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Introduction: Management of the patient with cirrhosis of the liver that requires surgical treatment has been relatively unexplored. In Mexico, there is currently no formal stance or expert recommendations to guide clinical decision-making in this context. Aims: The present position paper reviews the existing evidence on risks, prognoses, precautions, special care, and specific management or procedures for patients with cirrhosis that require surgical interventions or invasive procedures. Our aim is to provide recommendations by an expert panel, based on the best published evidence, and consequently ensure timely, quality, efficient, and low-risk care for this specific group of patients. Results: Twenty-seven recommendations were developed that address preoperative considerations, intraoperative settings, and postoperative follow-up and care. Conclusions: The assessment and care of patients with cirrhosis that require major surgical or invasive procedures should be overseen by a multidisciplinary team that includes the anesthesiologist, hepatologist, gastroenterologist, and clinical nutritionist. With respect to decompensated patients, a nephrology specialist may be required, given that kidney function is also a parameter involved in the prognosis of these patients. Resumen: Introducción: El terreno del paciente con cirrosis que requiere de una intervención quirúrgica ha sido poco explorado. En México, a la fecha no contamos con un posicionamiento formal o recomendaciones de expertos que ayuden a la toma de decisiones clínicas en este contexto. Objetivos: Revisar la evidencia existente sobre el riesgo, pronóstico, precauciones, cuidados especiales y manejo o proceder específico para los pacientes con cirrosis que requieren ser intervenidos quirúrgicamente o mediante procedimientos invasivos, para emitir recomendaciones por un panel experto, basadas en la mejor evidencia publicada para la atención oportuna, de calidad, eficiente y con el menor riesgo posible en este grupo específico de pacientes. Resultados: Se obtuvieron 27 recomendaciones, en donde se abordan el terreno preoperatorio, el escenario transoperatorio y el seguimiento y cuidados postoperatorios. Conclusiones: La valoración y cuidado del paciente con cirrosis que requiere un procedimiento quirúrgico o invasivo mayor, debe estar a cargo de un equipo multidisciplinario que brinde soporte al cirujano, durante todo el perioperatorio, este equipo debe incluir al anestesiólogo, hepatólogo, gastroenterólogo, nutriólogo clínico. En el paciente descompensado, puede ser necesario involucrar especialistas en nefrología ya que la función renal es un parámetro implicado también en el pronóstico de estos pacientes.

Resumen: Introducción: El terreno del paciente con cirrosis que requiere una intervención quirúrgica ha sido poco explorado. En México, a la fecha no contamos con un posicionamiento formal o recomendaciones de expertos que ayuden a la toma de decisiones clínicas en este contexto. Objetivos: Revisar la evidencia existente sobre el riesgo, pronóstico, precauciones, cuidados especiales y manejo o proceder específico para los pacientes con cirrosis que requieren ser intervenidos quirúrgicamente o mediante procedimientos invasivos, para emitir recomendaciones por un panel experto, basadas en la mejor evidencia publicada para la atención oportuna, de calidad, eficiente y con el menor riesgo posible en este grupo específico de pacientes. Resultados: Se obtuvieron 27 recomendaciones, en donde se abordan el terreno preoperatorio, el escenario transoperatorio y el seguimiento y cuidados postoperatorios. Conclusiones: La valoración y el cuidado del paciente con cirrosis que requiere un procedimiento quirúrgico o invasivo mayor debe estar a cargo de un equipo multidisciplinario que brinde soporte al cirujano durante todo el perioperatorio; este equipo debe incluir al anestesiólogo, al hepatólogo, al gastroenterólogo y al nutriólogo clínico. En el paciente descompensado puede ser necesario involucrar especialistas en nefrología, ya que la función renal es un parámetro implicado también en el pronóstico de estos pacientes. Abstract: Introduction: Management of the patient with cirrhosis of the liver that requires surgical treatment has been relatively unexplored. In Mexico, there is currently no formal stance or expert recommendations to guide clinical decision-making in this context. Aims: The present position paper reviews the existing evidence on risks, prognoses, precautions, special care, and specific management or procedures for patients with cirrhosis that require surgical interventions or invasive procedures. Our aim is to provide recommendations by an expert panel, based on the best published evidence, and consequently ensure timely, quality, efficient, and low-risk care for this specific group of patients. Results: Twenty-seven recommendations were developed that address preoperative considerations, intraoperative settings, and postoperative follow-up and care. Conclusions: The assessment and care of patients with cirrhosis that require major surgical or invasive procedures should be overseen by a multidisciplinary team that includes the anesthesiologist, hepatologist, gastroenterologist, and clinical nutritionist. With respect to decompensated patients, a nephrology specialist may be required, given that kidney function is also a parameter involved in the prognosis of these patients.

