Gilmar de Souza Lacerda1, Thalia Medeiros2, Natalia Fonseca do Rosário2, Regina Helena Saramago Peralta3, Mauro Jorge Cabral-Castro4, Eliane Bordalo Cathalá Esberard5, Thaís Guaraná de Andrade5, Analúcia Rampazzo Xavier6, Andrea Alice Silva7. 1. Laboratório Multiusuário de Apoio à Pesquisa em Nefrologia e Ciências Médicas, Departamento de Medicina Clínica, Faculdade de Medicina, Universidade Federal Fluminense, Rio de Janeiro, Brazil; Departamento de Patologia, Faculdade de Medicina, Universidade Federal Fluminense, Rio de Janeiro, Brazil. 2. Laboratório Multiusuário de Apoio à Pesquisa em Nefrologia e Ciências Médicas, Departamento de Medicina Clínica, Faculdade de Medicina, Universidade Federal Fluminense, Rio de Janeiro, Brazil. 3. Departamento de Patologia, Faculdade de Medicina, Universidade Federal Fluminense, Rio de Janeiro, Brazil. 4. Instituto de Microbiologia Prof Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil. 5. Centro de Referência de Tratamento em Hepatites/HUAP, Serviço de Gastroenterologia, Departamento de Medicina Clínica, Faculdade de Medicina, Universidade Federal Fluminense, Rio de Janeiro, Brazil. 6. Laboratório Multiusuário de Apoio à Pesquisa em Nefrologia e Ciências Médicas, Departamento de Medicina Clínica, Faculdade de Medicina, Universidade Federal Fluminense, Rio de Janeiro, Brazil; Departamento de Patologia, Faculdade de Medicina, Universidade Federal Fluminense, Rio de Janeiro, Brazil. Electronic address: analuciaxavier@id.uff.br. 7. Laboratório Multiusuário de Apoio à Pesquisa em Nefrologia e Ciências Médicas, Departamento de Medicina Clínica, Faculdade de Medicina, Universidade Federal Fluminense, Rio de Janeiro, Brazil; Departamento de Patologia, Faculdade de Medicina, Universidade Federal Fluminense, Rio de Janeiro, Brazil. Electronic address: aasilva@id.uff.br.
Abstract
BACKGROUND: Hepatitis C virus is known to be highly dependent of lipid metabolism to infect new cells and replicate. AIMS: To investigate lipid and apolipoprotein profile in chronic HCV patients according to treatment response. METHODS: Patients recruited from the Hepatitis Treatment Center at Niteroi (Brazil) who received interferon (IFN)-based therapies were separated into two groups, those who achieved sustained virological response (SVR) or not (non-SVR). Another group of patients treated with IFN-free direct-acting antiviral (DAA) therapies was followed from before starting the treatment until one year after therapy. Triglycerides, total cholesterol and fractions were determined by colorimetric and/or electrophoresis techniques. Lecithin cholesterol acyltransferase (LCAT) activity and serum levels of apolipoproteins A1, A2, B, C2, C3 and E were assessed by enzymatic and multiplex assays, respectively. RESULTS: We studied 114 patients, and SVR was reached in 28 (39.4%) patients treated with IFN-therapy and in all (100%) patients who received DAA. Non-SVR patients (n = 43) presented altered liver parameters post-treatment. Levels of total cholesterol, LDL-C, VLDL-C and triglycerides were significant higher in SVR group. In contrast, LCAT activity and HDL-C levels were elevated in non-SVR patients. Only apolipoproteins B, C2 and C3 levels were increased in SVR group. The follow-up of SVR-DAA patients (n = 43) revealed a significant and progressive increase in serum levels of total cholesterol, LDL-C, VLDL-C and triglycerides. CONCLUSIONS: After a successful treatment, chronic hepatitis C patients experienced a reestablishment of lipid metabolism. Our results suggest that the monitoring of serum lipids could be a practical and routine laboratory tool to be applied during the treatment follow-up.
BACKGROUND:Hepatitis C virus is known to be highly dependent of lipid metabolism to infect new cells and replicate. AIMS: To investigate lipid and apolipoprotein profile in chronic HCVpatients according to treatment response. METHODS:Patients recruited from the Hepatitis Treatment Center at Niteroi (Brazil) who received interferon (IFN)-based therapies were separated into two groups, those who achieved sustained virological response (SVR) or not (non-SVR). Another group of patients treated with IFN-free direct-acting antiviral (DAA) therapies was followed from before starting the treatment until one year after therapy. Triglycerides, total cholesterol and fractions were determined by colorimetric and/or electrophoresis techniques. Lecithin cholesterol acyltransferase (LCAT) activity and serum levels of apolipoproteins A1, A2, B, C2, C3 and E were assessed by enzymatic and multiplex assays, respectively. RESULTS: We studied 114 patients, and SVR was reached in 28 (39.4%) patients treated with IFN-therapy and in all (100%) patients who received DAA. Non-SVR patients (n = 43) presented altered liver parameters post-treatment. Levels of total cholesterol, LDL-C, VLDL-C and triglycerides were significant higher in SVR group. In contrast, LCAT activity and HDL-C levels were elevated in non-SVR patients. Only apolipoproteins B, C2 and C3 levels were increased in SVR group. The follow-up of SVR-DAApatients (n = 43) revealed a significant and progressive increase in serum levels of total cholesterol, LDL-C, VLDL-C and triglycerides. CONCLUSIONS: After a successful treatment, chronic hepatitis Cpatients experienced a reestablishment of lipid metabolism. Our results suggest that the monitoring of serum lipids could be a practical and routine laboratory tool to be applied during the treatment follow-up.