Drug Monograph
Aspirin (Acetylsalicylic Acid)
Bayer Aspirin, Ecotrin, Vazalore (PL-ASA), Durlaza (ER)
Pharmacokinetic Profile
Half-Life (ASA)
15–20 min
Half-Life (Salicylate)
2–4.5 h (dose-dependent)
Metabolism
Hepatic esterase hydrolysis
Protein Binding
50–80% (albumin, concentration-dependent)
Bioavailability
~68% (plain tablet)
Volume of Distribution
0.1–0.2 L/kg
Clinical Information
Drug Class
Salicylate / NSAID / Antiplatelet
Available Doses
81 mg, 325 mg, 500 mg, 650 mg (suppository); 162.5 mg (ER capsule)
Route
Oral, Rectal
Renal Adjustment
Avoid in severe impairment (CrCl <10)
Hepatic Adjustment
Avoid in severe hepatic insufficiency
Pregnancy
Avoid ≥20 weeks (NSAID doses); low-dose may be used under guidance
Lactation
Low-dose (75–150 mg) compatible; avoid analgesic doses
Schedule / Legal Status
OTC (analgesic/antipyretic); Rx for specific CV indications
Generic Available
Yes
Indications
| Indication | Approved Population | Therapy Type | Status |
|---|---|---|---|
| Acute coronary syndrome (STEMI/NSTEMI/UA) | Adults | Combination (with P2Y12 inhibitor) | FDA Approved |
| Secondary prevention of cardiovascular events | Adults with established ASCVD | Monotherapy or combination | FDA Approved |
| Secondary prevention of ischaemic stroke / TIA | Adults | Monotherapy or combination | FDA Approved |
| Post-coronary revascularisation (PCI / CABG) | Adults | Combination (DAPT) | FDA Approved |
| Mild-to-moderate pain and fever | Adults & children ≥12 years | Monotherapy | FDA Approved |
| Inflammatory conditions (e.g., rheumatic fever) | Adults | Monotherapy | FDA Approved |
| Kawasaki disease | Children (typically <5 years) | Combination (with IVIG) | FDA Approved |
Aspirin remains the cornerstone antiplatelet agent for patients with established atherosclerotic cardiovascular disease. Its role in secondary prevention is well-supported by decades of randomised trial data, with consistent reductions in recurrent myocardial infarction, ischaemic stroke, and vascular death. For acute coronary syndromes, aspirin is administered as a loading dose at first medical contact and continued as lifelong maintenance therapy. In paediatric practice, aspirin is used in Kawasaki disease for both its anti-inflammatory and antiplatelet properties.
Off-Label Uses
Primary prevention of ASCVD (ages 40–70, high risk): The 2019 ACC/AHA guideline gives a class IIb recommendation for low-dose aspirin in select adults 40–70 years with elevated ASCVD risk who are not at increased bleeding risk. The 2022 USPSTF recommends against initiation in adults ≥60 years. Evidence: High
Pre-eclampsia prevention: ACOG and USPSTF recommend low-dose aspirin (81 mg daily) starting at 12–16 weeks of gestation in women at high risk of pre-eclampsia. Evidence: High
Colorectal cancer chemoprevention: Observational data and meta-analyses suggest aspirin use for ≥5 years reduces colorectal cancer incidence, but routine use for this purpose alone is not broadly recommended following the ASPREE trial results. Evidence: Moderate
Pericarditis: High-dose aspirin (650–1000 mg TID) is first-line treatment for acute pericarditis per ESC guidelines. Evidence: High
Dosing
Adult Dosing by Clinical Scenario
| Clinical Scenario | Starting Dose | Maintenance Dose | Maximum Dose | Notes |
|---|---|---|---|---|