Coagulation management in the patient with cirrhosis has undergone a significant transformation since the beginning of this century, with the concept of a rebalancing between procoagulant and anticoagulant factors. The paradigm that patients with cirrhosis have a greater bleeding tendency has changed, as a result of this rebalancing. In addition, it has brought to light the presence of complications related to thrombotic events in this group of patients.These guidelines detail aspects related to pathophysiologic mechanisms that intervene in the maintenance of hemostasis in the patient with cirrhosis, the relevance of portal hypertension, mechanical factors for the development of bleeding, modifications in the hepatic synthesis of coagulation factors, and the changes in the reticuloendothelial system in acute hepatic decompensation and acute-on-chronic liver failure. They address new aspects related to the hemorrhagic complications in patients with cirrhosis, considering the risk for bleeding during diagnostic or therapeutic procedures, as well as the usefulness of different tools for diagnosing coagulation and recommendations on the pharmacologic treatment and blood-product transfusion in the context of hemorrhage. These guidelines also update the knowledge regarding hypercoagulability in the patient with cirrhosis, as well as the efficacy and safety of treatment with the different anticoagulation regimens. Lastly, they provide recommendations on coagulation management in the context of acute-on-chronic liver failure, acute liver decompensation, and specific aspects related to the patient undergoing liver transplantation. Resumen: El manejo de la coagulación en el paciente con cirrosis ha sufrido una transformación significativa a partir de principios de este siglo, con el concepto de un rebalanceo entre factores procoagulantes y anticoagulantes. Esto ha cambiado el paradigma de que los pacientes con cirrosis tienen una mayor tendencia a la hemorragia, ya que existe un rebalanceo entre factores procoagulantes y anticoagulantes. Además, ha traído a la luz la presencia de complicaciones relacionadas a eventos trombóticos en este grupo de pacientes.En estas guías se detallan aspectos relacionados con los mecanismos fisiopatológicos que intervienen en el mantenimiento de la hemostasia en el paciente con cirrosis, la relevancia de la hipertensión portal, factores mecánicos para el desarrollo de sangrado, modificaciones en la síntesis hepática de factores de coagulación, y los cambios en el sistema reticuloendotelial en la descompensación hepática aguda e insuficiencia hepática aguda sobre crónica (IHAC). Se abordan nuevos aspectos relacionados a las complicaciones hemorrágicas en pacientes con cirrosis, considerando el riesgo de hemorragia durante procedimientos diagnósticos o terapéuticos, así como la utilidad de diferentes herramientas diagnósticas de la coagulación y recomendaciones en el tratamiento farmacológico y transfusión de hemoderivados en el contexto de hemorragia. En estas guías se actualiza el conocimiento respecto al diagnóstico y abordaje de complicaciones relacionadas a hipercoagulabilidad en el paciente con cirrosis, así como la eficacia y seguridad del tratamiento con diferentes esquemas de anticoagulación. Finalmente, se mencionarán recomendaciones en el manejo de la coagulación en el contexto de IHAC, descompensación hepática aguda y aspectos específicos relacionados al paciente en protocolo de trasplante hepático.

