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)

In an open clinical study the efficacy and tolerability of [1-(p-chlorobenzoyl)-5-methoxy-2-methylindole-3-acetoxy] acetic acid (acemetacin, TV 1322, Rantudil) were studied in 15 patients (2 female and 13 male) suffering from acute arthritis urica. Basing on the heterogeneity of the patients it was possible to estimate the minimal dose of acemetacin necessary to treat slight, moderately severe and extremely severe forms of the complaint. With the exception of one patient who suffered from an extremely severe attack of gout, all patients were completely free from pain within 7 days of therapy. The same results were also valid for the parameters reddening, swelling and functional and impairment. In 12 of 15 cases the assessment of therapy was given as "good" by the patients as well as the physicians. In only one instance was it necessary to give colchizin concomitantly to ensure that the patient was free from pain. In this case, the gout, had over many years, assumed a chronic character and during acute attacks manifested to an almost generalised arthritis. Despite the relatively high daily doses--in some cases up to 600 mg/day--only one case of slight gastric disorder was recorded as an undesired side effect. This, however, did not necessitate withdrawing the drug. It can thus be concluded that acemetacin in the doses used in this study is effective in the therapy of acute gout and is well tolerated at relatively high daily doses.
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PMID:[Therapy of acute attacks of gout using acemetacin (author's transl)]. 719 17

Indomethacin is a nonsteroidal anti-inflammatory drug (NSAID) used for the treatment of acute gout and inflammation. However, its use is limited due to side effects. Acemetacin is a prodrug of indomethacin that exhibits better gastric tolerability in preclinical and clinical trials. The aim of this study was to examine if the systemic administration of acemetacin involved the sequential participation of nitric oxide (NO) or K+ channel pathways to confer its antinociceptive effect, as compared to indomethacin. The antinociceptive effect of both drugs was studied with the formalin test. Equimolar doses of acemetacin or indomethacin were administered orally. The intraplantar administration of either L-NAME, glibenclamide, apamin or charybdotoxin plus indomethacin or acemetacin was studied using the formalin test and the anti-inflammatory and antihyperalgesic effects were measured. The antinociceptive effect of acemetacin or indomethacin was not significantly different when pretreatment with L-NAME, glibenclamide, apamin or charybdotoxin was done. The antihyperalgesic and antiinflammatory effects were also similar for both indomethacin and acemetacin. Our results suggest that the antinociceptive effect of indomethacin or acemetacin is not mediated by NO or K+ channel activation.
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PMID:Acemetacin antinociceptive mechanism is not related to NO or K+ channel pathways. 2040 46