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To achieve WHO's goal of eliminating hepatitis C virus (HCV), innovative strategies must be designed to diagnose and treat more patients. Therefore, we aimed to describe an implementation strategy to identify patients with HCV who were lost to follow-up (LTFU) and offer them re-linkage to HCV care. We conducted an implementation study utilizing a strategy to contact patients with HCV who were not under regular follow-up in 13 countries from Latin America. Patients with HCV were identified by the international classification of diseases (ICD-9/10) or equivalent. Medical records were then reviewed to confirm the diagnosis of chronic HCV infection defined by anti-HCV+ and detectable HCV-RNA. Identified patients who were not under follow-up by a liver specialist were contacted by telephone or email, and offered a medical reevaluation. A total of 10,364 patients were classified to have HCV. After reviewing their medical charts, 1349 (13%) had undetectable HCV-RNA or were wrongly coded. Overall, 9015 (86.9%) individuals were identified with chronic HCV infection. A total of 5096 (56.5%) patients were under routine HCV care and 3919 (43.5%) had been LTFU. We were able to contact 1617 (41.3%) of the 3919 patients who were LTFU at the primary medical institution, of which 427 (26.4%) were cured at a different institutions or were dead. Of the remaining patients, 906 (76.1%) were candidates for retrieval. In our cohort, about one out of four patients with chronic HCV who were LTFU were candidates to receive treatment. This strategy has the potential to be effective, accessible and significantly impacts on the HCV care cascade.

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Twenty-nine HCV-infected patients were treated with pegylated interferon alpha. Diagnosis was based on serum HCV RNA-PCR positive results and liver biopsy. All patients had elevated serum levels of alanine aminotransferase at the time of the study, but liver disease was compensated. Patients were evaluated at baseline treatment and after 4 and 12 weeks of antiviral treatment with the Medical Outcomes Study 36-item Short-Form Health Survey. The Mini-International Neuropsychiatric Interview was used to exclude previous or current psychiatric diagnoses. Both patients and psychiatrists were blind to the HCV RNA status, and serum HCV RNA test results only became available after the visit at week 12. After antiviral treatment, 16 patients (55.2%) were classified as nonresponders and 13 (44.8%) were classified as responders. When compared to nonresponders, responders had a greater improvement in the HRQOL scores for the mental health domain (P < .019). Differences in other domains were not significant. The present study confirms that active viral infection is one possible reason for the poor Health-Related Quality of Life in this population.

