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Abstract
Objectives. To investigate clinical features of dimethylacetamide-induced hepatic injuries (DIHIs). Methods. Workers exposed to dimethylacetamide (DMAc) in two spandex factories were monitored for DIHI. We identified 38 DIHI cases as study subjects between 2001 and 2004. DMAc exposure was estimated with urinary N-methylacetamide (NMAc) results from 2003 to 2004. Results. All 38 cases showed hepatocellular-type liver injury. The interval between first exposure and identification of hepatic injury (latent period) was mostly less than two months and never exceeded six months. In addition, three repeat DIHI cases showed much shorter latent periods for recurrence than their initial latent periods of hepatic injury. A 50% decline of serum alanine aminotransferase (ALT) levels after the cessation of DMAc exposure took less than 14 days and a 90% decline less than 31 days. The median urinary NMAc level of DIHI group (samples from the department of DIHI cases) was 25.1 mg/g Cr; higher than that of all other urinary NMAc results (11.8 mg/g Cr). Conclusions. Our data suggest that DMAc can induce hepatocellular-type liver injury and the mechanism of DIHI may be idiosyncratic. Although our exposure estimation was incomplete, the workers with DIHIs might be exposed to higher levels of environmental DMAc than the workers who did not develop DIHIs. All workers exposed to DMAc need to be closely observed for occurrence of hepatic injury for at least six months.