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Yamamoto-Furusho K, et al. Hepatobiliary diseases are well recognized in inflammatory bowel disease (IBD) frequently presenting as abnormal serum liver biochemistry. The associated liver and biliary tract disease range from minor conditions, such as liver fatty changes, to severe diseases including primary sclerosing cholangitis and autoimmune hepatitis. The reported prevalence of IBD associated to hepatobiliary diseases has varied from 3% to greater than 50%. In this issue, Yamamoto-Furusho, et al., report their prospective single center study to investigate the prevalence of abnormal serum liver biochemical tests and risk factors associated with their development in Mexican patients with ulcerative colitis (UC). This is noteworthy as UC in Latin America may be genetically and phenotypically different to other populations. From January 1, 2007 to December 31, 2008 at the Instituto Nacional de Ciencias Médicas y Nutrición Hospital in Mexico, 200 patients (94 females, 106 males) with UC, who did not consume a significant amount of alcohol, were evaluated. A high prevalence of abnormal serum liver biochemical tests was found in 40%. The pattern of abnormal serum tests was hepacellular (70%), cholestatic (20%) and mixed (10%). The most common occurrence of the abnormal serum tests was a transient elevation in 63%, presumably not reflective of significant hepatobiliary disease. The hepatobiliary diseases resulting in the abnormal tests were: fatty liver disease (11.2%), primary sclerosing cholangitis (6.3%), drug-toxicity (6%) and other conditions (13.5%) including chronic hepatitis C, total parenteral nutrition associated disease, granulomatous and ischemic hepatitis. Factors found to be associated with the abnormal serum liver biochemistry included: intermittent activity of UC, surgical procedure including colectomy, active UC, abdominal sepsis and the presence of a positive ANA serology.

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2010-10-27   |   682 visitas   |   Evalua este artículo 0 valoraciones

Vol. 9 Núm.4. Octubre-Diciembre 2010 Pags. 387-389 Ann Hepatol 2010; 9(4)