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14-September-2008 18:38:39 - Aspirin Aspirin Systematic IUPAC name 2-ethanoylhydroxybenzoic acid Identifiers CAS number 50-78-2 ATC code A01AD05 B01AC06, N02BA01 PubChem 2244 DrugBank APRD00264 Chemical data Formula C9H8O4 Mol. mass 180.160 g/mol SMILES eMolecules PubChem Synonyms 2-acetyloxybenzoic acid 2-acetyloxybenzoic acid acetylsalicylate acetylsalicylic acid O-acetylsalicylic acid Physical data Density 1.40 g/cm³ Melt. point 135 °C 275 °F Boiling point 140 °C 284 °F decomposes Solubility in water 10 mg/mL 20 °C Pharmacokinetic data Bioavailability Rapidly and completely absorbed Protein binding 99.6% Metabolism Hepatic Half life 300-650 mg dose: 3.1-3.2hrs 1 g dose: 5 hours 2 g dose: 9 hours Excretion Renal Therapeutic considerations Pregnancy cat. CAU CUS Legal status UnscheduledAU GSLUK OTCUS Routes Most commonly oral, also rectal. Lysine acetylsalicylate may be given IV or IM Aspirin, or acetylsalicylic acid A.S.A. IPA: /əˌsÉ›tɨlsælɨˌsɪlɨk ˈæsɨd/, is a salicylate drug, often used as an analgesic to relieve minor aches and pains, as an antipyretic to reduce fever, and as an anti-inflammatory medication. In countries where Aspirin is a registered trademark owned by Bayer, the generic term is A.S.A. Aspirin also has an antiplatelet or anti-clotting effect and is used in long-term, low doses to prevent heart attacks, strokes and blood clot formation in people at high risk for developing blood clots.1 It has also been established that low doses of aspirin may be given immediately after a heart attack to reduce the risk of another heart attack or of the death of cardiac tissue.23 The main undesirable side effects of aspirin are gastrointestinal-ulcers and stomach bleeding-and tinnitus, especially in higher doses. In children under 19 years of age, aspirin is no longer used to control flu-like symptoms or the symptoms of chickenpox, due to the risk of Reye's syndrome.4 Aspirin was the first-discovered member of the class of drugs known as non-steroidal anti-inflammatory drugs NSAIDs, not all of which are salicylates, although they all have similar effects and most have some mechanism of action which involves non-selective inhibition of the enzyme cyclooxygenase. Today, aspirin is one of the most widely used medications in the world, with an estimated 40,000 metric tons of it being consumed each year.5 Contents 1 History 2 Therapeutic uses 2.1 Experimental uses 2.2 Veterinary uses 3 Mechanism of action 4 Chemistry 4.1 Synthesis 4.2 Polymorphism 5 Pharmacokinetics 6 Contraindications and resistance 7 Adverse effects 7.1 Gastrointestinal side effects 7.2 Central effects 7.3 Pediatrics 7.4 Other effects 8 Interactions 9 Dosage 10 Overdose 10.1 Symptoms 10.2 Toxicity 10.3 Treatment 10.4 Epidemiology 11 See also 12 References 13 External links History Main article: History of aspirin Medicines containing derivatives of salicylic acid, structurally similar to aspirin, have been in medical use since ancient times. Salicylate-rich willow bark extract became recognized for its specific effects on fever, pain and inflammation in the mid-eighteenth century. By the nineteenth century pharmacists were experimenting with and prescribing a variety of chemicals related to salicylic acid, the active component of willow extract. A French chemist, Charles Frederic Gerhardt, was the first to prepare acetylsalicylic acid named aspirin in 1899 in 1853. In the course of his work on the synthesis and properties of various acid anhydrides, he mixed acetyl chloride with a sodium salt of salicylic acid sodium salicylate. A vigorous reaction ensued, and the resulting melt soon solidified.6 Since no structural theory existed at that time, Gerhardt called the compound he obtained salicylic-acetic anhydride wasserfreie Salicylsäure-Essigsäure. This preparation of aspirin salicylic-acetic anhydride was one of the many reactions Gerhardt conducted for his paper on anhydrides, and he did not pursue it further. Advertisement for Aspirin, Heroin, Lycetol, Salophen Advertisement for Aspirin, Heroin, Lycetol, Salophen Six years later, in 1859, von Gilm obtained analytically pure acetylsalicylic acid which he called acetylierte Salicylsäure, acetylated salicylic acid by a reaction of salicylic acid and acetyl chloride.7 In 1869 Schröder, Prinzhorn and Kraut repeated both Gerhardt's from sodium salicylate and von Gilm's from salicylic acid syntheses and concluded that both reactions gave the same compound-acetylsalicylic acid. They were first to assign to it the correct structure with the acetyl group connected to the phenolic oxygen.8 In 1897, scientists at the drug and dye firm Bayer began investigating acetylsalicylic acid as a less-irritating replacement for standard common salicylate medicines. By 1899, Bayer had dubbed this drug Aspirin and was selling it around the world.9The name Aspirin is derived from A = Acetyl and Spirsäure = an old German name for salicylic acid.10 Aspirin's popularity grew over the first half of the twentieth century, spurred