| Acute coronary syndrome (STEMI / NSTEMI / UA) | 162–325 mg chewed immediately | 75–100 mg daily | 325 mg daily | Use non-enteric-coated, chewed for rapid absorption; combine with P2Y12 inhibitor 2025 ACC/AHA ACS guideline: prefer 75–100 mg maintenance |
| Secondary CV prevention (stable ASCVD, post-MI, post-stroke) | 75–100 mg daily | 75–100 mg daily | 325 mg daily | Lifelong therapy; no loading dose needed for chronic use 81 mg most common US dose |
| Post-PCI (with stent placement) | 325 mg pre-procedure | 81 mg daily | 325 mg daily | DAPT duration varies by stent type and bleeding risk; typically 6–12 months Transition to 81 mg after initial period per 2021 ACC/AHA/SCAI |
| Primary CV prevention (select adults 40–70) | 75–100 mg daily | 75–100 mg daily | 100 mg daily | Only if ≥10% 10-year ASCVD risk, not at increased bleeding risk 2022 USPSTF: against initiation ≥60 years |
| Analgesia / antipyresis (adults) | 325–650 mg q4–6h | 325–650 mg q4–6h | 4,000 mg/day | Short-term use preferred; take with food or milk OTC label: max 12 tablets (325 mg) per 24 hours |
| Anti-inflammatory (rheumatic fever, pericarditis) | 650–1,000 mg TID | 3–6 g/day divided | 6,000 mg/day | Target salicylate levels 15–30 mg/dL; taper over weeks Monitor for tinnitus as early sign of toxicity |
| Pre-eclampsia prevention | 81 mg daily | 81 mg daily | 150 mg daily | Initiate at 12–16 weeks gestation; continue until delivery ACOG recommends for women with ≥1 high-risk factor |
Paediatric Dosing
| Clinical Scenario | Starting Dose | Maintenance Dose | Maximum Dose | Notes |
|---|---|---|---|---|
| Kawasaki disease — acute febrile phase | 80–100 mg/kg/day divided QID | 80–100 mg/kg/day divided QID | 100 mg/kg/day | Continue until afebrile for 48–72 h; give with IVIG 2 g/kg AHA recommendation; some centres use 30–50 mg/kg/day |
| Kawasaki disease — convalescent phase | 3–5 mg/kg/day once daily | 3–5 mg/kg/day once daily | 5 mg/kg/day | Continue 6–8 weeks if no coronary abnormalities; indefinitely if aneurysms persist Ensure influenza and varicella vaccination is current |
Clinical Pearl: Enteric-Coated vs. Plain Aspirin
For acute coronary syndromes, always use non-enteric-coated aspirin, chewed for rapid buccal absorption. Enteric-coated formulations have erratic absorption and may result in delayed and inadequate platelet inhibition, particularly in obese or diabetic patients. For chronic secondary prevention, plain low-dose aspirin (75–100 mg) is generally preferred over enteric-coated formulations for more reliable bioavailability.
Pharmacology
Mechanism of Action
Aspirin irreversibly acetylates a serine residue (Ser-530) in the active site of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). This covalent modification permanently blocks the enzyme’s ability to convert arachidonic acid into prostaglandin H2, the precursor of thromboxane A2 (TXA2) and other prostaglandins. In platelets, which lack a nucleus and cannot synthesise new COX protein, inhibition of TXA2 production is irreversible for the lifespan of the platelet (approximately 7–10 days). This accounts for aspirin’s potent antiplatelet effect at low doses (75–100 mg). At higher doses, aspirin also inhibits COX-2 in nucleated cells, producing anti-inflammatory, analgesic, and antipyretic effects. The anti-inflammatory dose range (3–6 g/day) substantially exceeds the antiplatelet dose because nucleated cells regenerate COX enzyme within hours.
