acceptable at low aspirin doses (75–100 mg). PPI cover with pantoprazole is mandatory. Alternative antidepressants: mirtazapine or agomelatine.
Mechanism
Additive antiplatelet effect via different targets: aspirin irreversibly blocks platelet cyclooxygenase; clopidogrel inhibits the P2Y12 receptor. The combination raises bleeding risk 1.5- to 2-fold versus monotherapy.
Symptoms
Gum bleeding, epistaxis, bruising without trauma. Severe cases: GI bleeding.
Management
The combination (dual antiplatelet therapy) is standard after acute coronary syndrome or coronary stenting. Limit duration to 1–6 months based on thrombosis and bleeding risk. Aspirin 75–100 mg/day. Mandatory PPI cover with pantoprazole.
Sources
Mechanism
Additive ulcerogenic effect. Dexamethasone suppresses GI mucosal repair; aspirin blocks protective prostaglandins.
Symptoms
Epigastric pain, nausea, heartburn. With prolonged therapy: peptic ulcer and GI bleeding risk (black stools, vomiting blood or coffee-ground material). Older patients and prior peptic ulcer disease: higher risk.
Management
For short dexamethasone courses, cardioprotective aspirin is acceptable with pantoprazole cover. For prolonged systemic glucocorticoid therapy, watch dyspepsia symptoms; consider stool occult blood testing as needed.
Mechanism
High aspirin doses can reduce renal digoxin clearance via prostaglandin-dependent renal blood flow suppression. The effect is clinically significant at analgesic aspirin doses (above 1 g/day), not cardioprotective ones.
Symptoms
Nausea, anorexia, visual disturbances (yellow-green halos around lights), arrhythmias at aspirin doses above 1 g/day.
Management
Cardioprotective aspirin doses are acceptable without adjustment. At high doses, check digoxin level at 1 week. For chronic analgesia on digoxin: paracetamol.
Mechanism
Diltiazem impairs platelet function via calcium channel blockade; aspirin is an antiplatelet. Mild additive bleeding risk, rarely clinically significant.
Symptoms
Usually asymptomatic. In patients with bleeding risk factors (peptic ulcer, older age): rare gum bleeding and epistaxis.
Management
Standard combination in ischaemic heart disease. Cardioprotective aspirin doses (75–100 mg) are acceptable without special measures. In patients with bleeding risk factors: PPI cover with pantoprazole.
Mechanism
Duloxetine (SNRI) depletes the platelet serotonin pool, impairing primary haemostasis. Additively with aspirin's antiplatelet effect: GI bleeding risk roughly doubles.
Symptoms
Gum bleeding, epistaxis, bruising without trauma, black or tarry stools. Severe cases: GI bleeding.
Management
The combination is acceptable at low aspirin doses (75–100 mg). PPI cover with pantoprazole is mandatory. Alternative antidepressants with minimal platelet effect: mirtazapine or agomelatine.
Mechanism
High aspirin doses (above 1 g/day) weaken the hypotensive and cardioprotective effects of the ACE-I via vasodilator prostaglandin suppression. At cardioprotective doses (75–100 mg/day), the clinical effect is minimal.
Symptoms
Gradual blood pressure rise at high aspirin doses. At cardioprotective doses, no significant changes.
Management
Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high aspirin doses, monitor blood pressure and increase enalapril if needed. Alternative analgesic: paracetamol.
Sources
Mechanism
SSRIs block serotonin reuptake into platelets, impairing primary haemostasis. Additively with aspirin's antiplatelet effect: upper GI bleeding risk roughly doubles.
Symptoms
Gum bleeding, epistaxis, bruising without trauma. Severe cases: GI bleeding.
Management
The combination is acceptable at low aspirin doses (75–100 mg as cardioprotection). PPI cover with pantoprazole is mandatory. Alternative antidepressants with minimal platelet effect: mirtazapine or agomelatine.