by its effectiveness in the wake of Spanish flu pandemic of 1918, and aspirin's profitability led to fierce competition and the proliferation of aspirin brands and products.11 Aspirin's popularity declined after the market releases of paracetamol acetaminophen in 1956 and ibuprofen in 1969.12 In the 1960s and 1970s, John Vane and others discovered the basic mechanism of aspirin's effects, while clinical trials and other studies from the 1960s to the 1980s established aspirin's efficacy as an anti-clotting agent that reduces the risk of clotting diseases.13 Aspirin sales revived considerably in the last decades of the twentieth century, and remain strong in the twenty-first, thanks to widespread use as a preventive treatment for heart attacks and strokes.14 Therapeutic uses Aspirin is one of the most frequently used drugs in the treatment of mild to moderate pain, including that of migraines and fever.1516 It is often combined with other non-steroidal anti-inflammatory drugs and opioid analgesics in the treatment of moderate to severe pain.17 In high doses, aspirin and other salicylates are used in the treatment of rheumatic fever, rheumatic arthritis, and other inflammatory joint conditions. In lower doses, aspirin also has properties as an inhibitor of platelet aggregation, and has been shown to decrease the incidence of transient ischemic attacks and unstable angina in men, and can be used prophylactically. It is also used in the treatment of pericarditis, coronary artery disease, and acute myocardial infarction.1819 Low doses of aspirin are also recommended for the prevention of stroke, and myocardial infarction in patients with either diagnosed coronary artery disease or who have an elevated risk of cardiovascular disease. Experimental uses Aspirin has been theorized to reduce cataract formation in diabetic patients, but one study showed it was ineffective for this purpose.20 The role of aspirin in reducing the incidence of many forms of cancer has also been widely studied. In several studies, aspirin use did not reduce the incidence of prostate cancer.2122 Its effects on the incidence of pancreatic cancer are mixed; one study published in 2004 found a statistically significant increase in the risk of pancreatic cancer among women,23 while a meta-analysis of several studies, published in 2006, found no evidence that aspirin or other NSAIDs are associated with an increased risk for the disease.24 The drug may be effective in reduction of risk of various cancers, including those of the colon,25262728 lung,2930 and possibly the upper GI tract, though some evidence of its effectiveness in preventing cancer of the upper GI tract has been inconclusive.313231 Its preventative effect against adenocarcinomas may be explained by its inhibition of COX-2 enzymes expressed in them.33 An older studycitation needed claimed that aspirin may reduce the neurotoxicity of THC, the active drug in cannabis. However, this theory has been discred, as newer studiescitation needed indicate THC to be neuroprotective rather than neurotoxic. Veterinary uses Aspirin has been used to treat pain and arthritis in veterinary medicine, primarily in cats and dogs, although it is often not recommended for this purpose, as there are newer medications available with fewer side effects in these animals. Dogs, for example, are particularly susceptible to the gastrointestinal side effects associated with salicylates.34 Horses have also been given aspirin for pain relief, although it is not commonly used due to its relatively short-lived analgesic effects. Horses are also fairly sensitive to the gastrointestinal side effects. Nevertheless, it has shown promise in its use as an anticoagulant, mostly in cases of laminitis.35 Aspirin should only be used in animals under the direct supervision of a veterinarian. Mechanism of action Main article: Mechanism of action of aspirin Structure of COX-2 inactivated by Aspirin. In the active site of each of the two monomers, Serine 530 has been acetylated. Also visible is the salicylic acid which has transferred the acyl group, and the heme cofactor. Structure of COX-2 inactivated by Aspirin. In the active site of each of the two monomers, Serine 530 has been acetylated. Also visible is the salicylic acid which has transferred the acyl group, and the heme cofactor. In 1971, British pharmacologist John Robert Vane, then employed by the Royal College of Surgeons in London, showed that aspirin suppressed the production of prostaglandins and thromboxanes.3637 For this discovery, he was awarded both a Nobel Prize in Physiology or Medicine in 1982 and a knighthood. Aspirin's ability to suppress the production of prostaglandins and thromboxanes is due to its irreversible inactivation of the cyclooxygenase COX enzyme. Cyclooxygenase is required for prostaglandin and thromboxane synthesis. Aspirin acts as an acetylating agent where an acetyl group is covalently attached to a serine residue in the active site of the COX enzyme. This makes aspirin different from other NSAIDs such as