ADME Profile
| Parameter | Value | Clinical Implication |
|---|---|---|
| Absorption | Rapid from stomach and upper GI; Tmax 1–2 h (plain); bioavailability ~68% due to first-pass hydrolysis | Pre-systemic hydrolysis in portal circulation achieves platelet COX-1 inhibition before drug reaches systemic circulation; chewed administration further accelerates onset to ~15 min |
| Distribution | Vd 0.1–0.2 L/kg; 50–80% protein-bound to albumin (concentration-dependent); crosses placenta and enters breast milk | Low Vd reflects high albumin binding; at toxic concentrations (>300 mcg/mL), binding sites saturate, increasing free salicylate and toxicity risk |
| Metabolism | Rapid hydrolysis by esterases to salicylic acid (active metabolite); further hepatic conjugation via glycine (salicyluric acid, 75%), glucuronidation, and oxidation to gentisic acid | Glycine conjugation pathway saturates at therapeutic doses, producing dose-dependent (Michaelis-Menten) kinetics; half-life of salicylate extends from 2–4.5 h at low doses to 15–30 h in overdose |
| Elimination | Renal: salicyluric acid (75%), free salicylic acid (10%), salicyl phenolic glucuronide (10%), ASA glucuronide (5%), gentisic acid (<1%); strongly pH-dependent | Alkalinisation of urine to pH 7.5–8 increases renal clearance 10–20-fold; this principle underpins urinary alkalinisation therapy in salicylate toxicity |
Side Effects
≥10%
Very Common
| Adverse Effect | Incidence | Clinical Note |
|---|---|---|
| Dyspepsia / epigastric discomfort | 15–25% | Most common GI complaint; occurs even at low doses; prevalence increases with dose and duration; PPI co-therapy reduces symptoms |
| Nausea | 10–15% | More frequent with analgesic/anti-inflammatory doses; take with food to mitigate |
1–10%
Common
| Adverse Effect | Incidence | Clinical Note |
|---|---|---|
| Gastroesophageal reflux | 5–10% | Reported as most frequent GI symptom in LDA survey data; contributes to non-adherence |
| Easy bruising | 5–8% | Reflects irreversible platelet COX-1 inhibition; prolonged bleeding time for 7–10 days after last dose |
| Tinnitus | 1–5% | Dose-related; occurs at salicylate levels approaching 200 mcg/mL; an early warning signal of toxicity; reversible on dose reduction |
| Minor GI bleeding (occult) | 2–4% | Chronic occult blood loss may produce iron-deficiency anaemia; faecal occult blood testing may be positive in asymptomatic users |
| Increased bleeding time | 1–3% | Clinically significant in surgical settings; discontinue 7–10 days before elective procedures if antiplatelet effect not needed |
Serious
Serious (Regardless of Frequency)
| Adverse Effect | Estimated Frequency | Typical Onset | Required Action |
|---|---|---|---|
| Major upper GI bleeding (haematemesis/melaena) | 1–2 per 1,000 patient-years (LDA) | Any time; risk does not attenuate with duration | Discontinue aspirin; urgent endoscopy; transfuse as needed; consider PPI co-therapy on reinitiation; weigh CV benefit vs GI risk before restarting |
| Intracranial haemorrhage | 0.2–0.4 per 1,000 patient-years | Any time | Emergency neurosurgical evaluation; discontinue all antiplatelet/anticoagulant therapy; platelet transfusion may be considered |
| Aspirin-exacerbated respiratory disease (AERD) | 0.3–0.9% general population; ~7% of all asthmatics; up to 30–40% in asthmatics with nasal polyps | 30 min to 3 h after ingestion | Immediate discontinuation; bronchodilators and epinephrine if severe; absolute contraindication to future NSAID use unless desensitised |
| Reye syndrome | Very rare (children/adolescents only) | 3–7 days after viral illness | Aspirin is contraindicated in children <12 with febrile viral illness; ICU management if suspected; permanent avoidance of aspirin in recovered patients |
| Peptic ulcer perforation | Rare (<0.1%/year) | Weeks to months | Surgical emergency; discontinue aspirin; H. pylori eradication if positive |
