Hepatitis E: ¿Un virus infrecuente o un agente infrecuentemente pensado?

Se describen dos casos con diferente presentación clínica de infección por virus de hepatitis E que fueron asistidos en nuestra Unidad de Hepatología y Trasplante Hepático. Uno de los pacientes adquirió la enfermedad sobre un hígado con hepatopatía previa, presentando una evolución más tórpida, mientras que el otro solo desarrolló una hepatitis aguda autolimitada

Group 2 innate lymphoid cells exhibit progressively higher levels of activation during worsening of liver fibrosis

Introduction: The interleukin-33/interleukin-13 pathway is involved in the immunopathology of liver fibrosis and recently characterized group 2 innate lymphoid cells (ILC2) were identified as profibrotic immune cells in the liver of mouse models. Our aim was to elucidate whether ILC2 might be present in human liver tissue and whether ILC2 contribute to liver fibrosis. Materials and methods: To identify ILC2 in liver tissue and blood, we purified mononuclear immune cells from needle biopsies, cirrhotic explant specimen, and paired peripheral blood samples. Cell suspensions were incubated with specific markers for ILC2 and analyzed by flow cytometry. The CD69 marker was included to assess the activation level of ILC2. In addition, we determined the IL-33 plasma level. Results: Results were correlated with the METAVIR fibrotic score of patients enrolled in this study. We detected ILC2 in a higher percentage of CD45+ cells in liver tissue than in paired peripheral blood. The number of ILC2 was significantly increased in fibrotic tissue, but only slightly increased in paired peripheral blood. A higher percentage of CD69+ ILC2 was observed in fibrotic tissue, and this increase correlates positively with aggravation of liver fibrosis measured by fibrotic METAVIR score. A higher level of plasma IL-33 was only detected in samples obtained from cirrhotic patients. Conclusion: Our study indicates that ILC2 are present in the human liver and are activated in tissue contributing to the immunopathology of human liver fibrosis, independently ofthe etiology; which might be a potential new therapeutic target.Fil: Gonzalez Polo, Virginia. Universidad Favaloro; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Medicina Traslacional, Trasplante y Bioingeniería. Fundación Favaloro. Instituto de Medicina Traslacional, Trasplante y Bioingeniería; ArgentinaFil: Pucci Molineris, Melisa Eliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Medicina Traslacional, Trasplante y Bioingeniería. Fundación Favaloro. Instituto de Medicina Traslacional, Trasplante y Bioingeniería; Argentina. Universidad Favaloro; ArgentinaFil: Cervera, Victorio. Universidad Favaloro; ArgentinaFil: Gambaro, Sabrina Eliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Medicina Traslacional, Trasplante y Bioingeniería. Fundación Favaloro. Instituto de Medicina Traslacional, Trasplante y Bioingeniería; Argentina. Universidad Favaloro; ArgentinaFil: Yantorno, Silvina E.. Fundación Favaloro; ArgentinaFil: Descalzi, Valeria. Fundación Favaloro; ArgentinaFil: Tiribelli, Claudio. Italian Liver Foundation; ItaliaFil: Gondolesi, Gabriel Eduardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Medicina Traslacional, Trasplante y Bioingeniería. Fundación Favaloro. Instituto de Medicina Traslacional, Trasplante y Bioingeniería; Argentina. Universidad Favaloro; ArgentinaFil: Meier, Dominik. Universidad Favaloro; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Medicina Traslacional, Trasplante y Bioingeniería. Fundación Favaloro. Instituto de Medicina Traslacional, Trasplante y Bioingeniería; Argentin

Group 2 innate lymphoid cells exhibit progressively higher levels of activation during worsening of liver fibrosis

Introduction: The interleukin-33/interleukin-13 pathway is involved in the immunopathology of liver fibrosis and recently characterized group 2 innate lymphoid cells (ILC2) were identified as profibrotic immune cells in the liver of mouse models. Our aim was to elucidate whether ILC2 might be present in human liver tissue and whether ILC2 contribute to liver fibrosis. Materials and methods: To identify ILC2 in liver tissue and blood, we purified mononuclear immune cells from needle biopsies, cirrhotic explant specimen, and paired peripheral blood samples. Cell suspensions were incubated with specific markers for ILC2 and analyzed by flow cytometry. The CD69 marker was included to assess the activation level of ILC2. In addition, we determined the IL-33 plasma level. Results: Results were correlated with the METAVIR fibrotic score of patients enrolled in this study. We detected ILC2 in a higher percentage of CD45+ cells in liver tissue than in paired peripheral blood. The number of ILC2 was significantly increased in fibrotic tissue, but only slightly increased in paired peripheral blood. A higher percentage of CD69+ ILC2 was observed in fibrotic tissue, and this increase correlates positively with aggravation of liver fibrosis measured by fibrotic METAVIR score. A higher level of plasma IL-33 was only detected in samples obtained from cirrhotic patients. Conclusion: Our study indicates that ILC2 are present in the human liver and are activated in tissue contributing to the immunopathology of human liver fibrosis, independently of the etiology; which might be a potential new therapeutic target.Consejo Nacional de Investigaciones Científicas y TécnicasFacultad de Ciencias Médica

How Common Is Delayed Cyclosporine Absorption Following Liver Transplantation?

The mean time to peak absorption of cyclosporine (CsA) in liver transplant patients is approximately 2 hours, but in some patients the peak occurs later. The goal of this study was, therefore, to investigate the incidence of delayed absorption in 27 de novo liver transplant recipients receiving CsA >10 mg/kg/day (C 2 monitoring) and in 15 maintenance patients. Patients were categorized as 'normal' absorbers (C 2 exceeding C 4 and C 6 ) or 'delayed' absorbers (C 4 or C 6 exceeding C 2 ), and as 'good' (>800 ng/mL at C 0 , C 2 , C 4 , or C 6 ) or 'poor' absorbers (C 0 , C 2 , C 4 and C 6 <800 ng/mL) on the day of study. Among de novo patients, 15 (56%) had 'normal' CsA absorption and 12 (44%) 'delayed' absorption. Good CsA absorption occurred in 16 patients (59%) and poor absorption in 11 (41%). The proportion of poor absorbers was similar in patients with normal (6 / 15, 40%) or delayed (5 / 12, 42%) absorption. Among the 12 delayed absorbers, 11 had peak CsA concentration at C 4 . Mean C 0 level was significantly higher in delayed absorbers (282 ؎ 96 ng/mL) than in normal absorbers (185 ؎ 88ng/mL; P ‫؍‬ .01). Delayed absorbers reverted to normal absorption (C 2 > C 4 ) after a median of 6 days from the day of study, and no cases of delayed absorption were found among maintenance patients. In conclusion, almost 50% of the patients had delayed CsA absorption early posttransplant; around half of these exhibited normal CsA exposure. Measurement of C 4 in addition to C 2 differentiates effectively between delayed and poor absorbers of CsA such that over-or underimmunosuppression can be avoided. (Liver Transpl 2005;11:167-173.