Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aspirin (acetylsalicylic acid), the first of the NSAIDs (introduced in 1899), was initially never referred to as an anti-inflammatory agent. It was the advent of cortisone in 1949 that demonstrated dramatically that corticosteroids had anti-inflammatory properties and the term 'non-steroidal anti-inflammatory drug' was first used when phenylbutazone was introduced 3 years later. Since then, the NSAIDs have proliferated. There is to date no good evidence that they halt progression of rheumatoid disease, but by easing pain and diminishing swelling they make life much easier in osteoarthrosis, rheumatoid arthritis and many other types of arthritis, and are the drugs of first choice in acute gout. Their mode (or modes) of action are obscure and though inhibition of cyclo-oxygenase (prostaglandin synthetase) is clearly important, other mechanisms are also involved. The assessment of the anti-inflammatory action of these agents has received considerable attention in clinical trials because, whatever their action may be in experimental animal models, their action in inflamed joints in human patients must be ascertained, since there may be little parallel between the two. Different experimental animal models give different results with various agents and often bear little relation to their therapeutic action in man. No attempt has been made here to review in depth all the NSAIDs that have appeared since 1952. All have anti-inflammatory and analgesic activity and all can cause gastrointestinal side effects, though effectiveness and toxicity vary from drug to drug and patient to patient, there being very great interpatient variability. Non-reactors, patients who apparently fail to respond to certain agents, need further study, for it seems that these subjects may metabolise these agents differently from others. Considerable ingenuity has been shown not only in evolving new NSAIDs but in finding new ways of administering them. The number and variety of NSAIDs in their various forms varies greatly from country to country, depending largely on the regulatory bodies of those countries. In the meantime, the search for a better, less toxic compound continues with the hope that one may be found which has a deeper and more basic action on the underlying disease process.
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PMID:Non-steroidal anti-inflammatory drugs. Current status and rational therapeutic use. 636 85

Most physicians regard to newer short-acting anti-inflammatory drugs as a substitute for aspirin because they are less toxic. Although these drugs cannot induce remissions of rheumatoid arthritis, they do afford symptomatic relief and exert both a moderate algesic and anti-inflammatory effect in conditions like osteoarthritis, gout, pseudogout, and a variety of musculoskeletal syndromes. The many adverse reactions and toxic effects associated with these drugs are probably related to the inhibition of prostaglandin synthetase, which in turn reduces the biosynthesis of prostaglandins in widespread areas of the body. Thus limited in number, these compounds cannot play an effective role in the body's defense mechanisms. Researchers postulate that this failure accounts for the gastrointestinal and renal lesions--as well as other, as yet unexplained toxic manifestations--noted in patients taking these drugs. For safety's sake, the newer anti-inflammatory drugs should be used with large doses of aspirin, other agents that inhibit prostaglandin synthetase, or drugs that are potentially nephro-toxic.
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PMID:The new nonsteroidal anti-inflammatory drugs. 697 17

We present a patient in whom indomethacin treatment for acute gouty arthritis induced reversible azotaemia and hyperkalaemia. Re-introduction of the drug under controlled conditions of metabolic balance resulted in recurrence of hyperkalaemia and azotaemia, and was associated with a fall in plasma renin activity, but no change was observed in plasma aldosterone. Since potassium retention and hyperkalaemia occurred in the absence of hypoaldosteronism, other factors must be invoked to explain the observed upset in potassium homeostasis. This, and other recent case reports suggest that prostaglandin synthetase inhibitors such as indomethacin should be used with caution, especially in patients with pre-existing azotaemia, congestive heart failure, or gout.
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PMID:Indomethacin-induced azotaemia and hyperkalaemia: a case study. 703 49