diclofenac and ibuprofen, which are reversible inhibitors. Low-dose, long-term aspirin use irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation. This anticoagulant property makes aspirin useful for reducing the incidence of heart attacks.38 40 mg of aspirin a day is able to inhibit a large proportion of maximum thromboxane A2 release provoked acutely, with the prostaglandin I2 synthesis being little affected; however, higher doses of aspirin are required to attain further inhibition.39 Prostaglandins are local hormones produced in the body and have diverse effects in the body, including the transmission of pain information to the brain, modulation of the hypothalamic thermostat, and inflammation. Thromboxanes are responsible for the aggregation of platelets that form blood clots. Heart attacks are primarily caused by blood clots, and low doses of aspirin are seen as an effective medical intervention for acute myocardial infarction. The major side-effect of this is that because the ability of blood to clot is reduced, excessive bleeding may result from the use of aspirin. There are at least two different types of cyclooxygenase: COX-1 and COX-2. Aspirin irreversibly inhibits COX-1 and modifies the enzymatic activity of COX-2. Normally COX-2 produces prostanoids, most of which are pro-inflammatory. Aspirin-modified COX-2 produces lipoxins, most of which are anti-inflammatory. Newer NSAID drugs called COX-2 selective inhibitors have been developed that inhibit only COX-2, with the intent to reduce the incidence of gastrointestinal side-effects.5 However, several of the new COX-2 selective inhibitors, such as Vioxx, have been recently withdrawn, after evidence emerged that COX-2 inhibitors increase the risk of heart attack. It is proposed that endothelial cells lining the microvasculature in the body express COX-2, and, by selectively inhibiting COX-2, prostaglandins specifically PGI2; prostacyclin are downregulated with respect to thromboxane levels, as COX-1 in platelets is unaffected. Thus, the protective anti-coagulative effect of PGI2 is decreased, increasing the risk of thrombus and associated heart attacks and other circulatory problems. Since platelets have no DNA, they are unable to synthesize new COX once aspirin has irreversibly inhibited the enzyme, an important difference with reversible inhibitors. Furthermore, aspirin has been shown to have at least three additional modes of action. It uncouples oxidative phosphorylation in cartilaginous and hepatic mitochondria, by diffusing from the inner membrane space as a proton carrier back into the mitochondrial matrix, where it ionizes once again to release protons.40 In short, aspirin buffers and transports the protons. When high doses of aspirin are given, aspirin may actually cause fever due to the heat released from the electron transport chain, as opposed to the antipyretic action of aspirin seen with lower doses. Additionally, aspirin induces the formation of NO-radicals in the body, which have been shown in mice to have an independent mechanism of reducing inflammation. This reduced leukocyte adhesion, which is an important step in immune response to infection; however, there is currently insufficient evidence to show that aspirin helps to fight infection.41 More recent data also suggests that salicylic acid and its derivatives modulate signaling through NF-κB.42 NF-κB is a transcription factor complex that plays a central role in many biological processes, including inflammation. Chemistry Aspirin is an acetyl derivative of salicylic acid that is a white, crystalline, weakly acidic substance, with melting point 135°C. Acetylsalicylic acid decomposes rapidly in solutions of ammonium acetate or of the acetates, carbonates, citrates or hydroxides of the alkali metals. Acetylsalicylic acid is stable in dry air, but gradually hydrolyses in contact with moisture to acetic and salicylic acids. In solution with alkalis, the hydrolysis proceeds rapidly and the clear solutions formed may consist entirely of acetate and salicylate.43 Synthesis The synthesis of aspirin is classified as an esterification reaction, where the alcohol group from the salicylic acid reacts with an acid derivative acetic anhydride, yielding aspirin and acetic acid as a byproduct. Small amounts of sulfuric acid are often used as a catalyst. This method is commonly employed in undergraduate teaching labs.44 Formulations containing high concentrations of aspirin often smell like vinegar.45 This is because aspirin can decompose in moist conditions, yielding salicylic acid and acetic acid.46 The acid dissociation constant pKa for acetylsalicylic acid is 3.5 at 25 °C.47 Polymorphism Polymorphism, or the ability of a substance to form more than one crystal structure, is important in the development of pharmaceutical ingredients. Many drugs are receiving regulatory approval for only a single crystal form or polymorph. For a long time, only one crystal structure for aspirin was known, although there had been indications that aspirin might have a