Mechanism
Additive nephrotoxicity. Aspirin suppresses prostaglandin-dependent renal blood flow (at high doses); gentamicin causes direct tubulotoxicity.
Symptoms
Reduced urine output, rising creatinine. Symptoms appear earlier in older patients and chronic kidney disease.
Management
Cardioprotective aspirin doses (75–100 mg) do not require withdrawal. At high doses, check creatinine before and 3–5 days into gentamicin therapy. Ensure adequate hydration; consider switching to a less nephrotoxic antibiotic (a cephalosporin, carbapenem).
Sources
Mechanism
High aspirin doses displace glibenclamide from albumin binding and suppress hepatic gluconeogenesis. Hypoglycaemia risk at aspirin doses above 3 g/day.
Symptoms
Sweating, tremor, hunger, tachycardia, confusion. Severe cases: seizures and coma. Symptoms appear 1–2 days after starting high aspirin doses.
Management
Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high doses, monitor glucose 4 times daily in the first week; reduce glibenclamide if needed.
Mechanism
High aspirin doses (above 1 g/day) weaken the ARB's antihypertensive effect via vasodilator prostaglandin suppression. At cardioprotective doses, the effect is clinically minor.
Symptoms
Gradual blood pressure rise at high aspirin doses. At cardioprotective doses, no significant changes.
Management
Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high doses, monitor blood pressure and increase losartan if needed. Alternative analgesic: paracetamol.
Sources
Mechanism
Meloxicam is preferentially COX-2 selective and weakly displaces aspirin from COX-1. Additive GI bleeding risk persists from the ulcerogenic effect of both drugs.
Symptoms
Gum bleeding, epistaxis, bruising without trauma, black or tarry stools. Severe cases: GI bleeding.
Management
Aspirin's cardioprotective effect is preserved better than with ibuprofen/naproxen. PPI cover with pantoprazole is mandatory in chronic meloxicam therapy. Alternative analgesic: paracetamol or celecoxib.
Mechanism
Glucocorticoids damage the gastric mucosa and suppress protective prostaglandin production. Aspirin compounds the 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 methylprednisolone courses, cardioprotective aspirin is acceptable with pantoprazole cover. For prolonged systemic therapy, watch dyspepsia symptoms; consider stool occult blood testing if needed.
Mechanism
Naproxen (NSAID) may block aspirin's acetylation of platelet cyclooxygenase-1, reducing its cardioprotective effect. Plus additive GI bleeding risk from two antiplatelet and ulcerogenic drugs.
Symptoms
Gum bleeding, epistaxis, bruising without trauma, black or tarry stools. Severe cases: GI bleeding.
Management
If the patient takes aspirin for cardioprotection, give aspirin 30 minutes before or 8 hours after naproxen. Alternative analgesic without this issue: paracetamol or a selective COX-2 inhibitor (celecoxib).
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
High aspirin doses (above 1 g/day) may reduce the ARB's antihypertensive effect via vasodilator prostaglandin suppression. Cardioprotective doses (75–100 mg) are clinically minor.
Symptoms
Gradual blood pressure rise at high aspirin doses. At cardioprotective doses, no significant changes.
Management
Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high doses, monitor blood pressure and increase telmisartan if needed. Alternative analgesic: paracetamol.
Mechanism
Aspirin displaces valproate from albumin binding and suppresses its metabolism. The free valproate fraction rises, raising neurotoxicity risk (tremor, sedation, hyperammonaemia).
Symptoms
Tremor, drowsiness, nausea, confusion. Severe cases: hyperammonaemic encephalopathy. Symptoms appear within 1–2 weeks at high aspirin doses.
Management
Cardioprotective aspirin doses (75–100 mg) are usually acceptable. At high doses, check valproate level at 1 week. For chronic analgesia on valproate: paracetamol.
Mechanism
Analgesic aspirin doses weaken the ARB's antihypertensive effect via vasodilator prostaglandin suppression. Cardioprotective doses are clinically minor.