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A hepatite C é uma doença de endemicidade mundial, atingindo quase 200 milhões de pessoas em todo o mundo, sua historia natural é caleidoscópica, mas a fibrose hepática está presente em 80 por cento dos infectados. Constantemente, diversos estudos são realizados tentando definir fatores prognósticos de evolução para fibrose e de resposta ao tratamento. Nos últimos anos as alterações da homeostase da glicose, precisamente níveis de insulinemia e glicemia plasmáticos em jejum e resistência à insulina nos pacientes com Hepatite C crônica têm recebido muita atenção devido ao papel que a insulina exerce na fibrogênese hepática, assim como na refratariedade de resposta ao tratamento antiviral. Estudos recentes apontam ao vírus da hepatite C como fator indutor de resistência à insulina. Por todo o supracitado, parece ser relevante e apropriado estudar estes parâmetros para tentar achar fatores preditivos de evolução à fibrose assim, como à resposta terapêutica as drogas convencionais. Objetivos: 1. Avaliar a associação entre os níveis de insulinemia, glicemia em jejum, índice de resistência a insulina (HOMA-RI) e estágio de fibrose hepática em dois grupos de pacientes portadores de hepatite C crônica com doença de fígado compensada. 2. Analisar num destes grupos a relação entre os níveis de glicemia e insulinemia em jejum, valores de HOMA-RI e resposta terapêutica ao Interferon- alfa e Ribavirina avaliados em quatro momentos durante este tratamento antiviral. 3. Determinar a associação de resistência à insulina (RI) e fibrose hepática com variáveis como: índice de Massa Corpórea (IMC), circunferência de cintura, esteatose hepática, genótipo viral e níveis de transaminases assim como com outras variáveis demográficas. Estudo ambispectivo de série de casos, no qual foram analisados: 1°. Em 25 pacientes não obesos [amostra 1] a associação dos níveis de insulinemia e glicemia em jejum, índice de HOMA-RI após tratamento anti-viral com grau de fibrose de acordo a escala de METAVIR e com taxa de progressão da fibrose segundo o estudo histopatológico das biópsias hepáticas pré-tratamento. Foi avaliado num segundo grupo com 33 pacientes com IMC ≥ 30kg/m2 15 diabéticos e 18 não diabéticos [amostra 2] que participaram de um estudo longitudinal por 72 semanas, o comportamento da resistência à insulina durante quatro tempos no tratamento com Interferon D e Ribavirina. Neste grupo também foi realizado o estudo histopatológico das biópsias hepáticas pré-tratamento. Foi analisada a associação entre resistência a insulina (RI) e fibrose hepática assim como relação entre resistência a insulina e resposta ao tratamento nos 33 pacientes da amostra 2°. Análise estatística: foi realizada em SSPS versão 10, utilizado os testes de X2, Teste t e Mann-Whitney. A análise da amostra 1, quando foi utilizada variável dependente estágio de fibrose leve (F1 e F2) versus fibrose avançada (F3 e F4) e se relacionou com resistência a insulina (RI) não demonstrou diferenças estatisticamente significativas entre os dois grupos assim como, quando foi avaliada a associação de RI com a taxa da progressão da fibrose. Quando nesta amostra a variável dependente estudada foi RI versus Não RI, o IMC, a circunferência de cintura e insulinemia em jejum foram maiores no grupo com RI existindo diferença estatística significativa. Quando na amostra 2 com 33 pacientes foi estudada variável dependente estágio de fibrose leve (F1 e F2) versus fibrose moderada (F3 e F4) os níveis da enzima aspartato aminotransferase (AST) estiveram significativamente mais altos no grupo com fibrose avançada (F3 e F4). O genótipo 1 esteve associado a níveis de HOMA-RI= 3 quando os pacientes tinham um grau de fibrose F3 e HOMA-RI = 2,90 quando os pacientes apresentavam um estágio de fibrose F4. Quando foi analisada RI versus Não RI como variável dependente, uma idade maior esteve associada com RI. Quando foi analisada nesta amostra como variável dependente resposta sustentável ao tratamento (RS) versus Não resposta (NR) a presença de esteatose, genótipo 1, HOMA>3,1 O; insulinemia em jejum> 9,76μUI,IMC>31,31kg/m2, circunferência de cintura >104 cm associaram-se a não resposta ao tratamento anti-viral. Um estágio mais avançado de fibrose associou-se com parâmetros antropométricos maiores, com níveis de AST mais elevados, com níveis mais elevados de glicemia em jejum 2. O genótipo 1 no grupo obeso teve um índice de HOMA-RI maior associado com fibrose avançada. 3. No grupo de não obesos a circunferência de cintura e insulinemia em jejum se relacionaram com resistência à insulina (RI) enquanto que no grupo de obesos esta associação não foi achada. 4. Não resposta ao tratamento antiviral esteve associado a um índice de RI elevado assim como a níveis de insulinemia elevados, à presença de esteatose na biópsia hepática, a genótipo 1 e à índices antropométricos maiores.