second crystalline form since the 1960s. The elusive second polymorph was first discovered by Vishweshwar and coworkers in 2005,48 and fine structural details were given by Bond et al.49 A new crystal type was found after attempted co-crystallization of aspirin and levetiracetam from hot acetonitrile. The form II is only stable at 100 K and reverts back to form I at ambient temperature. In the unambiguous form I, two salicylic molecules form centrosymmetric dimers through the acetyl groups with the acidic methyl proton to carbonyl hydrogen bonds, and in the newly claimed form II, each salicylic molecule forms the same hydrogen bonds with two neighboring molecules instead of one. With respect to the hydrogen bonds formed by the carboxylic acid groups both polymorphs form identical dimer structures. Pharmacokinetics Salicylic acid is a weak acid, and very little of it is ionized in the stomach after oral administration. Acetylsalicylic acid is poorly soluble in the acidic conditions of the stomach, which can delay absorption of high doses for 8 to 24 hours. In addition to the increased pH of the small intestine, aspirin is rapidly absorbed there due to the increased surface area, which in turn allows more of the salicylate to dissolve. Due to the issue of solubility, however, aspirin is absorbed much more slowly during overdose, and plasma concentrations can continue to rise for up to 24 hours after ingestion.505152 About 50-80% of salicylate in the blood is bound by protein while the rest remains in the active, ionized state; protein binding is concentration-dependent. Saturation of binding sites leads to more free salicylate and increased toxicity. The volume of distribution is 0.1-0.2 l/kg. Acidosis increases the volume of distribution because of enhancement of tissue penetration of salicylates.52 As much as 80% of therapeutic doses of salicylic acid is metabolized in the liver. Conjugation with glycine forms salicyluric acid and with glucuronic acid forms salicyl acyl and phenolic glucuronide. These metabolic pathways have only a limited capacity. Small amounts of salicylic acid are also hydroxylated to gentisic acid. With large salicylate doses, the kinetics switch from first order to zero order, as metabolic pathways become saturated and renal excretion becomes increasingly important.52 Salicylates are excreted mainly by the kidneys as salicyluric acid 75%, free salicylic acid 10%, salicylic phenol 10% and acyl 5% glucuronides, and gentisic acid 1%. When small doses less than 250 mg in an adult are ingested, all pathways proceed by first order kinetics, with an elimination half-life of about 2 to 4.5 hours.5354 When higher doses of salicylate are ingested more than 4 g, the half-life becomes much longer 15-30 hours55 because the biotransformation pathways concerned with the formation of salicyluric acid and salicyl phenolic glucuronide become saturated.56 Renal excretion of salicylic acid becomes increasingly important as the metabolic pathways become saturated, because it is extremely sensitive to changes in urinary pH. There is a 10 to 20 fold increase in renal clearance when urine pH is increased from 5 to 8. The use of urinary alkalinization exploits this particular aspect of salicylate elimination.57 Contraindications and resistance Aspirin should be avoided by those known to be allergic to ibuprofen or naproxen,5859 or to have salicylate intolerance6061 or a more generalized drug intolerance to NSAIDs, and caution should be exercised in those with asthma or NSAID-precipitated bronchospasm. Due to its effect on the stomach lining, manufacturers recommend that patients with kidney disease, peptic ulcers, mild diabetes, gout or gastritis talk to their doctors before using aspirin.5862 Even if none of these conditions are present, there is still an increased risk of stomach bleeding when aspirin is taken with alcohol or warfarin.5859 Patients with hemophilia or other bleeding tendencies should not take aspirin or other salicylates.5862 Aspirin is known to cause hemolytic anemia in people who have the genetic disease glucose-6-phosphate dehydrogenase deficiency G6PD, particularly in large doses and depending on the severity of the disease.6364 Aspirin should not be given to children or adolescents to control cold or influenza symptoms as this has been linked with Reye's syndrome.4 Use of aspirin during Dengue Fever is not recommended due to increased bleeding tendency.65 For some people, aspirin does not have as strong an effect on platelets as for others, an effect known as aspirin resistance or insensitivity. One study has suggested that women are more likely to be resistant than men6667 and a different, aggregate study of 2,930 patients found 28% to be resistant.68 Adverse effects Gastrointestinal side effects Aspirin use has been shown to increase the risk of gastrointestinal bleeding.69 Although some enteric coated formulations of aspirin are advertised as being gentle to the stomach, in one study enteric coating did not seem to reduce this risk.69 Combining aspirin