| Salicylate toxicity (chronic or acute) | Rare at therapeutic doses | Chronic: insidious; Acute: hours | Check serum salicylate level; urinary alkalinisation; haemodialysis if level >100 mg/dL or clinical deterioration; activated charcoal if <3 h post-ingestion |
| Anaphylaxis / angioedema | Very rare | Minutes to hours | Emergency care with epinephrine; permanent avoidance; refer for allergy evaluation and possible desensitisation if aspirin is essential |
Discontinuation
Discontinuation Rates
Low-Dose Aspirin (CV prevention)
~10–15% over first year
Top reasons: Dyspepsia, GI discomfort, bleeding concerns, physician recommendation
Analgesic / Anti-inflammatory Dose
~20–25% within treatment course
Top reasons: GI symptoms, nausea, tinnitus, bleeding events
| Reason for Discontinuation | Incidence | Context |
|---|---|---|
| Dyspepsia / GI intolerance | 5–10% | Most frequent reason; PPI co-therapy can improve adherence significantly |
| Overt GI bleeding | 1–2% | May prompt permanent discontinuation unless CV risk strongly favours reinitiation |
| Tinnitus / hearing changes | 1–3% | Predominantly at anti-inflammatory doses; reversible on dose reduction |
| Planned surgery | Variable | Typically held 7–10 days pre-operatively unless the cardiovascular risk of stopping outweighs bleeding risk |
Managing GI Risk in Chronic Aspirin Users
For patients on long-term low-dose aspirin who have risk factors for GI complications (prior ulcer or GI bleed, age >70, concurrent NSAIDs or anticoagulants, H. pylori infection), co-prescription of a proton pump inhibitor is strongly recommended. The ACC Foundation/ACG/AHA expert consensus recommends PPI therapy for at-risk aspirin users. Testing for and eradicating H. pylori before initiating aspirin further reduces ulcer and bleeding risk in patients with a history of peptic ulcer disease.
Drug Interactions
Aspirin is metabolised primarily through hepatic esterases and glycine/glucuronide conjugation rather than cytochrome P450 enzymes, so classic CYP-mediated interactions are not a major concern. However, aspirin’s antiplatelet activity, protein-binding displacement capacity, and prostaglandin-mediated renal effects generate clinically significant interactions with anticoagulants, other NSAIDs, and several drug classes.
Major
Warfarin / DOACs
MechanismAdditive antihaemostatic effect; aspirin inhibits platelet function while anticoagulants impair clotting cascade
EffectSubstantially increased bleeding risk, particularly GI and intracranial haemorrhage
ManagementLimit to lowest effective aspirin dose (75–81 mg); use PPI; closely monitor INR with warfarin; minimise triple-therapy duration
ACC/AHA Guidelines
Major
Methotrexate
MechanismAspirin reduces renal clearance of methotrexate and displaces it from albumin binding sites
EffectElevated methotrexate levels with increased risk of pancytopenia, mucositis, and hepatotoxicity
ManagementAvoid concurrent use with high-dose methotrexate; for low-dose methotrexate (RA), use lowest aspirin dose and monitor CBC/renal function closely
FDA PI
Moderate
Ibuprofen / Naproxen (NSAIDs)
MechanismNSAIDs compete with aspirin for binding to the serine residue in COX-1 active site; reversible binding by NSAID blocks aspirin’s irreversible acetylation
EffectReduced antiplatelet efficacy of aspirin; increased GI bleeding risk from additive COX inhibition
ManagementIf ibuprofen needed, administer aspirin ≥2 h before ibuprofen or ≥8 h after ibuprofen; naproxen has less interaction but still exercise caution
FDA PI
Moderate
ACE Inhibitors / ARBs
MechanismAspirin inhibits renal prostaglandin synthesis, reducing the vasodilatory and natriuretic effects of ACE inhibitors and ARBs
EffectBlunted antihypertensive effect; potential worsening of renal function in susceptible patients
ManagementClinically significant primarily at aspirin doses ≥325 mg/day; low-dose aspirin for CV prevention generally does not meaningfully blunt ACE inhibitor efficacy; monitor BP and renal function
Lexicomp
Moderate