Resumen: El manejo de la coagulación en el paciente con cirrosis ha sufrido una transformación significativa a partir de principios de este siglo con el concepto de un rebalanceo entre los factores procoagulantes y anticoagulantes. Esto ha cambiado el paradigma de que las personas con esta enfermedad tienen una mayor tendencia a la hemorragia. Además, ha traído a la luz la presencia de complicaciones relacionadas a eventos trombóticos en este grupo de sujetos.En estas guías se detallan aspectos asociados con los mecanismos fisiopatológicos que intervienen en el mantenimiento de la hemostasia en el paciente con cirrosis, la relevancia de la hipertensión portal, los factores mecánicos para el desarrollo de sangrado, las modificaciones en la síntesis hepática de los factores de coagulación, y los cambios en el sistema reticuloendotelial en la descompensación hepática aguda e insuficiencia hepática aguda sobre crónica (IHAC). Se abordan nuevos aspectos vinculados a las complicaciones hemorrágicas en sujetos con esta entidad, considerando el riesgo de hemorragia durante los procedimientos diagnósticos o terapéuticos, así como la utilidad de diferentes herramientas diagnósticas de la coagulación y recomendaciones en el tratamiento farmacológico y transfusión de hemoderivados en el contexto de hemorragia. En estas guías se actualiza el conocimiento respecto al diagnóstico y abordaje de las complicaciones relacionadas con la hipercoagulabilidad en estos casos, así como la eficacia y seguridad de la terapia con diferentes esquemas de anticoagulación. Finalmente, se mencionarán recomendaciones en el manejo de la coagulación en el contexto de IHAC, descompensación hepática aguda y aspectos específicos relacionados al paciente en protocolo de trasplante hepático (TH). Abstract: Coagulation management in the patient with cirrhosis has undergone a significant transformation since the beginning of this century, with the concept of a rebalancing between procoagulant and anticoagulant factors. The paradigm that patients with cirrhosis have a greater bleeding tendency has changed, as a result of this rebalancing. In addition, it has brought to light the presence of complications related to thrombotic events in this group of patients.These guidelines detail aspects related to pathophysiologic mechanisms that intervene in the maintenance of hemostasis in the patient with cirrhosis, the relevance of portal hypertension, mechanical factors for the development of bleeding, modifications in the hepatic synthesis of coagulation factors, and the changes in the reticuloendothelial system in acute hepatic decompensation and acute-on-chronic liver failure. They address new aspects related to the hemorrhagic complications in patients with cirrhosis, considering the risk for bleeding during diagnostic or therapeutic procedures, as well as the usefulness of different tools for diagnosing coagulation and recommendations on the pharmacologic treatment and blood-product transfusion in the context of hemorrhage. These guidelines also update the knowledge regarding hypercoagulability in the patient with cirrhosis, as well as the efficacy and safety of treatment with the different anticoagulation regimens. Lastly, they provide recommendations on coagulation management in the context of acute-on-chronic liver failure, acute liver decompensation, and specific aspects related to the patient undergoing liver transplantation.

Alcoholic liver disease (ALD) is a clinical-pathologic entity caused by the chronic excessive consumption of alcohol. The disease includes a broad spectrum of anomalies at the cellular and tissual level that can cause acute-on-chronic (alcoholic hepatitis) or chronic (fibrosis, cirrhosis, hepatocellular cancer) injury, having a great impact on morbidity and mortality worldwide. Alcohol is metabolized mainly in the liver. During alcohol metabolism, toxic metabolites, such as acetaldehyde and oxygen reactive species, are produced. At the intestinal level, alcohol consumption can cause dysbiosis and alter intestinal permeability, promoting the translocation of bacterial products and causing the production of inflammatory cytokines in the liver, perpetuating local inflammation during the progression of ALD. Different study groups have reported systemic inflammatory response disturbances, but reports containing a compendium of the cytokines and cells involved in the pathophysiology of the disease, from the early stages, are difficult to find. In the present review article, the role of the inflammatory mediators involved in ALD progression are described, from risky patterns of alcohol consumption to advanced stages of the disease, with the aim of understanding the involvement of immune dysregulation in the pathophysiology of ALD. Resumen: La enfermedad hepática alcohólica (EHA) es una entidad clínico-patológica, ocasionada por el consumo excesivo y crónico de alcohol. La enfermedad incluye un amplio espectro de anomalías a nivel celular y tisular que pueden causar daño agudo sobre crónico (hepatitis alcohólica) o crónico (fibrosis, cirrosis, cáncer hepatocelular), teniendo un gran impacto en la morbilidad y mortalidad a nivel mundial. El alcohol es metabolizado principalmente en el hígado. Durante el metabolismo del alcohol son generados metabolitos tóxicos como el acetaldehído y las especies reactivas de oxígeno. A nivel intestinal, el consumo de alcohol puede producir disbiosis y alteración de la permeabilidad intestinal, promoviendo la translocación de productos bacterianos, y provocando la producción de citocinas proinflamatorias en el hígado, lo cual perpetua la inflamación local durante la evolución de la EHA. Diferentes grupos de estudio han reportado alteraciones de la respuesta inflamatoria a nivel sistémico, sin embargo, es difícil encontrar reportes que contengan un compendio de las células y citocinas involucradas en la fisiopatología de la enfermedad desde sus etapas tempranas. En este trabajo de revisión se describe el papel de los mediadores inflamatorios involucrados en la progresión de la EHA, desde los patrones de consumo de riesgo hasta etapas avanzadas de la enfermedad, con la finalidad de comprender la implicación de la desregulación inmunológica en la fisiopatología de esta enfermedad.