with other NSAIDs has also been shown to further increase this risk.69 Using aspirin in combination with clopidogrel or warfarin also increases the risk of upper GI bleeding.70 Central effects Large doses of salicylate, a metabolite of aspirin, have been proposed to cause tinnitus, based on the experiments in rats, via the action on arachidonic acid and NMDA receptors cascade.71 Pediatrics See also: Reye's syndrome Reye's syndrome can occur when children or pediatric patients are given aspirin for a fever or other illnesses or infections. In one study, 213 patients under the age of 18 were reported for Reye's syndrome from the nationwide Reye's syndrome surveillance system. Out of 213 patients 211 had known that had another antecedent illness: 89% reported being ill severe vomiting, mental strain, respiratory illness, vericella or gastrointestinal illness two weeks before onset of Reye's syndrome. Salicylate levels, the active acid in aspirin, were present in 162 of the 213 patients. 72 Reye's syndrome is due to fatty deterioration of liver cells. In another study, 12 livers were obtained from children who had died from Reye's syndrome, and another liver from a child who died of accidental causes was used as a control. The autopsy stated in seven of the 12 livers, micro vesicular fatty change was present.73 Other effects Aspirin can cause prolonged bleeding after operations for up to 10 days. In one study, thirty patients were observed after their various surgeries. Twenty of the thirty patients had to have an additional unplanned operation because of postoperative bleeding.74 This diffuse bleeding was associated with aspirin alone or in combination with another NSAID in 19 out of the 20 who had to have another operation due to bleeding after their operation. The average recovery time for the second operation was 11 days. Aspirin can induce angioedema in some people. In one study, angioedema appeared 1-6 hours after ingesting aspirin in some of the patients participating in the study. However, when the aspirin was taken alone it did not cause angioedema in these patients; the aspirin was either taken in combination with another NSAID-induced drug when angioedema appeared.75 Interactions Aspirin is known to interact with other drugs. For example, acetazolamide and ammonium chloride have been known to enhance the intoxicating effect of salicyclates, and alcohol also enhances the gastrointestinal bleeding associated with these types of drugs as well.5859 Aspirin is known to displace a number of drugs from protein binding sites in the blood, including the anti-diabetic drugs tolbutamide and chlorpropamide, the immunosuppressant methotrexate, phenytoin, probenecid, valproic acid as well as interfering with beta oxidation, an important part of valproate metabolism and any nonsteroidal anti-inflammatory drug. Corticosteroids may also reduce the concentration of aspirin. The pharmacological activity of spironolactone may be reduced by taking aspirin, and aspirin is known to compete with Penicillin G for renal tubular secretion.76 Aspirin may also inhibit the absorption of vitamin C.777879 Dosage Coated 325 mg aspirin tablets Coated 325 mg aspirin tablets For adults doses are generally taken four times a day for fever or arthritis,80 with doses near the maximal daily dose used historically for the treatment of rheumatic fever.81 For the prevention of myocardial infarction in someone with documented or suspected coronary artery disease, much lower doses are taken once daily.80 For those under 12 years of age, the dose previously varied with the age, but aspirin is no longer routinely used in children due to the association with Reye's syndrome; paracetamol known as acetaminophen in North America or other NSAIDs, such as ibuprofen, are now used instead. Kawasaki disease remains one of the few indications for aspirin use in children, with aspirin taken at dosages based on body weight, initially four times a day for up to two weeks and then at a lower dose once daily for a further six to eight weeks.82 Overdose It has been suggested that this section be split into a new article entitled salicylate intoxication. Discuss Aspirin overdose can be acute or chronic. In acute poisoning, a single large dose is taken; in chronic poisoning, supratherapeutic doses are taken over a period of time. Acute overdose has a mortality rate of 2%. Chronic overdose is more commonly lethal with a mortality rate of 25%; chronic overdose may be especially severe in children.83 Symptoms Aspirin overdose has potentially serious consequences, sometimes leading to significant morbidity and death. Patients with mild intoxication frequently have nausea and vomiting, abdominal pain, lethargy, tinnitus, and dizziness. More significant symptoms occur in more severe poisonings and include hyperthermia, tachypnea, respiratory alkalosis, metabolic acidosis, hyperkalemia, hypoglycemia, hallucinations, confusion, seizure, cerebral edema, and coma. The most common cause of death following an aspirin overdose is cardiopulmonary