Valproic Acid
MechanismAspirin displaces valproic acid from albumin and inhibits its beta-oxidation, reducing clearance
EffectIncreased free valproic acid levels with potential for toxicity (tremor, hepatotoxicity, thrombocytopenia)
ManagementMonitor free valproic acid levels; consider alternative analgesic; use lowest effective aspirin dose
Lexicomp
Moderate
SSRIs / SNRIs
MechanismSSRIs impair serotonin-mediated platelet aggregation; additive antihaemostatic effect with aspirin
EffectApproximately 2-fold increase in risk of GI bleeding compared with either agent alone
ManagementAdd PPI for GI protection in patients on both agents; counsel patients regarding signs of GI bleeding
Meta-analysis data
Minor
Corticosteroids
MechanismCorticosteroids increase renal clearance of salicylates; withdrawal of corticosteroids may increase salicylate levels
EffectReduced salicylate efficacy during steroid use; risk of salicylate toxicity on steroid withdrawal
ManagementMonitor salicylate levels if dose adjustment is needed; increase GI bleed vigilance when both agents are used concurrently
FDA PI
Minor
Probenecid / Sulfinpyrazone
MechanismAspirin (even at low doses) blocks renal tubular secretion of uric acid, antagonising the uricosuric effect of probenecid
EffectReduced uric acid excretion; potential gout flare
ManagementAvoid combination if possible; if CV aspirin is essential, consider alternative urate-lowering therapy (allopurinol, febuxostat)
LexicompMonitoring
-
CBC with Platelets
Baseline; annually for chronic users
Routine Assess for iron-deficiency anaemia from chronic occult GI blood loss; check haemoglobin and MCV; evaluate platelet count before invasive procedures -
Renal Function
Baseline; annually
Routine Serum creatinine and eGFR; aspirin can impair renal prostaglandin-mediated haemodynamics, particularly in patients with pre-existing renal disease, heart failure, or concurrent ACE inhibitor/ARB use -
Signs of GI Bleeding
Every visit
Routine Ask about melaena, haematemesis, epigastric pain, and unexplained fatigue; consider faecal occult blood testing or iron studies if anaemia is suspected -
Salicylate Level
PRN (anti-inflammatory dosing)
Trigger-based Therapeutic range 15–30 mg/dL for anti-inflammatory effect; levels approaching 200 mcg/mL suggest toxicity; levels >300 mcg/mL are clearly toxic; check if tinnitus, confusion, or tachypnoea develop -
Liver Function
Baseline; PRN
Trigger-based Hepatic transaminase elevation occurs rarely but can be seen at high anti-inflammatory doses; check ALT/AST if hepatic symptoms develop; Reye syndrome surveillance in paediatric patients -
Blood Pressure
Every visit
Routine Monitor in patients taking concurrent antihypertensives; aspirin at analgesic/anti-inflammatory doses can blunt the effect of ACE inhibitors and ARBs -
Bleeding Time / Coagulation
Pre-operative
Trigger-based Assess before surgical or dental procedures; aspirin irreversibly inhibits platelet function for 7–10 days; consult with surgeon regarding timing of discontinuation
Contraindications & Cautions
Absolute Contraindications
- Known aspirin or NSAID hypersensitivity: Including urticaria, angioedema, bronchospasm, or anaphylaxis triggered by aspirin or any NSAID
- Active peptic ulcer disease or GI bleeding: Aspirin will worsen existing haemorrhage or ulceration
- Haemorrhagic disorders: Including haemophilia, von Willebrand disease, or severe thrombocytopenia
- Pregnancy ≥20 weeks (NSAID/analgesic doses): FDA 2020 safety communication warns of oligohydramnios risk from reduced fetal renal function; also risk of premature ductus arteriosus closure and increased maternal/neonatal bleeding. Does not apply to low-dose aspirin (81 mg) for pre-eclampsia prevention
- Children and adolescents (<19 years) with febrile viral illness: Association with Reye syndrome (chickenpox, influenza); absolute contraindication except in Kawasaki disease under specialist care
