Chemical formula: C₉H₈O₄ Molecular mass: 180.157 g/mol PubChem compound: 2244
Acetylsalicylic acid interacts in the following cases:
Concomitant administration of alcohol and acetylsalicylic acid increases the risk of gastrointestinal bleeding.
The excretion of acetylsalicylic acid is increased by alkaline urine, which can occur with some antacids.
Salicylics may increase the hypoglycaemic effect of sulphonylureas.
Anticoagulants e.g. coumarin, heparin, warfarin: Increased risk of bleeding due to inhibited thrombocyte function, injury of the duodenal mucosa and displacement of oral anticoagulants from their plasma protein binding sites. The bleeding time should be monitored.
Anti-platelet agents (e.g clopidogrel and dipyridamole): Increased risk of gastrointestinal bleeding.
Diuretics: Risk of acute renal failure due to the decreased glomerual filtration via decreased renal prostaglandin synthesis. Hydrating the patient and monitoring renal function at the start of the treatment is recommended.
NSAIDs may decrease the antihypertensive effects of antihypertensive agents. As for other NSAIDs concomitant administration with ACE-inhibitors increases the risk of acute renal insufficiency.
Selective serotonin reuptake inhibitors (SSRIs; such as sertraline or paroxetine): Increased risk of gastrointestinal bleeding.
Co-administration of acetylsalicylic acid and carbonic anhydrase inhibitors (acetazolamide) may result in severe acidosis and increased central nervous system toxicity.
The risk of gastrointestinal ulceration and bleeding may be increased when acetylsalicylic acid and corticosteroids are co-administered.
Increased risk of ulcerations and gastrointestinal bleeding due to synergistic effects.
Concomitant administration of acetylsalicylic acid and crystalline penicillin G causes a decrease in half-life of crystalline penicillin G.
Concomitant use of NSAIDs and ciclospoin or tacrolimus may increase the nephrotoxic effect of ciclosporin and tacrolimus. The renal function should be monitored in case of concomitant use of these agents and acetylsalicylic acid.
Acetylsalicylic acid impairs the renal excretion of digoxin, resulting in increased plasma concentrations. Monitoring of plasma concentrations of digoxin is recommended when initiating and terminating treatment with acetylsalicylic acid. Dose adjustment may be necessary.
Concomitant administration of acetylsalicylic acid and furosemide can cause intoxication of salicylates, while can reduce natriuretic action of furosemide.
Griseofulvin may reduce the efficacy of acetylsalicylic acid. Griseofulvin should be avoided if possible when therapy with anti-inflammatory doses of salicylate are required.
Experimental data suggest that ibuprofen may inhibit the effect of low dose acetylsalicylic acid on platelet aggregation when they are dosed concomitantly. However, the limitations of these data and the uncertainties regarding extrapolation of ex vivo data to the clinical situation imply that no firm conclusions can be made for regular ibuprofen use, and no clinically relevant effect is considered to be likely for occasional ibuprofen use.
Acetylsalicylic acid may increase the toxicity of ketorolac. Caution should be advised in patients receiving concomitant medications which could increase the risk of ulceration or bleeding, such as oral corticosteroids, selective serotonin-reuptake inhibitors or anti-platelet agents such as aspirin.
Acetylsalicylic acid impairs the renal excretion of lithium, resulting in increased plasma concentrations. Monitoring of plasma concentrations of lithium is recommended when initiating and terminating treatment with acetylsalicylic acid. Dose adjustment may be necessary.
Co-administration of acetylsalicylic acid and metoclopramide would increase their absorption. Repeated doses of the combined treatment are efficient and well-tolerated. According to a trial, efficacy appeared to increase according to the number of doses when headache was initially severe.
Co-administration of acetylsalicylic acid and phenylbutazone increases the risk of ulcers in the gastrointestinal tract.
Co-administration of acetylsalicylic acid and valproic acid may increase levels of free valproate in serum.
Co-administration of acetylsalicylic acid and spironolactone may involve reduction of the diuretic action of spironolactone. Aldosterone injected i.m. decreased the release of renomedullary PGEs and the index (urinary Na/K ratio) in conscious normotensive intact and adrenalectomized rats. Coadministration of spironolactone increased the release of PGEs as well as the index (urinary Na/K ratio). The effect of spironolactone was partly inhibited by aspirin injected in a ratio 5:1 (aspirin:spironolactone), and effect which could be reversed by the infusion of a synthetic prostaglandin (PGA2) in a subhypotensive dose.
Coadministration of telmisartan and acetylsalicylic acid may increase the risk of acute renal failure and hyperkalemia. Combination of aspirin with telmisartan suppresses the augmented TGFβ/smad signaling during the development of streptozotocin-induced type I diabetic nephropathy.