arrest usually due to pulmonary edema.84 Toxicity The acutely toxic dose of aspirin is generally considered greater than 150 mg per kg of body mass.55 Moderate toxicity occurs at doses up to 300 mg/kg, severe toxicity occurs between 300 to 500 mg/kg, and a potentially lethal dose is greater than 500 mg/kg.85 This is the equivalent of many dozens of the common 325 mg tablets, depending on body weight. Chronic toxicity may occur following doses of 100 mg/kg per day for two or more days.85 Treatment All overdose patients should be conveyed to a hospital for assessment immediately. Initial treatment of an acute overdose includes gastric decontamination. This is achieved by administering activated charcoal, which adsorbs the aspirin in the gastrointestinal tract. Stomach pumps are no longer routinely used in the treatment of poisonings but are sometimes considered if the patient has ingested a potentially lethal amount less than 1 hour previously.86 Inducing emesis with syrup of ipecac is not recommended.55 Repeated doses of charcoal have been proposed to be beneficial in aspirin overdose;87 although, one study found that repeat dose charcoal might not be of significant value.88 However, most clinical toxicologists will administer additional charcoal if serum salicylate levels are increasing. Patients are monitored until their peak salicylate blood level has been determined.57 Blood levels are usually assessed four hours after ingestion and then every two hours after that to determine the maximum level. Maximum levels can be used as a guide to toxic effects expected.89 There is no antidote to salicylate poisoning. Monitoring of biochemical parameters such as electrolytes, liver and kidney function, urinalysis, and complete blood count is undertaken along with frequent checking of salicylate and blood sugar levels. Arterial blood gas assessments are performed to test for respiratory alkalosis and metabolic acidosis. Patients are monitored and often treated according to their individual symptoms, patients may be given intravenous potassium chloride to counteract hypokalemia, glucose to restore blood sugar levels, benzodiazepines for any seizure activity, fluids for dehydration, and importantly sodium bicarbonate to restore the blood's sensitive pH balance. Sodium bicarbonate also has the effect of increasing the pH of urine, which in turn increases the elimination of salicylate. Additionally, hemodialysis can be implemented to enhance the removal of salicylate from the blood. Hemodialysis is usually used in severely poisoned patients; for example, patients with significantly high salicylate blood levels, significant neurotoxicity agitation, coma, convulsions, renal failure, pulmonary edema, or cardiovascular instability are hemodialyzed.57 Hemodialysis also has the advantage of restoring electrolyte and acid-base abnormalities while removing salicylate;57 hemodialysis is often life-saving in severely ill patients. Epidemiology In the later part of the 20th century the number of salicylate poisonings has declined mainly due to the popularity of other over-the-counter analgesics such as paracetamol acetaminophen. Fifty-two deaths involving single-ingredient aspirin were reported in the United States in 2000. However, in all but three cases, the reason for the ingestion of lethal doses was intentional, predominantly suicides.90 See also Pharmacy and Pharmacology portal Aspergum Copper aspirinate Non-steroidal anti-inflammatory drug History of aspirin Salicylic acid References ^ Lewis, H D; J W Davis, D G Archibald, W E Steinke, T C Smitherman, J E Doherty, H W Schnaper, M M LeWinter, E Linares, J M Pouget, S C Sabharwal, E Chesler, H DeMots 1983-08-18. Protective effects of aspirin against acute myocardial infarction and death in men with unstable angina. Results of a Veterans Administration Cooperative Study. The New England journal of medicine 309 7: 396-403. ISSN 00284793. ^ Julian, D G; D A Chamberlain, S J Pocock 1996-09-24. A comparison of aspirin and anticoagulation following thrombolysis for myocardial infarction the AFTER study: a multicentre unblinded randomised clinical trial. BMJ 313 7070: 1429-1431. British Medical Journal. PMID 8973228. Retrieved on 2007-10-04. ^ Krumholz, Harlan M.; Martha J. Radford, Edward F. Ellerbeck, John Hennen, Thomas P. Meehan, Marcia Petrillo, Yun Wang, Timothy F. Kresowik, Stephen F. Jencks 1995-11-15. Aspirin in the Treatment of Acute Myocardial Infarction in Elderly Medicare Beneficiaries : Patterns of Use and Outcomes. Circulation 92 10: 2841-2847. PMID 7586250. Retrieved on 2008-05-15. ^ a b Macdonald S 2002. Aspirin use to be banned in under 16 year olds. BMJ 325 7371: 988. doi:10.1136/bmj.325.7371.988/c. PMID 12411346. ^ a b Warner, T. D.; Warner TD, Mitchell JA. 2002-10-15. Cyclooxygenase-3 COX-3: filling in the gaps toward a COX continuum?. Proc Natl Acad Sci U S a 99 21: 13371-3. doi:10.1073/pnas.222543099. PMID 12374850. Retrieved on 2008-05-08. ^ German Gerhardt C 1853. Untersuchungen über die wasserfreien organischen