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Anti Inflammatory Analgesics
Several chemically unrelated series of complex organic acids have the ability to relieve mild to moderate pain through actions that reduce inflammation at its source. Acetylsalicylic acid, or aspirin, is the most widely used mild analgesic, although more potent antipyretic (fever-reducing) analgesics, such as acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs), are available. Like aspirin, many of the drugs of this class reduce fever, and those that resemble aspirin most closely share what is presumed to be its molecular mechanism of action—namely, inhibition of the synthesis of prostaglandins (natural products of inflamed leukocytes) that induce the responses in local tissue that include pain and inflammation.
Research has shown that small doses of certain prostaglandins can mimic almost all the signs and symptoms of localized inflammation. Prostaglandins are naturally occurring by-products of arachidonic acid synthesis. They are thought to be released at the site of inflammation when leukocytes are attracted to injured or inflamed areas. All cells except red blood cells can produce prostaglandins, and when injured, the cells release large amounts of these substances. All aspirin-like analgesics, including NSAIDs, inhibit prostaglandin synthesis and release.
The NSAIDs (e.g., ibuprofen, naproxen, and fenoprofen) produce their therapeutic action by inhibition of the cyclooxygenase (COX) enzyme, which is responsible for the synthesis of prostaglandins and related compounds. There are two forms of the COX enzyme, COX-1 and COX-2. COX-1 is found in most normal tissues, while COX-2 is induced in the presence of inflammation. Because COX-2 is not normally expressed in the stomach, the use of COX-2 inhibitors (e.g., rofecoxib, celecoxib) seems to result in less gastric ulceration than occurs with other anti-inflammatory analgesics. However, COX-2 inhibitors do not reduce the ability of platelets to form clots.
As might be expected from their common mechanisms of action, many of the anti-inflammatory analgesic drugs share similar side effects. Hypersensitivity responses to aspirin-like drugs are thought to be due to an accumulation of prostaglandins after the pathways that break down prostaglandins are blocked. These responses can be fatal when very strong anti-inflammatory compounds are given. Inhibition of prostaglandin synthesis may result in other serious side effects, such as peptic ulcers (which may also be due in part to the irritant activity of large doses of aspirin on the lining of the stomach) and a reduced ability of platelets in the blood to aggregate and form clots. The latter effect, however, has given aspirin an added use as a prophylactic antithrombotic drug to reduce chances of cardiac or cerebral vascular thrombosis. Some of these aspirin-like analgesics also have specific toxic effects: liver damage occasionally occurs after administration of acetaminophen, and renal toxicity is sometimes seen with use of NSAIDs. Aspirin is thought to be a causative agent of Reye syndrome, a rare and serious degenerative disease of the brain and fatty tissue of the liver that accompanies certain viral infections in children and young adults.
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