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Drug Detailed Description (Generic name) - Aspirin



Aspirin is an analgesic, antipyretic, and anti-inflammatory agent. Anti-inflammatory properties are related to the inhibition of prostaglandin biosyn-thesis. Aspirin nonselectively inhibits cyclo-oxygenase-1 (COX-1), which is asso-ciated with GI and renal effects and inhibition of platelet aggregation, and cyclo-oxygenase-2 (COX-2), which is associated with the inflammatory response. Unlike other NSAIDs, its antiplatelet effect is irreversible and permanent (because of transacetylation of platelet COX) for the life of the platelet (8–11 days). Salicy-lates without acetyl groups (eg, sodium salicylate) have essentially no antiplatelet effect but retain analgesic, antipyretic, and anti-inflammatory activities. Low dosages (1–2 g/day) decrease urate excretion; high dosages (>5 g/day) induce uri-cosuria.

Administration and Adult Dosage

PO or PR for fever or minor pain 325– 1000 mg q 4-6 hr, to a maximum of 4 g/day. PO for arthritis and rheumatic conditions 3.6–5.4 g/day in 3–4 divided doses. PO for acute rheumatic fever 5–8 g/day in divided doses. PO for prevention of TIAs or stroke 81– 325 mg/day.PO for myocardial infarction risk reduction (primary prevention in healthy men >50 yr with at least one major cardiovascular risk factor) 81–325 mg/day; (secondary prevention) 162–325 mg/day.PO for unstable angina 162–325 mg/day.PO for prevention of coronary artery bypass graft occlu-sion 325 mg/day started 6 hr postoperatively and continued for 1 yr.PO for nonrheumatic atrial fibrillation (patients who are poor candidates for, or de-cline, oral anticoagulants) 325 mg/day; (patients <75 yr with no risk factors for stroke) 325 mg/day.The optimum dosage for platelet inhibition has not been determined; doses as low as 50 mg/day inhibit platelet aggregation and provide effective protection against thrombosis.

Special Populations

Pediatric Dosage

PO for juvenile rheumatoid arthritis 60–110 mg/kg/day in divided doses. PO for acute rheumatic fever 100 mg/kg/day in divided doses initially for 2 weeks, then 75 mg/kg/day in di-vided doses for 4–6 weeks. PO for Kawasaki disease 80–120 mg/kg/day; de-crease to 10 mg/kg/day after fever resolves.

Geriatric Dosage

Use minimal effective dosages; elderly are more susceptible to GI bleeding and acute renal insufficiency. PO for MI risk reduction (healthy men >50 yr for primary prevention with cardiovascular risk factors) 81– 325 mg/day. Other Conditions. Uremia or reduced albumin levels are likely to produce higher unbound drug levels that can increase pharmacologic or toxic effects. Dosage re-duction might be required in these patients (eg, kidney disease, malnutrition).

Dosage Forms

Chew Tab 81 mg; EC Tab 81, 165, 325, 500, 650, 975 mg; SR Tab 650, 800 mg; Tab 81, 325, 500 mg; Supp 120, 200, 300, 600 mg.

Patient Instructions

Children and teenagers (<16 yr) should not use aspirin-containing medications for chickenpox or flu symptoms because of the association with Reye’s syndrome, a rare but serious illness. Take this drug with food, milk, or a full glass of water to minimize stomach upset; report any symptoms of gas-trointestinal ulceration or bleeding. Contact your physician if ringing in the ears or gastrointestinal pain occurs. Do not crush or chew enteric-coated or sustained-re-lease preparations. Avoid other products containing aspirin or nonsteroidal anti-inflammatory drugs. Missed Doses. If you take this drug on a regular schedule and you miss a dose, take it as soon as you remember. If it is about time for the next dose, take that dose only. Do not double the dose or take extra.