Symptoms
Gradual blood pressure rise at high aspirin doses. At cardioprotective doses, no significant changes.
Management
Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high doses, monitor blood pressure and increase valsartan if needed. Alternative analgesic: paracetamol.
Mechanism
Venlafaxine (SNRI) depletes the platelet serotonin pool, impairing primary haemostasis. With aspirin: additive GI bleeding risk.
Symptoms
Gum bleeding, epistaxis, bruising without trauma, black or tarry stools. Severe cases: GI bleeding.
Management
The combination is acceptable at low aspirin doses (75–100 mg). PPI cover with pantoprazole is mandatory. Alternative antidepressants with minimal platelet effect: mirtazapine or agomelatine.
Mechanism
At high doses, aspirin weakens verapamil's antihypertensive effect via vasodilator prostaglandin suppression. At cardioprotective doses, there is no clinically significant effect.
Symptoms
Gradual blood pressure rise at high aspirin doses. At cardioprotective doses, no significant changes.
Management
Cardioprotective aspirin doses (75–100 mg) are acceptable without adjustment. At high doses, monitor blood pressure and increase verapamil if needed. Alternative analgesic: paracetamol.
Mechanism
Antacids accelerate renal aspirin elimination via urinary alkalinisation. At cardioprotective doses (75–100 mg/day), the effect is clinically minimal.
Symptoms
The combination usually causes no specific symptoms. Each drug's individual side effects remain.
Management
At cardioprotective aspirin doses, no adjustment needed. At high anti-inflammatory doses (over 3 g/day) with simultaneous antacid for several days, efficacy may slightly drop — separate dosing by 2 hours.
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FDA pregnancy categories were retired in 2015 (PLLR). Full analgesic doses are avoided throughout pregnancy and strictly contraindicated after 30 weeks due to premature closure of the ductus arteriosus. Low-dose aspirin (81–150 mg daily) for preeclampsia prevention in high-risk women is started at week 12 and continued until delivery per USPSTF 2021, ACOG Committee Opinion 743, NICE NG133, and WHO 2011 (the previous «stop at week 36» rule has been dropped — there is no evidence supporting earlier discontinuation).
Excreted in breast milk. Low antiplatelet doses (75–100 mg) are acceptable during breastfeeding. High analgesic doses are not recommended.
Reference information, not a clinical decision. Discuss feeding pauses or changes with your physician or an IBCLC.
Acetylsalicylic acid is evaluated for the following indications with varying evidence strength: Established ASCVD, secondary prevention (evidence tier A), Primary cardiovascular prevention with aspirin (evidence tier C), Anti-aging and longevity (evidence tier F). See the full indication matrix with dosing and citations above on this page.
Common side effects of Acetylsalicylic acid (≥ 1 in 100): Dyspepsia, heartburn, Increased bleeding tendency (epistaxis, bruising), Nausea. See the Safety section for uncommon and serious reactions.
FDA category D. FDA pregnancy categories were retired in 2015 (PLLR). Full analgesic doses are avoided throughout pregnancy and strictly contraindicated after 30 weeks due to premature closure of the ductus arteriosus. Low-dose aspirin (81–150 mg daily) for preeclampsia prevention in high-risk women is started at week 12 and continued until delivery per USPSTF 2021, ACOG Committee Opinion 743, NICE NG133, and WHO 2011 (the previous «stop at week 36» rule has been dropped — there is no evidence supporting earlier discontinuation).
Excreted in breast milk. Low antiplatelet doses (75–100 mg) are acceptable during breastfeeding. High analgesic doses are not recommended.
Acetylsalicylic acid is contraindicated in: Active GI bleeding; Severe thrombocytopenia; Hemorrhagic diathesis; Aspirin allergy or aspirin-exacerbated respiratory disease; Severe hepatic failure. Full list in the Safety section.