Hepatotoxicidade ao esquema rifampicina, isoniazida e pirazinamidano tratamento da tuberculose em pacientes com e sem a síndrome daimunodeficiência humana adquirida

• Ano de defesa: 2009
• Autor(a) principal: Maria Natalia Simao Saldanha de Magalhaes Coca
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais
• Palavras-chave em Português: HIV; Antituberculosos/uso terapêutico; Tuberculose; Antituberculosos/toxicidade
• Link de acesso: https://hdl.handle.net/1843/ECJS-7WYFYK

Previous studies suggest that human infection by HIV increases the frequency of hepatotoxicity to antituberculosis drugs. In this study, the prevalence and the risk factors for hepatotoxicity to rifampicin, isoniazid and pyrazinamide have been evaluated in HIVinfected and non-infected. 162 patients with tuberculosis have been selected, in the age range of 18 to 80 years, and admitted to the Hospital Eduardo de Menezes, in BeloHorizonte, 2005-2007. Patients were divided into two groups: 1) comprising 30 HIVinfected individuals; and 2) 132 controls. This is a case-control study. Three definitions for hepatotoxicity were used: a) hepatotoxicity I: a 3 times increase in the lower normal value (LNV) of alanine-aminotransferase; b) hepatotoxicity II: a 3 times increase in the normal superior value (NSV) of alanine-aminotransferase; c) hepatotoxicity III: a 3 times increase in the normal superior value (NSV) of alanine-aminotransferase and 2 times the normal superior value of total bilirubin. The medical records were retrieved from the hospital filesand information was transferred to an eletronic data bank and analyzed by SPSS 12.0. In groups I and II the frequency of hepatotoxicity I was 77% and 46%, respectively (p< 0.01). Using the hepatotoxicity II definition the frequency was 20% and 9.1%, respectively (p=0.107). For hepatotoxicity III the frequency was 20% and 8.3%, respectively (p=0,09). Hepatotoxicity was more frequent in men of both groups (77% in group 1 and 71% ingroup 2; p> 0.05). The mean age was similar for both groups (36 years in group 1 and 44 in group 2; p> 0.05). Of 17 patients with hepatotoxicity (definition III), 3 did not present symptoms and treatment with antituberculous drugs was continued. On the other hand, of 22 who suspended treatment, 8 (36.4%) did not fulfill the definition of hepatoxicity III and treatment was interrupted because they presented symptoms attributed to causes other than toxic hepatitis. In the two groups, alcohol abuse was similar (68% in group 1 and 64% in group 2; p> 0.05) and was associated to hepatotoxicity only for definition I. In relation to the time until the development of hepatotoxicity (definition I), the median was 14 days in group 1 and of 11 days in group 2 (p> 0.05). There was no relation between hepatotoxicity and the use of antiretroviral drugs. In summary, the frequency of hepatotoxicity is depend on the definition. Alcohol use was a factor associated with hepatotoxicity independently ofserological status for HIV. Mortality was not higher among HIV-infected individuals. The clinical symptoms in the post-treatment do not always define hepatotoxicity; the presence of symptoms can not always be attributed to the hepatotoxicity.