Acetylsalicylic acid increases the activity of ticlopidine. Combination therapy increases both efficacy and potency of ticlopidine allowing for reduction of the dose.
Acetylsalicylic acid may decrease the effectiveness of trandolapril. Coadministration with aspirin may attenuate the vasodilator and hypotensive effects of ACE inhibitors. In addition, the benefits of ACE inhibitors on morbidity and mortality in post-acute myocardial infarction, coronary heart disease, and particularly congestive heart failure may be compromised or even nullified by aspirin.
Urine acidifiers (e.g. vitamin C), results in a reduction of salicylate excretion by the kidneys.
Caution should be taken in patients with glucose-6-phosphate dehydrogenase deficiency as haemolytic anaemia may occur.
Acetylsalicylic acid increases the activity of divalproex sodium.
Clinical studies indicate that doses up to 100mg/day for restricted obstetrical use, which require specialised monitoring, appear safe.
There is insufficient clinical experience regarding the use of doses above 100mg/day up to 500mg/day. Therefore, the recommendations below for doses of 500mg/day and above apply also for this dose range.
Inhibition of prostaglandin synthesis may adversely affect the pregnancy and/or the embryo/foetal development. Data from epidemiological studies suggest an increased risk of miscarriage and of cardiac malformation and gastroschisis after use of a prostaglandin synthesis inhibitor in early pregnancy. The absolute risk for cardiovascular malformation was increased from less than 1%, up to approximately 1.5%. The risk is believed to increase with dose and duration of therapy. In animals, administration of a prostaglandin synthesis inhibitor has been shown to result in increased pre- and post-implantation loss and embryo-foetal lethality. In addition, increased incidences of various malformations, including cardiovascular, have been reported in animals given a prostaglandin synthesis inhibitor during the organogenetic period. During the first and second trimester of pregnancy, acetylsalicylic acid should not be given unless clearly necessary. If acetylsalicylic acid is used by a woman attempting to conceive, or during the first and second trimester of pregnancy, the dose should be kept as low and duration of treatment as short as possible.
During the third trimester of pregnancy, all prostaglandin synthesis inhibitors may expose the foetus to:
The mother and the neonate, at the end of pregnancy, to:
Consequently, acetylsalicylic acid at doses of 100 mg/day and higher is contraindicated during the third trimester of pregnancy.
Low quantities of salicylates and of their metabolites are excreted into the breast milk. Since adverse effects for the infant have not been reported up to now, short-term use of the recommended dose does not require suspending lactation. In cases of long-term use and/or administration of higher doses, breastfeeding should be discontinued.
No studies on the effects on the ability to drive and use machines have been performed with acetylsalicylic acid.
Based on the pharmacodynamic properties and the side effects of acetylsalicylic acid, no influence on the reactivity and the ability to drive or use machines is expected.
Side effects are grouped on the basis of System Organ Class. Within each system organ class the frequencies are defined as: very common (≥1/10), common (≥1/100 to <1/10), uncommon (≥1/1,000 to <1/100), rare (≥1/10,000 to <1/1,000), very rare (<1/10,000) and not known (cannot be estimated from the available data).
Common: Increased bleeding tendencies.
Rare: Thrombocytopenia, granulocytosis, aplastic anaemia.
Not known: Cases of bleeding with prolonged bleeding time such as epistaxis, haematuria, purpura, ecchymoses, haemoptysis, haematoma, cerebral haemorrhage and gingival bleeding.
Symptoms may persist for a period of 4–8 days after acetylsalicylic acid discontinuation. As a result there may be an increased risk of bleeding during surgical procedures.
Acetylsalicylic acid decreases platelet adhesiveness and, in large doses, may cause hypoprothrombinaemia.
Existing (haematemesis, melaena) or occult gastrointestinal bleeding, which may lead to iron deficiency anaemia (more common at higher doses).
Haemolytic anaemia can occur in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency.
Rare: Hypersensitivity reactions, skin rashes, urticarial, asthma, bronchospasm, angio-oedema, allergic oedema, anaphylactic reactions including shock.
Not known: Hyperuricemia.
Rare: Intracranial haemorrhage.
Not known: Headache, vertigo.
Not known: Reduced hearing ability; tinnitus.
Rare: Hemorrhagic vasculitis.
Uncommon: Rhinitis, dyspnoea.
Rare: Bronchospasm, asthma attacks.
Rare: Menorrhagia.
Common: Dyspepsia.
Rare: Severe gastrointestinal haemorrhage, nausea, vomiting, gastritis.
Not known: Gastric or duodenal ulcers and perforation, diarrhoea.
Not known: Hepatic insufficiency.
Uncommon: Urticaria.
Rare: Steven-Johnsons syndrome, Lyells syndrome, purpura, erythema nodosum, erythema multiforme.
Not known: Impaired renal function, salt and water retention, urate kidney stones.
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