Phenylbutazone was introduced in 1949, followed soon there- after by its metabolite oxyphenbutazone. Both are potent anti- inflammatory drugs, but are associated with significant adverse effects, and hence have been withdrawn from routine use in several countries. They are still available in India. Their use should be restricted to acute gout and acute exacerbations of rheumatoid arthritis and ankylosing spondylitis.
Related drugs include aminopyrine, antipyrine, amidopy- rine, azapropazone, dipyrone, noramidoprine, phenazone, and sulfinpyrazone.
Phenylbutazone interferes with prostaglandin synthesis via inhibition of the cyclo-oxygenase pathway. It is irritating to the mucosa of the gastrointestinal tract.
· Main features of overdose with phenylbutazone/oxyphenbuta- zone include vomiting, abdominal pain, acid-base and elec- trolyte disturbances, pulmonary oedema, vertigo, seizures, hypotension, coma, and respiratory and cardiac arrest.
· Salicylate-like symptoms including stimulation of the respiratory center, respiratory alkalosis, and metabolic
· Other reported effects include hyperglycaemia, hypocal- caemia, cyanosis, paraesthesias, tinnitus, erythematous rash, profuse sweating, and dyspnoea.
· Renal, hepatic, and haematological complications soon follow. Renal dysfunction is common, including protein- uria, haematuria, anuria, oliguria and in one fatal case, acute nephritis. Urine may be red due to a pyrazolone metabolite.
· Blood dyscrasias (agranulocytosis, thrombocytopenia, aplastic anaemia) are more common with dipyrone. Methaemoglobinemia has been reported with antipyrine. Pancytopenia has been reported after overdose with phenylbutazone and oxyphenbutazone.
· Moderate to marked hepatocellular injury has been reported with chronic ingestion (less than 6 weeks) of therapeutic doses. Gastric ulceration was reported in a few patients.
· Fatal dose is highly variable (4 to 40 gm).
· Phenylbutazone enhances the effects of tolbutamide and other sulphonylurea antidiabetic agents, and coumarin anticoagulants, and may enhance the effects of phenytoinand some sulfonamides.
· Ferric chloride test.
· Obtain a baseline CBC, renal and liver function tests, and urinalysis in symptomatic patients.
· After 24 hours, a red discolouration of the urine may be seen, due to rubazonic acid, a pyrazolone metabolite.
· Stomach wash, activated charcoal. Ipecac-induced emesis is not recommended because of the potential for CNS depres-sion and seizures.
· Treat convulsions in the usual manner.
· It is postulated that the excretion of phenylbutazone, like salicylate, may be enhanced in an alkaline urine. This may be considered in very severely intoxicated patients. However, alkaline diuresis is of questionable value since pyrazoles are extensively metabolised, and only 1 to 5% of the drug is eliminated unchanged by the kidneys.
· Haemoperfusion in life-threatening cases. Because of the low water solubility and high protein binding, haemodi-alysis is not likely to be effective.
· Plasmapheresis is claimed to be beneficial in severe poisoning, and has been tried successfully in a case of phenylbutazone overdose.
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