Vinyl chloride-induced hepatic coproporphyrinuria with transition to chronic hepatic porphyria.
A chronic hepatic disorder of porphyrin metabolism was found in 36 workers with vinyl chloride (VC)-induced hepatic injury following long-time industrial exposure. Pathologic porphyrinuria, especially secondary coproporphyrinuria with transition to subclinical chronic hepatic porphyria, is a consistent pathobiochemical parameter for the recognition of VC hepatic lesions. The porphyrinuria is of diagnostic value for the incipient toxic phase. Erythrocyte uroporphyrinogen decarboxylase activity studied in six cases with initial chronic hepatic porphyria was normal, suggesting that VC affects only this enzyme in the liver.
D002617:Chemical Industry; D056486:Chemical and Drug Induced Liver Injury; D002908:Chronic Disease; D003306:Coproporphyrins / Q000652:urine*; D004912:Erythrocytes / Q000187:drug effects; D006801:Humans; D008111:Liver Function Tests; D008297:Male; D009784:Occupational Diseases / Q000139:chemically induced*; D011143:Polyvinyl Chloride / Q000138:chemical synthesis; D011164:Porphyrias / Q000139:chemically induced*; D011166:Porphyrins / Q000652:urine*; D014575:Uroporphyrinogen Decarboxylase / Q000097:blood; D014752:Vinyl Chloride / Q000009:adverse effects*; D014753:Vinyl Compounds / Q000009:adverse effects*
D003306:Coproporphyrins; D011166:Porphyrins; D014753:Vinyl Compounds; D011143:Polyvinyl Chloride; D014575:Uroporphyrinogen Decarboxylase; D014752:Vinyl Chloride