Introduction
Aspirin is one of the most commonly used drug in the world. The generic name is acetyl salicylic acid and the drug belongs to the group of non- steroidal anti-inflammatory medicines, which works by inhibiting the production of compounds in the body that cause pain, fever, inflammation, and blood clots (Koester, 1993). Aspirin is also a member of the salicylate family of compounds as it is synthesized from salicylic acid, which was discovered in Oxford (UK) by Edward stone in 1793 and first synthesized in the laboratory in 1897 by a German scientist, Felix Hoffmann of the Bayer company (Rinsema, 1999). The drug is also known as Acetoxybenzoic acid, Acylpyrin, Ecotrin, Acenterine, Polopiryna, Acetosal, Colfarit and is prescribed for e.g. migraine, headache, back and muscle pain, arthritis, heart attacks and strokes. Aspirin is used in both human and veterinary medicine.
Chemical and physical characteristics
The chemical formula of aspirin is C9H8O4 with a molecular weight of: 180.16 g/mol. Its chemical structure is composed of an aromatic ring, an ester group and a carboxylic acid group. During the chemical reaction for aspirin production, salicylic acid reacts by acetylation with acetic anhydride to generate aspirin and acetic acid. Sulfuric or phosphoric acid is often used in small quantity as a catalyst.
Aspirin has a white colour, a crystalline structure and is weakly acidic. The melting and boiling points are 136 °C and 140 °C respectively.
Mechanism of action in the body
In the body, aspirin has two main actions. It can act as an anti-prostaglandin (anti-inflammation, fever-reducing, pain reliever) compound and also as an anti-platelet aggregation (blood thinner) agent. The molecule works by inhibiting cyclooxygenase (COX), the enzyme that metabolizes arachidonic acid, the precursor to prostaglandins (named A to I), which are hormones that trigger inflammation and pain in the body (Vane &Potty, 2003). There are two types of COX and both are irreversibly inhibited by aspirin. The first (COX1) produces prostaglandins in a normal physiological condition and the second (COX2) mediates pain and inflammation in response to tissue damage. The therapeutic target of aspirin is COX2. Its activity is inhibited by a formation of a covalent bond between the drug and the enzyme leading to an obstruction of the enzyme active site and a blockage of prostaglandin synthesis.
For fever release, aspirin acts directly on the hypothalamus, a small gland at the base of the brain, by inhibiting the productions of the prostaglandins that stimulate the hypothalamus to increase the body's temperature set-point. This results in a vasodilation of blood vessels, sweating and reduction of the body temperature.
For an anti-clotting effect, aspirin inhibits thromboxane-A synthetase, an enzyme found in platelets that converts prostaglandin H2 into thromboxane. Thromboxane is a sort of glue that cause the platelets to aggregate and provoke blood clotting. For treatment of heart attacks, this process prevents irreversibly the platelet to aggregate and adhere to the blood vessel walls and block the blood flow.
Forms and doses
Aspirin is produced in various forms including tablets, caplets, quick chew tablets, and express packs, which contain varying concentrations of the molecules (e.g. 80, 325, 550 mg). The dose of aspirin to be taken vary according to many factors such age, medical condition, body weight and other medications. Physicians decide the appropriate dose for each patient. Examples of doses are: 325-650 mg every 4-6 hours for an adult dosage for pain and fever with a maximum daily dose of 4000 mg and 650 mg twice daily for blood clots prevention after surgery. Aspirin is not usually prescribed to children for fever, but if prescribed by a physician for pain, the indicative dose is 10-15 mg/kg of body weight every 6 hours. In all case the prescribed dose should be respected as an overdose can be deadly.
Adverse effects and precautions
As for all medicines, the use of aspirin presents various side effects. These can be mild or severe and are not experienced by all users. Side effects occur more frequently with high doses and long period treatment and involves more commonly the gastrointestinal system. Use of aspirin can cause ulcers, stomach bleeding and in some cases, perforation of the stomach (Kwok & Loke, 2010). This is due to the interaction of the drug with COX-1 in the gastrointestinal tract. COX-1 is important for maintaining a tick stomach lining and when the enzyme is disabled by a regular use of the drug, a thinning of the mucus that protects the stomach from the gastric juices occurs, causing the side effects mentioned above. Other side effects include e.g. heartburn or indigestion, abdominal cramps or discomfort, dizziness, nausea or vomiting, mouth and throat swelling and symptoms of an allergic reaction. In any cases, the use of the drug should be stopped immediately and a medical attention sought.
Use of aspirin is not appropriate for everyone. It is not advisable for children, teenagers and young adults that suffer of chickenpox, influenza or flu-like illnesses as it increases their risk for Reye's syndrome, a serious health condition that may cause liver or brain damage. Other cases of unsuitability are e.g. people suffering of diabetes, gout, liver and kidney malfunction, pregnant and breast- feeding women, before surgeries or when using other medications such as anticoagulants, corticosteroids, ibuprofen, naproxen, insulin.
Conclusion
Aspirin is an important drug used to treat various health conditions. The full beneficial attributes are yet to be discovered. Many research projects showed that the drug is a promising candidate treatment for other diseases such as cancer, Alzheimer's disease and dementia. However due to serious side effects that can occur with regular use of the medicine, it is recommended to seek medical advice before using the drug and to respect the prescribed dose and treatment period.
References
Koester, M.C. (1993). An overview of the physiology and pharmacology of aspirin and Non-steroidal anti-inflammatory Drugs. Journal of Athletic Training, 28 (3), 252-259.
Kwok, C.S., Loke, Y.K. (2010). Critical Overview on the Benefits and Harms of Aspirin. Pharmaceuticals, 3, 1491-1506.
Rinsema, T.J. (1999). One Hundred Years of Aspirin. Medical History, 43, 502-507.
Van, J.R., Botting, R.M. (2003). The mechanism of action of aspirin. Thrombosis Research, 110 (5-6), 255-258.