Relative Contraindications (Specialist Input Recommended)
- Uncontrolled hypertension: Increased risk of haemorrhagic stroke; optimise BP before initiating aspirin for primary prevention
- Severe renal impairment (CrCl <10 mL/min): Impaired salicylate elimination; risk of accumulation and toxicity
- Severe hepatic insufficiency: Altered metabolism and increased bleeding risk; avoid or use with extreme caution
- Concurrent therapeutic anticoagulation: Combined use with full-dose warfarin or DOACs substantially increases bleeding; requires documented risk-benefit discussion and GI protection
- History of aspirin-exacerbated respiratory disease (AERD): Aspirin desensitisation may be performed by an allergist if aspirin is essential (e.g., post-stent DAPT)
- G6PD deficiency: Large doses may precipitate haemolysis
Use with Caution
- Elderly (≥70 years): Increased absolute risk of GI and intracranial bleeding; 2022 USPSTF recommends against initiating aspirin for primary prevention in this age group
- History of peptic ulcer disease (healed): Co-prescribe PPI; confirm H. pylori eradication
- Concurrent use of SSRIs, corticosteroids, or antiplatelet agents: Each independently increases bleeding risk
- Pre-operative patients: Discuss timing of discontinuation (typically 7–10 days before elective surgery) with surgical team; for high CV risk patients, continuation may be appropriate for minor procedures
- Gout: Low-dose aspirin may increase serum uric acid by impairing renal urate excretion
FDA Safety Communication
NSAIDs and Pregnancy: After 20 Weeks
In October 2020, the FDA issued a safety communication advising against the use of NSAIDs, including aspirin at analgesic/anti-inflammatory doses, at 20 weeks or later in pregnancy unless specifically directed by a clinician. NSAID use in this period may cause oligohydramnios from reduced fetal renal function, potentially resulting in complications including limb contractures and impaired pulmonary development. This communication does not apply to low-dose aspirin (81 mg) used for pre-eclampsia prevention, which remains recommended by ACOG for high-risk women.
FDA Class-Wide Regulatory Warning
Reye Syndrome in Children and Adolescents
Aspirin and aspirin-containing products carry a warning against use in children and teenagers who have or are recovering from chickenpox or influenza-like illness due to the association with Reye syndrome, a rare but potentially fatal condition characterised by acute hepatic failure and encephalopathy. This warning applies to all OTC aspirin products and is a mandatory labelling requirement.
Patient Counselling
Purpose of Therapy
For patients prescribed low-dose aspirin for cardiovascular protection, explain that aspirin works by preventing blood platelets from sticking together to form clots. This significantly reduces the risk of heart attack and stroke in people who have already had a cardiovascular event or who are at high risk. It is important to take aspirin consistently every day as prescribed and not to stop without consulting a clinician, as sudden discontinuation can lead to a rebound increase in clotting risk.
How to Take
For cardiovascular prevention, take aspirin at the same time each day with a glass of water. It can be taken with or without food, though taking it with food may reduce stomach discomfort. Do not crush or chew enteric-coated tablets. For acute chest pain or suspected heart attack, chew a plain (non-enteric-coated) aspirin immediately for rapid absorption.
Stomach Upset and GI Bleeding
Tell patient
Even low-dose aspirin can irritate the stomach lining. Taking it with food or a full glass of water can help. If you develop persistent indigestion or heartburn, your clinician may prescribe a stomach-protective medication (PPI). Avoid alcohol as it increases GI bleeding risk.
Call prescriber
If you notice black or tarry stools, vomit that looks like coffee grounds, persistent stomach pain, or unexplained weakness or dizziness.
