Aspirin is one of the most widely used medicinal compounds in the world. It is an ingredient in hundreds medications and is approved for use as an analgesic, antiinflammatory, anticoagulant and antipyretic. Aspirin produces these effects by inhibiting the oxidation of arachadonic acid by cyclooxygenase 1 & 2.

Arachadonic acid is a ubiquitous membrane fatty acid released in response to injury or stress. Without aspirin, arachadonic acid is initially oxidized by cyclooxygenase to prostaglandin G₂, subsequent steps produce: Thromboxane A, prostacyclin I₂, prostaglandin E₂, prostaglandin D₂ and prostaglandin F_2a.

• Thromboxane A mediates platelet aggregation and vasoconstriction
• Prostacyclin I₂ decreases platelet aggregation, increases renal blood flow, increases vasodilation, inhibits gastric acid production of mucus
• Prostaglandin E₂ increases renal blood flow, vasodilation, natriuresis, inhibits gastric acid production
• Prostaglandin D₂ increases renal blood flow, inhibits gastric acid production
• Prostaglandin F_2a decreases progestrone, increases uterine contraction, increases vasoconstriction and bronchconstriction

Like other non-steroidal aniti-inflammatory drugs (NSAIDS), aspirin has a maximum dose ceiling and significant side effects including increased bleeding time and gastric ulceration.

Aspirin can cause gastric irritation and affects platelet function, thus increasing the risk of bleeding. Aspirin has also been linked to the development of Reye’s syndrome in children and teens. Reye's syndrome is a life threatening condition that causes acute encephalopathy and fatty infiltration of the liver and other organs in children recovering from viral infection.

Because of this association, aspirin should not be given to persons under the age of 20 unless ordered by a physician. Since 2003, the U.S. Food and Drug Administration (FDA) has required that all aspirin products contain a warning label describing the potential for the development of Reye’s syndrome.

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