The first clinical guidelines on hepatic encephalopathy were published in 2009. Almost 14 years since that first publication, numerous advances in the field of diagnosis, treatment, and special condition care have been made. Therefore, as an initiative of the Asociación Mexicana de Gastroenterología A.C., we present a current view of those aspects. The manuscript described herein was formulated by 24 experts that participated in six working groups, analyzing, discussing, and summarizing the following topics: Definition of hepatic encephalopathy; recommended classifications; epidemiologic panorama, worldwide and in Mexico; diagnostic tools; conditions that merit a differential diagnosis; treatment; and primary and secondary prophylaxis. Likewise, these guidelines emphasize the management of certain special conditions, such as hepatic encephalopathy in acute liver failure and acute-on-chronic liver failure, as well as specific care in patients with hepatic encephalopathy, such as the use of medications and types of sedation, describing those that are permitted or recommended, and those that are not. Resumen: La primera guía clínica sobre encefalopatía hepática se publicó en el año 2009, a casi catorce años de esta primera publicación, numerosos avances en el campo del diagnóstico, tratamiento y cuidados en condiciones especiales, han ocurrido; por ello, a iniciativa de la Asociación Mexicana de Gastroenterología A.C presentamos este manuscrito elaborado por 24 expertos que han trabajado en seis mesas de trabajo analizando, discutiendo y resumiendo los siguientes tópicos: Definición de encefalopatía hepática, clasificaciones que se recomiendan utilizar, panorama epidemiológico mundial y en México, herramientas para el diagnóstico, condiciones que ameritan hacer un diagnóstico diferencial, tratamiento y profilaxis primaria y secundaria. Así mismo, esta guía hace énfasis en el manejo de ciertas condiciones especiales como encefalopatía hepática en insuficiencia hepática aguda y en falla hepática aguda sobre crónica y cuidados específicos en pacientes con encefalopatía hepática como medicamentos que se deben evitar, por ejemplo, uso de analgésicos permitidos y no permitidos, y en caso de sedación para procedimientos cuales se permiten o sugieren y cuáles no.

Resumen: La primera guía clínica sobre la encefalopatía hepática se publicó en el año 2009, a casi 14 años de esta primera publicación, numerosos avances en el campo del diagnóstico, tratamiento y cuidados en condiciones especiales, han ocurrido; por ello, a iniciativa de la Asociación Mexicana de Gastroenterología AC presentamos este manuscrito elaborado por 24 expertos que han trabajado en 6 mesas de trabajo analizando, discutiendo y resumiendo los siguientes tópicos: Definición de encefalopatía hepática, clasificaciones que se recomiendan utilizar, panorama epidemiológico mundial y en México, herramientas para el diagnóstico, condiciones que ameritan hacer un diagnóstico diferencial, tratamiento y profilaxis primaria y secundaria. Así mismo, esta guía hace énfasis en el manejo de ciertas condiciones especiales como encefalopatía hepática en insuficiencia hepática aguda y en falla hepática aguda sobre crónica y cuidados específicos en pacientes con encefalopatía hepática como medicamentos que se deben evitar, por ejemplo, uso de analgésicos permitidos y no permitidos, y en caso de sedación para procedimientos cuales se permiten o sugieren y cuáles no. Abstract: The first clinical guidelines on hepatic encephalopathy were published in 2009. Almost 14 years since that first publication, numerous advances in the field of diagnosis, treatment, and special condition care have been made. Therefore, as an initiative of the Asociación Mexicana de Gastroenterología A.C., we present a current view of those aspects. The manuscript described herein was formulated by 24 experts that participated in six working groups, analyzing, discussing, and summarizing the following topics: Definition of hepatic encephalopathy; recommended classifications; epidemiologic panorama, worldwide and in Mexico; diagnostic tools; conditions that merit a differential diagnosis; treatment; and primary and secondary prophylaxis. Likewise, these guidelines emphasize the management of certain special conditions, such as hepatic encephalopathy in acute liver failure and acute-on-chronic liver failure, as well as specific care in patients with hepatic encephalopathy, such as the use of medications and types of sedation, describing those that are permitted or recommended, and those that are not.