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Apoptosis es un término griego que significa ¶caída de las hojas viejas de los árboles en otoño÷. Esta palabra describe el proceso por el cual células indeseables, dañadas o senescentes son eliminadas de los organismos multicelulares. La muerte cellular patológica en el hígado fue siempre referida como necrosis, pero procesos fisiopatológicos en este órgano pueden conducir a injuria celular tanto por apoptosis como por necrosis. Apoptosis difiere de necrosis porque la primera es controlada activamente y la membrana celular es mantenida, evitando la extravasación de material intracelular con la consecuente respuesta inflamatoria. El proceso de apoptosis puede ocurrir por dos mecanismos: el de receptor de muerte (DR) o extrínseco o por el mecanismo mitochondrial llamado también intrínseco. Las células hepaticas expresan diferentes receptores de muerte: Fas, TNF-R1, TRAIL-R1 y TRAIL-R2. Las células estelares expresan Fas y TRAIL cuando están activadas y transformadas fenotípicamente en miofibroblastos, y éstas también sufren apoptosis durante la resolución de la injuria hepática. Los colangiocitos parecen ser células tipo II (en éstas el mecanismo de apoptosis mitochondrial parece ser esencial). Apoptosis mediada por estos receptors juega un rol importante en una variedad de procesos biológicos tales como el daño tisular, protección contra microorganismos patógenos, y su papel central en la injuria hepática y posterior progresión a la fibrosis ha sido bien establecido en diferentes enfermedades hepáticas. Un factor importante en apoptosis cellular es que puede ocurrir en ausencia de elevación sérica de transaminasas hepáticas como ocurre en la necrosis celular. Este artículo es una revisión de este proceso.(AU)

Apoptosis is a Greek term that means "the fall of the old leaves of the autumn trees". This term describes the process by which undesirable, damaged or old cells are eliminated from the multicellular organisms. Pathologic cell death in the liver has traditionally been referred to as necrosis, but pathophysiologic process in the liver can lead to cell injury and death by apoptosis as well by necrosis. The first differs from the second, because it is actively controlled and the membrane integrity is maintained, avoiding extravasations of intracellular mate rial and inflammatory response. Apoptosis can occur by two mechanisms: death receptor (DR) or extrinsic mechanism and mitochondrial or intrinsic mechanism. Liver cells express different death receptors: hepatocytes express Fas, TNF-R1, TRAIL-R1, TRAIL-R2; Stellate Cell (HCS) express Fas and TRAIL when is activated into myofibroblast-like phenotype and undergo apoptosis during resolution of liver injury in vivo. Cholangiocytes seem to be type II cells (in which the mitochondrial mechanism to apoptotic is essential) regarding signaling of Fas endothelial cells from rat livers express Fas, and their activation may lead to apoptosis of endothelial cells from hepatic sinusoids. Apoptosis mediated by these receptors have a major role in a variety of biological processes as tissue injury, protection against pathogenic microorganisms, and the role on hepatic injury and posterior progression to fibrosis has been well established in different hepatic diseases. Apoptosis may occur in the absence of significant transaminase elevations as happen in cellular necrosis. This paper is a review of this process.(AU)

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Apoptosis es un término griego que significa “caída de las hojas viejas de los árboles en otoño”. Esta palabra describe el proceso por el cual células indeseables, dañadas o senescentes son eliminadas de los organismos multicelulares. La muerte cellular patológica en el hígado fue siempre referida como necrosis, pero procesos fisiopatológicos en este órgano pueden conducir a injuria celular tanto por apoptosis como por necrosis. Apoptosis difiere de necrosis porque la primera es controlada activamente y la membrana celular es mantenida, evitando la extravasación de material intracelular con la consecuente respuesta inflamatoria. El proceso de apoptosis puede ocurrir por dos mecanismos: el de receptor de muerte (DR) o extrínseco o por el mecanismo mitochondrial llamado también intrínseco. Las células hepaticas expresan diferentes receptores de muerte: Fas, TNF-R1, TRAIL-R1 y TRAIL-R2. Las células estelares expresan Fas y TRAIL cuando están activadas y transformadas fenotípicamente en miofibroblastos, y éstas también sufren apoptosis durante la resolución de la injuria hepática. Los colangiocitos parecen ser células tipo II (en éstas el mecanismo de apoptosis mitochondrial parece ser esencial). Apoptosis mediada por estos receptors juega un rol importante en una variedad de procesos biológicos tales como el daño tisular, protección contra microorganismos patógenos, y su papel central en la injuria hepática y posterior progresión a la fibrosis ha sido bien establecido en diferentes enfermedades hepáticas. Un factor importante en apoptosis cellular es que puede ocurrir en ausencia de elevación sérica de transaminasas hepáticas como ocurre en la necrosis celular. Este artículo es una revisión de este proceso.