Bruising and Bleeding Risk
Tell patient
You may bruise more easily or bleed slightly longer from minor cuts while taking aspirin. This is a normal effect of the medication and is not usually a cause for concern. Use caution with sharp objects and contact sports. Inform all healthcare providers, including dentists and surgeons, that you take aspirin.
Call prescriber
If you experience nosebleeds that won’t stop, blood in your urine, unusually heavy menstrual bleeding, or any signs of internal bleeding such as severe unexplained abdominal pain.
Interaction with Other Pain Relievers
Tell patient
Ibuprofen (Advil, Motrin) can interfere with aspirin’s heart-protective effect if taken at the wrong time. If you need ibuprofen, take your aspirin first and wait at least 2 hours before taking ibuprofen, or take ibuprofen at least 8 hours before your next aspirin dose. Paracetamol (acetaminophen/Tylenol) does not interfere with aspirin and is a safe alternative for occasional pain relief.
Call prescriber
Before starting any new medication, supplement, or herbal product, including over-the-counter NSAIDs, fish oil, or ginkgo biloba, as these can increase bleeding risk.
Tinnitus (Ringing in the Ears)
Tell patient
Ringing or buzzing in the ears can occur, particularly at higher doses used for inflammation. This is usually a sign that the aspirin level in your blood is at the upper end and typically resolves when the dose is reduced.
Call prescriber
If you develop persistent tinnitus, hearing changes, dizziness, or rapid breathing, as these may indicate salicylate toxicity requiring dose adjustment.
Do Not Stop Without Asking
Tell patient
If you are taking aspirin for heart or stroke prevention, do not stop suddenly without consulting your clinician. Abruptly stopping aspirin after long-term use may increase the risk of a cardiovascular event, particularly in patients with coronary stents.
Call prescriber
If you are scheduled for surgery or a dental procedure, contact your prescriber well in advance to discuss whether and when to temporarily stop aspirin.
Children, Viral Illness, and Reye Syndrome
Tell patient
Never give aspirin to children or teenagers who have a fever or viral illness such as the flu or chickenpox, as it has been linked to Reye syndrome, a rare but serious condition affecting the brain and liver. Use paracetamol or ibuprofen instead for children’s fevers.
Call prescriber
If a child on long-term aspirin (e.g., for Kawasaki disease) develops symptoms of a viral illness, contact the treating clinician to discuss temporary alternatives. Ensure the child receives annual influenza vaccination.
Sources
Regulatory (PI / SmPC)
- Bayer Aspirin (aspirin) OTC Label. DailyMed, National Library of Medicine. Updated November 2024. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7f5d9ebe-8119-49a2-9380-eca18a5e5e85 Primary OTC aspirin label with dosing, warnings, and contraindications for analgesic/antipyretic use.
- Durlaza (aspirin extended-release capsules) Prescribing Information. New Haven Pharmaceuticals, Inc. FDA approved September 2015. https://www.accessdata.fda.gov/drugsatfda_docs/label/2015/200671s000lbl.pdf FDA-approved extended-release aspirin label with detailed pharmacokinetics, adverse reactions, and cardiovascular indications.
- FDA Drug Safety Communication: FDA recommends avoiding use of NSAIDs in pregnancy at 20 weeks or later. October 2020. https://www.fda.gov/drugs/drug-safety-and-availability/fda-recommends-avoiding-use-nsaids-pregnancy-20-weeks-or-later Safety communication on NSAID use in pregnancy, including aspirin at analgesic doses, after 20 weeks of gestation.
Key Clinical Trials
- ISIS-2 Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet. 1988;332(8607):349–360. doi:10.1016/S0140-6736(88)92833-4 Landmark trial establishing aspirin (162.5 mg) as standard therapy in acute MI, demonstrating a 23% reduction in vascular mortality.