Säuren. Annalen der Chemie und Pharmacie 87: 149-179. doi:10.1002/jlac.18530870107. ^ German von Gilm H 1859. Acetylderivate der Phloretin- und Salicylsäure. Annalen der Chemie und Pharmacie 112 2: 180-185. doi:10.1002/jlac.18591120207. ^ German Schröder, Prinzhorn, Kraut K 1869. Uber Salicylverbindungen. Annalen der Chemie und Pharmacie 150 1: 1-20. doi:10.1002/jlac.18691500102. ^ Jeffreys, Diarmuid August 11, 2005. Aspirin: The Remarkable Story of a Wonder Drug. Bloomsbury USA, 73. ISBN 1582346003. ^ Ueber Aspirin. Pflügers Archiv : European journal of physiology, Volume: 84, Issue: 11-12 March 1, 1901, pp: 527-546. ^ Jeffreys, Aspirin, pp. 136-142 and 151-152 ^ Jeffreys, Aspirin, pp. 212-217 ^ Jeffreys, Aspirin, pp. 226-231 ^ Jeffreys, Aspirin, pp. 267-269 ^ Aukerman G, Knutson D, Miser WF 2002. Management of the acute migraine headache. Am Fam Phys 66 11: 2123-30. PMID 12484694. ^ Addy, D P 1983-04-09. Cold comfort for hot children. British Medical Journal Clinical research ed. 286 6372. ^ Barkin, Robert November/December 2001. Acetaminophen, Aspirin, or Ibuprofen in Combination Analgesic Products. American Journal of Therapeutics 8 6: 433-42. doi:10.1097/00045391-200111000-00008. Retrieved on 2008-05-02. ^ Krumholz, HM; Radford MJ, Ellerbeck EF, Hennen J, Meehan TP, Petrillo M, Wang Y, Kresowik TF, Jencks SF. 1995 November 15. Aspirin in the treatment of acute myocardial infarction in elderly Medicare beneficiaries. Patterns of use and outcomes. Circulation 92 10: 2841-7. PMID 7586250. Retrieved on 2008-05-02. ^ ISIS-2 Collaborative group 1988. Randomized trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet 2: 349-60. PMID 2899772. ^ Chew EY, Williams GA, Burton TC, Barton FB, Remaley NA, Ferris FL 1992. Aspirin effects on the development of cataracts in patients with diabetes mellitus. Early treatment diabetic retinopathy study report 16. Arch Ophthalmol 110 3: 339-42. PMID 1543449. ^ Bosetti, et al. 2006. Aspirin and the risk of prostate cancer. 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External links Wikimedia Commons has media related to: Aspirin DrugBank Aspirin Entry NextBio Aspirin Entry Reappraisal An aspirin a day keeps the doctor away Colour-enhanced scanning electron micrograph of aspirin crystals Aspirin research in the 1990s The History of Aspirin Aspirin and heart disease How Aspirin works Molview from bluerhinos.co.uk See Aspirin in 3D History of Aspro The science behind aspirin Take two: Aspirin, New uses and new dangers are still being discovered as aspirin enters its second century. Shauna Roberts, American Chemical Society Ling, Greg 2005. Aspirin. How Products are Made 1. Thomson Gale. A Gene Expression Omnibus entry of a genome-wide transcriptional expression data for bioactive small molecules Aspirin among them v d e Antithrombotics thrombolytics, anticoagulants and antiplatelet drugs B01 Antiplatelet drugs Glycoprotein IIb/IIIa inhibitors Abciximab Eptifibatide Tirofiban ADP receptor/P2Y12 inhibitors Clopidogrel Ticlopidine Prasugrel Prostaglandin analogue PGI2 Beraprost Prostacyclin Iloprost Treprostinil COX inhibitors Acetylsalicylic acid/Aspirin Aloxiprin Carbasalate calcium Other Ditazole Cloricromen Dipyridamole Indobufen Picotamide Triflusal Anticoagulants Vitamin K antagonists inhibit II, VII, IX, X Acenocoumarol Clorindione Coumatetralyl Dicoumarol Dicumarol Diphenadione Ethyl biscoumacetate Phenprocoumon Phenindione Tioclomarol Warfarin Heparin group/ glycosaminoglycans low molecular weight heparin Bemiparin, Certoparin, Dalteparin, Enoxaparin, Nadroparin, Parnaparin, Reviparin, Tinzaparin heparinoid Danaparoid, Sulodexide, Dermatan sulfate Direct thrombin II inhibitors Argatroban Bivalirudin Dabigatran Desirudin Hirudin Lepirudin Melagatran Ximelagatran Factor Xa inhibitors Apixaban Otamixaban Rivaroxaban oligosaccharides Fondaparinux, Idraparinux Other Defibrotide Ramatroban Antithrombin III Protein C Drotrecogin alfa Thrombolytic drugs/ fibrinolytics plasminogen activators: TPA Alteplase, Reteplase, Tenecteplase UPA Urokinase, Saruplase Streptokinase Anistreplase Monteplase other serine endopeptidases: Ancrod Fibrinolysin Brinase Non-medicinal Citrate EDTA Oxalate v d e Anti-inflammatory and antirheumatic products M01 Anti-inflammatory and antirheumatic products, non-steroids See also: NSAIDs Pyrazolidine/Butylpyrazolidines: · Ampyrone · Clofezone · Kebuzone · Metamizole · Mofebutazone · Oxyphenbutazone · Phenazone · Phenylbutazone · Sulfinpyrazone · Acetic acid derivatives and related substances: · Aceclofenac · Acemetacin · Alclofenac · Bromfenac · Bumadizone · Bufexamac · Diclofenac · Difenpiramide · Etodolac · Fentiazac · Indometacin · Ketorolac · Lonazolac · Oxametacin · Proglumetacin · Sulindac · Tolmetin · Zomepirac · Oxicams: · Ampiroxicam · Droxicam · Lornoxicam · Meloxicam · Piroxicam · Tenoxicam · Propionic acid derivatives: · Alminoprofen · Benoxaprofen · Dexibuprofen · Dexketoprofen · Fenbufen · Fenoprofen · Flunoxaprofen · Flurbiprofen · Ibuprofen · Ibuproxam · Indoprofen · Ketoprofen · Naproxen · Oxaprozin · Pirprofen · Suprofen · Tiaprofenic acid · Fenamates: · Flufenamic acid · Meclofenamic acid · Mefenamic acid · Tolfenamic acid · Coxibs: · Celecoxib · Etoricoxib · Lumiracoxib · Parecoxib · Rofecoxib · Valdecoxib · other anti-inflammatory and antirheumatic agents, non-steroids: · Nabumetone · Niflumic acid · Azapropazone · Glucosamine · Benzydamine · Glycosaminoglycan · Magnesium salicylate · Proquazone · Superoxide dismutase/Orgotein · Nimesulide · Feprazone · Diacerein · Morniflumate · Tenidap · Oxaceprol · Chondroitin sulfate · Specific antirheumatic agents Quinolines: · Oxycinchophen · Gold preparations: · Sodium aurothiomalate · Sodium aurothiosulfate · Auranofin · Aurothioglucose · Aurotioprol · Penicillamine/Bucillamine v d e Non-steroidal anti-inflammatory drug NSAID products primarily M01A and M02A, also N02BA Salicylates Aspirin acetylsalicylic acid · Aloxiprin · Benorylate · Diflunisal · Ethenzamide · Magnesium salicylate · Methyl salicylate · Salsalate · Salicin · Salicylamide · Sodium salicylate Arylalkanoic acids Diclofenac · Aceclofenac · Acemetacin · Alclofenac · Bromfenac · Etodolac · Indometacin · Indometacin farnesil · Nabumetone · Oxametacin · Proglumetacin · Sulindac · Tolmetin 2-Arylpropionic acids profens Ibuprofen · Alminoprofen · Benoxaprofen · Carprofen · Dexibuprofen · Dexketoprofen · Fenbufen · Fenoprofen · Flunoxaprofen · Flurbiprofen · Ibuproxam · Indoprofen†· Ketoprofen · Ketorolac · Loxoprofen · Miroprofen · Naproxen · Oxaprozin · Pirprofen · Suprofen · Tarenflurbil · Tiaprofenic acid N-Arylanthranilic acids fenamic acids Mefenamic acid · Flufenamic acid · Meclofenamic acid · Tolfenamic acid Pyrazolidine derivatives Phenylbutazone · Ampyrone · Azapropazone · Clofezone · Kebuzone · Metamizole†· Mofebutazone · Oxyphenbutazone · Phenazone · Sulfinpyrazone Oxicams Piroxicam · Droxicam · Lornoxicam · Meloxicam · Tenoxicam · Ampiroxicam COX-2 inhibitors Celecoxib · Deracoxib‡ · Etoricoxib · Firocoxib‡ · Lumiracoxib†· Parecoxib · Rofecoxib†· Valdecoxib†Sulphonanilides Nimesulide Topically used products Bendazac · Diclofenac · Etofenamate · Felbinac · Flurbiprofen · Ibuprofen · Indometacin · Ketoprofen · Naproxen · Piroxicam · Suprofen Others Fluproquazone · COX-inhibiting nitric oxide donator Items listed in bold indicate initially developed compounds of specific groups. †Withdrawn drugs. ‡Veterinary use medications. v d e Analgesic products N02A, N02B Opioids See also: Opioids template Opium alkaloids thereof Codeine · Morphine · Opium · Laudanum · Paregoric Semi-synthetic opium derivatives Acetyldihydrocodeine · Benzylmorphine · Desomorphine · Dihydrocodeine · Dihydromorphine · Ethylmorphine · Diamorphine · Hydrocodone · Hydromorphinol · Hydromorphone · Nicocodeine · Nicodicodeine · Nicomorphine · Oxycodone · Oxymorphone · Thebacon Synthetic opioids Alphaprodine · Anileridine · Buprenorphine · Butorphanol · Dextromoramide · Dextropropoxyphene · Dezocine · Fentanyl · Ketobemidone · Levorphanol · Methadone · Meptazinol · Nalbuphine · Pentazocine · Propoxyphene · Propiram · Pethidine · Phenazocine · Piminodine · Piritramide · Tapentadol · Tilidine · Tramadol Pyrazolones Ampyrone/Aminophenazone · Metamizole · Phenazone Cannabinoids Ajulemic acid · AM404 · Cannabidiol · Cannabis · Nabilone · Tetrahydrocannabinol Anilides Paracetamol acetaminophen · Phenacetin · Propacetamol Non-ateroidal anti-inflammatories See also: NSAIDs template Propionic acid class Fenoprofen · Flurbiprofen · Ibuprofen · Ketoprofen · Naproxen · Oxaprozin Oxicam class Meloxicam · Piroxicam Acetic acid class Diclofenac · Indometacin · Ketorolac · Nabumetone · Sulindac · Tolmetin COX-2 inhibitors Celecoxib · Rofecoxib Anthranilic acid fenamate class Meclofenamate · Mefenamic acid Salicylates Aspirin Acetylsalicylic acid · Benorylate · Diflunisal · Ethenzamide · Magnesium salicylate · Salicin · Salicylamide · Salsalate · Trisalate Atypical, adjunct miscellaneous Bicifadine · Clonidine · Cyclobenzaprine · Duloxetine · Flupirtine · Gabapentin · Glafenine · Nefopam · Orphenadrine · Tebanicline · Trazodone · Ziconotide Retrieved from http://en..org/wiki/Aspirin Categories: Aspirin | Non-steroidal anti-inflammatory drugs | Antiplatelet drugs | Acetates | Benzoic acids | Bayer brands | Equine medicationsHidden categories: Pages with DOIs broken since 2008 | All articles with statements | Articles with statements since August 2008 | articles to be split from August 2008 Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Türkçe العربية Asturianu বাংলা Bosanski БългарÑ?ки Català Česky Dansk Deutsch Eesti Ελληνικά Español Esperanto Ù?ارسی Français Galego í•œêµì–´ Hrvatski Bahasa Indonesia Ã?slenska Italiano עברית Kreyòl ayisyen Kurdî / كوردی Lietuvių Magyar Bahasa Melayu Nederlands 日本語 ‪Norsk bokmÃ¥l‬ ‪Norsk nynorsk‬ پښتو Polski Português Română РуÑ?Ñ?кий Simple English SlovenÄ?ina SlovenÅ¡Ä?ina СрпÑ?ки / Srpski Suomi Svenska தமிழà¯? ไทย Tiếng Việt Türkçe УкраїнÑ?ька Walon ä¸æ–‡ This page was last modified on 11 September 2008, at 19:34
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