Apoptosis is a Greek term that means "the fall of the old leaves of the autumn trees". This term describes the process by which undesirable, damaged or old cells are eliminated from the multicellular organisms. Pathologic cell death in the liver has traditionally been referred to as necrosis, but pathophysiologic process in the liver can lead to cell injury and death by apoptosis as well by necrosis. The first differs from the second, because it is actively controlled and the membrane integrity is maintained, avoiding extravasations of intracellular mate rial and inflammatory response. Apoptosis can occur by two mechanisms: death receptor (DR) or extrinsic mechanism and mitochondrial or intrinsic mechanism. Liver cells express different death receptors: hepatocytes express Fas, TNF-R1, TRAIL-R1, TRAIL-R2; Stellate Cell (HCS) express Fas and TRAIL when is activated into myofibroblast-like phenotype and undergo apoptosis during resolution of liver injury in vivo. Cholangiocytes seem to be type II cells (in which the mitochondrial mechanism to apoptotic is essential) regarding signaling of Fas endothelial cells from rat livers express Fas, and their activation may lead to apoptosis of endothelial cells from hepatic sinusoids. Apoptosis mediated by these receptors have a major role in a variety of biological processes as tissue injury, protection against pathogenic microorganisms, and the role on hepatic injury and posterior progression to fibrosis has been well established in different hepatic diseases. Apoptosis may occur in the absence of significant transaminase elevations as happen in cellular necrosis. This paper is a review of this process.

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Apoptosis is a Greek term that means "the fall of the old leaves of the autumn trees". This term describes the process by which undesirable, damaged or old cells are eliminated from the multicellular organisms. Pathologic cell death in the liver has traditionally been referred to as necrosis, but pathophysiologic process in the liver can lead to cell injury and death by apoptosis as well by necrosis. The first differs from the second, because it is actively controlled and the membrane integrity is maintained, avoiding extravasations of intracellular material and inflammatory response. Apoptosis can occur by two mechanisms: death receptor (DR) or extrinsic mechanism and mitochondrial or intrinsic mechanism. Liver cells express different death receptors: hepatocytes express Fas, TNF-R1, TRAIL-R1, TRAIL-R2; Stellate Cell (HCS) express Fas and TRAIL when is activated into myofibroblast-like phenotype and undergo apoptosis during resolution of liver injury in vivo. Cholangiocytes seem to be type II cells (in which the mitochondrial mechanism to apoptotic is essential) regarding signaling of Fas endothelial cells from rat livers express Fas, and their activation may lead to apoptosis of endothelial cells from hepatic sinusoids. Apoptosis mediated by these receptors have a major role in a variety of biological processes as tissue injury, protection against pathogenic microorganisms, and the role on hepatic injury and posterior progression to fibrosis has been well established in different hepatic diseases. Apoptosis may occur in the absence of significant transaminase elevations as happen in cellular necrosis. This paper is a review of this process.

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UNLABELLED: Incomplete septal cirrhosis is a form of macronodular cirrhosis characterized by fine and incomplete septa, which delimit rudimentary regeneration nodules. Its etiopathogeny is uncertain and is associated with various diseases such as regenerative nodular hyperplasia, idiopathic portal hypertension, and partial non-cirrhotic nodular transformation, as well as with progression and regression of cirrhosis of any etiology. Few studies are available in the literature describing the clinical and biological characteristics of incomplete septal cirrhosis. GOAL: The objective of the present descriptive study was to study this entity in the city of Salvador, Bahia, Brazil, and to compare the histopathological, biological and clinical data obtained with those reported in the specialized literature. MATERIALS AND METHODS: We reviewed eight cases of incomplete septal cirrhois of varieties etiologies. Hepatitis C, autoimmune hepatitis, alcoholic liver disease and criptogenic liver disease were present in our cases. Fibrosis progression as well as cirrhosis regression could be identified in these patients. CONCLUSIONS: We concluded that Incomplete septal cirrhosis is not a disease itself but it could be considered as a stage of progression and regression of liver fibrosis.

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