Resumen: La enfermedad hepática alcohólica (EHA) es una entidad clinicopatológica ocasionada por el consumo excesivo y crónico de alcohol. La enfermedad incluye un amplio espectro de anomalías celulares y tisulares que pueden causar daño agudo sobre crónico (hepatitis alcohólica) o crónico (fibrosis, cirrosis, cáncer hepatocelular), teniendo un gran impacto en la morbimortalidad en todo el mundo. El alcohol es metabolizado principalmente en el hígado. Durante el metabolismo del alcohol son generados metabolitos tóxicos como el acetaldehído y las especies reactivas de oxígeno. En el intestino el consumo de alcohol puede producir disbiosis y alteración de la permeabilidad intestinal, promoviendo la translocación de productos bacterianos y provocando la producción de citocinas proinflamatorias en el hígado, lo cual perpetúa la inflamación local durante la evolución de la EHA. Diferentes grupos de estudio han reportado alteraciones de la respuesta inflamatoria a nivel sistémico, sin embargo es difícil encontrar reportes que contengan un compendio de las células y citocinas involucradas en la fisiopatología de la enfermedad desde sus etapas tempranas. En este trabajo de revisión se describe el papel de los mediadores inflamatorios involucrados en la progresión de la EHA, desde los patrones de consumo de riesgo hasta etapas avanzadas de la enfermedad, con la finalidad de comprender la implicación de la desregulación inmunológica en la fisiopatología de esta enfermedad. Abstract: Alcoholic liver disease (ALD) is a clinical-pathologic entity caused by the chronic excessive consumption of alcohol. The disease includes a broad spectrum of anomalies at the cellular and tissual level that can cause acute-on-chronic (alcoholic hepatitis) or chronic (fibrosis, cirrhosis, hepatocellular cancer) injury, having a great impact on morbidity and mortality worldwide. Alcohol is metabolized mainly in the liver. During alcohol metabolism, toxic metabolites, such as acetaldehyde and oxygen reactive species, are produced. At the intestinal level, alcohol consumption can cause dysbiosis and alter intestinal permeability, promoting the translocation of bacterial products and causing the production of inflammatory cytokines in the liver, perpetuating local inflammation during the progression of ALD. Different study groups have reported systemic inflammatory response disturbances, but reports containing a compendium of the cytokines and cells involved in the pathophysiology of the disease, from the early stages, are difficult to find. In the present review article, the role of the inflammatory mediators involved in ALD progression are described, from risky patterns of alcohol consumption to advanced stages of the disease, with the aim of understanding the involvement of immune dysregulation in the pathophysiology of ALD.