Onset and Duration. PO onset of analgesia 30 min.Serum Levels. (Salicylate) 150–300 mg/L (1.1–2.2 mmol/L) for rheumatic dis-eases, often accompanied by mild toxic symptoms. Tinnitus occurs at 200– 400 mg/L (1.5–2.9 mmol/L), hyperventilation at >350 mg/L (2.6 mmol/L), acido-sis at >450 mg/L (3.3 mmol/L), and severe or fatal toxicity at >900 mg/L (6.6 mmol/L) 6 hr after acute ingestion.


Rapidly absorbed from the GI tract; oral bioavailability of aspirin is 80–100%. Enteric coating does not adversely affect absorption.A single analgesic/antipyretic dose produces peak salicylate levels of 30–60 mg/L (0.22– 0.44 mmol/L). Aspirin is 49% plasma protein bound, decreased in uremia; Vd is 0.15 ± 0.03 L/kg; Cl is 0.56 ± 0.07 L/hr/kg. Aspirin is rapidly hydrolyzed to sali-cylate, which also is pharmacologically active. Salicylate is metabolized primarily in the liver to 4 metabolites (salicyluric acid, phenolic and acyl glucuronides, and gentisic acid). Salicylate plasma protein binding is dose dependent, 95% at 15 mg/L and 80% at 300 mg/L, and decreased in uremia, hypoalbuminemia, neonates, and pregnancy; Vd is 0.17 ± 0.03 L/kg; Cl is dose dependent, 0.012 L/hr/kg at 134–157 mg/L, and decreased in hepatitis and neonates. Only 1% of a dose of aspirin is excreted unchanged in the urine. t¹/2. (Aspirin) 0.25 ± 0.03 hr.(Salicylate) dose dependent: 2.4 hr with 0.25 g, 5 hr with 1 g, 6.1 hr with 1.3 g, 19 hr with 10–20 g.

Adverse Reactions

Hearing impairment, GI upset, and occult bleeding are fre-quent, with acute hemorrhage from gastric erosion also likely. As with other NSAIDs, aspirin can cause renal dysfunction, particularly in those with pre-exist-ing renal disease or CHF. Rare hepatotoxicity occurs, primarily in children with rheumatic fever or rheumatoid arthritis and adults with SLE or pre-existing liver disease;the syndrome of asthma, angioedema, and nasal polyps can be provoked in susceptible patients.A single analgesic dose can suppress platelet aggregation and prolong bleeding time for up to 1 week; large dosages can prolong PT.


Bleeding disorders; asthma; hypersensitivity to other NSAIDs or tartrazine dye.


Use with caution in patients with renal disease, gastric ulcer, bleed-ing tendencies, hypoprothrombinemia, or history of asthma, or during anticoagu-lant therapy. Because of the association with Reye’s syndrome, the use of salicy-lates in children and teenagers with flu-like symptoms or chickenpox is not recommended.Those developing bronchospasm with aspirin can develop similar reactions to other NSAIDs.Sodium salicylate and other nonacetylated salicylates (except diflunisal) are usually well tolerated in these patients.

Drug Interactions

Alkalinizing agents (eg, acetazolamide, antacids) can reduce salicylate levels; acetazolamide also can enhance CNS penetration of salicylate. Corticosteroids can reduce serum salicylate levels. Large doses of salicylates can increase oral anticoagulant effect; even small doses can increase risk of bleeding with oral anticoagulants or heparin because of the antiplatelet effect of aspirin. Al-cohol and salicylate increase the risk of GI blood loss. Salicylates can cause an in-creased response to sulfonylureas, especially chlorpropamide. Salicylate decreases the uricosuric effect of uricosuric agents (eg, probenecid, sulfinpyrazone). Salicy-late, especially in large doses, can decrease renal elimination of methotrexate and displace it from plasma protein binding sites. Parameters to Monitor. Monitor for abnormal bleeding or bruising and occult GI blood loss (periodic hematocrit) in patients who ingest salicylates regularly. Serum salicylate level determinations are recommended with higher dosage regi-mens because of the wide variation among patients in serum levels produced. Monitor renal function and hearing changes (tinnitus); however, using tinnitus as an index of maximum salicylate tolerance is not recommended.55

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