- CURRENT-OASIS 7 Investigators. Dose comparisons of clopidogrel and aspirin in acute coronary syndromes. N Engl J Med. 2010;363(10):930–942. doi:10.1056/NEJMoa0909475 Randomised trial comparing high-dose (300–325 mg) vs. low-dose (75–100 mg) aspirin in ACS; no difference in ischaemic events but increased minor bleeding with higher dose.
- McNeil JJ, Wolfe R, Woods RL, et al. Effect of aspirin on cardiovascular events and bleeding in the healthy elderly (ASPREE). N Engl J Med. 2018;379(16):1509–1518. doi:10.1056/NEJMoa1805819 Key trial showing no cardiovascular benefit of aspirin for primary prevention in healthy adults ≥70 years, with increased major haemorrhage risk.
- Gaziano JM, Brotons C, Coppolecchia R, et al. Use of aspirin to reduce risk of initial vascular events in patients at moderate risk of cardiovascular disease (ARRIVE). Lancet. 2018;392(10152):1036–1046. doi:10.1016/S0140-6736(18)31924-X Primary prevention trial in moderate-risk adults; aspirin did not reduce cardiovascular events but increased GI bleeding.
Guidelines
- Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease. Circulation. 2019;140(11):e596–e646. doi:10.1161/CIR.0000000000000678 Current ACC/AHA guideline on aspirin for primary prevention: class IIb for ages 40–70 at higher CV risk, class III (harm) for >70 years.
- US Preventive Services Task Force. Aspirin Use to Prevent Cardiovascular Disease: US Preventive Services Task Force Recommendation Statement. JAMA. 2022;327(16):1577–1584. doi:10.1001/jama.2022.4983 2022 USPSTF recommendation: individualise for ages 40–59 with ≥10% 10-year CVD risk; recommend against initiation for ≥60 years.
- Lawton JS, Tamis-Holland JE, Bangalore S, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation. 2025. doi:10.1161/CIR.0000000000001309 Most recent ACS guideline: aspirin loading 162–325 mg at presentation, maintenance 75–100 mg daily with uncoated formulation preferred.
- McCrindle BW, Rowley AH, Newburger JW, et al. Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease: A Scientific Statement from the American Heart Association. Circulation. 2017;135(17):e927–e999. doi:10.1161/CIR.0000000000000484 AHA scientific statement with current dosing recommendations for aspirin in Kawasaki disease, including acute and convalescent phases.
Mechanistic / Basic Science
- Patrono C, García Rodríguez LA, Landolfi R, Baigent C. Low-dose aspirin for the prevention of atherothrombosis. N Engl J Med. 2005;353(22):2373–2383. doi:10.1056/NEJMra052717 Comprehensive review of aspirin’s mechanism of COX-1 acetylation, dose-response relationships, and the pharmacological basis for low-dose antiplatelet therapy.
Pharmacokinetics / Special Populations
- Needs CJ, Brooks PM. Clinical pharmacokinetics of the salicylates. Clin Pharmacokinet. 1985;10(2):164–177. doi:10.2165/00003088-198510020-00004 Classic reference on aspirin and salicylate PK including absorption kinetics, protein binding, Michaelis-Menten metabolism, and renal elimination.
- Bhatt DL, Grosser T, Dong JF, et al. Enteric coating and aspirin nonresponsiveness in patients with type 2 diabetes mellitus. J Am Coll Cardiol. 2017;69(6):603–612. doi:10.1016/j.jacc.2016.11.050 Demonstrates impaired bioavailability of enteric-coated aspirin versus plain aspirin in diabetic patients, supporting use of uncoated formulations.
- Lanas A, Wu P, Medin J, Mills EJ. Low doses of acetylsalicylic acid increase risk of gastrointestinal bleeding in a meta-analysis. Clin Gastroenterol Hepatol. 2011;9(9):762–768.e6. doi:10.1016/j.cgh.2011.05.020 Meta-analysis quantifying the approximately 2-fold increase in GI bleeding risk with low-dose aspirin compared to placebo across multiple RCTs.