Resumen: Introducción: La combinación de sofosbuvir-velpatasvir (SOF/VEL) es una terapia antiviral de acción directa que está autorizada y disponible en México. Esto hace que la evaluación de la respuesta virológica sostenida (RVS) 12 semanas después del tratamiento, por medio de la realización de una revisión multicentro en el mundo real, sea una tarea relevante. Métodos: Se efectuó una revisión retrospectiva de los registros de 241 casos de pacientes atendidos en 20 hospitales en México para evaluar el tratamiento contra la hepatitis C con la combinación SOF/VEL (n = 231) y sofosbuvir/velpatasvir/ribavirin (SOF/VEL/RBV) (n = 10). El objetivo de eficacia primario fue el porcentaje de pacientes que lograron la RVS 12 semanas posterior a la finalización del tratamiento. Resultados: En general, la RVS fue de 98.8% (IC 95% 97.35 a 100%). Solo tres pacientes no lograron la RVS, de los cuales dos padecían cirrosis y una tenía historia previa de tratamiento con interferón pegilado (peg-IFN). De los subgrupos analizados, todos los casos con infección de virus de la inmunodeficiencia humana (VIH), tres con genotipo 3 y aquellos tratados con la combinación SOF/VEL/RBV, lograron RVS. Los subgrupos con tasas menores de éxito fueron los pacientes que tenían experiencia con tratamiento (96.8%) y pacientes con fibrosis F1 (95.5%). Los eventos adversos más frecuentes fueron fatiga, cefalea e insomnio. No se reportaron eventos adversos graves. Conclusión: Los tratamientos con SOF/VEL y SOF/VEL/RBV fueron altamente seguros y efectivos y los resultados coinciden con los de otros estudios internacionales realizados en el mundo real. Abstract: Introduction: The sofosbuvir-velpatasvir (SOF/VEL) combination is a direct-acting antiviral therapy that is authorized and available in Mexico, making the performance of a real-world multicenter study that evaluates the sustained virologic response at 12 weeks post-treatment a relevant undertaking. Methods: A retrospective review of the case records of 241 patients seen at 20 hospitals in Mexico was conducted to assess hepatitis C treatment with the SOF/VEL combination (n = 231) and the sofosbuvir/velpatasvir/ribavirin (SOF/VEL/RBV) combination (n = 10). The primary efficacy endpoint was the percentage of patients that achieved SVR at 12 weeks after the end of treatment. Results: Overall SVR was 98.8% (95% CI 97.35-100%). Only three patients did not achieve SVR, two of whom had cirrhosis and a history of previous treatment with peg-IFN. Of the subgroups analyzed, all the patients with HIV coinfection, three patients with genotype 3, and the patients treated with the SOF/VEL/RBV combination achieved SVR. The subgroups with the lower success rates were patients that were treatment-experienced (96.8%) and patients with F1 fibrosis (95.5%). The most frequent adverse events were fatigue, headache, and insomnia. No serious adverse events were reported. Conclusion: Treatments with SOF/VEL and SOF/VEL/RBV were highly safe and effective, results coinciding with those of other international real-world studies.

Resumen: El término colestasis se refiere a la retención de ácidos biliares ya sea dentro del hepatocito o en los ductos biliares de cualquier calibre. Por laboratorio, se define por la elevación de fosfatasa alcalina arriba de 1.67 veces su valor normal. Las enfermedades colestásicas pueden asociarse a un proceso inflamatorio de la glándula hepática que provoca destrucción de los hepatocitos (hepatitis), a ictericia (coloración amarillenta de piel y mucosas asociada a elevación en niveles séricos de bilirrubinas) o ambas, aunque estos tres conceptos no deben considerarse sinónimos. Los padecimientos colestásicos pueden clasificarse como intra o extrahepáticos dependiendo de su etiología, y esto es importante para elegir los estudios diagnósticos adecuados y la terapéutica indicada en cada uno de los casos. Una historia clínica completa, aunada a exploración física exhaustiva y estudios iniciales básicos como el ultrasonido hepático y las pruebas de funcionamiento del hígado, pueden ayudar al clínico a decidir el camino a seguir al enfrentarse al paciente con colestasis. La Asociación Mexicana de Hepatología, la Asociación Mexicana de Gastroenterología y la Asociación Mexicana de Endoscopia Gastrointestinal decidieron trabajar en el primer posicionamiento científico mexicano sobre este tema. Abstract: The term cholestasis refers to bile acid retention, whether within the hepatocyte or in the bile ducts of any caliber. Biochemically, it is defined by a level of alkaline phosphatase that is 1.67-times higher than the upper limit of normal. Cholestatic diseases can be associated with an inflammatory process of the liver that destroys hepatocytes (hepatitis), with jaundice (yellowing of the skin and mucus membranes, associated with elevated serum bilirubin levels), or with both, albeit the three concepts should not be considered synonymous. Cholestatic diseases can be classified as intrahepatic or extrahepatic, depending on their etiology. Knowing the cause of the condition is important for choosing the adequate diagnostic studies and appropriate treatment in each case. A complete medical history, together with a thorough physical examination and basic initial studies, such as liver ultrasound and liver function tests, aid the clinician in deciding which path to follow, when managing the patient with cholestasis. In a joint effort, the Asociación Mexicana de Hepatología (AMH), the Asociación Mexicana de Gastroenterología (AMG) and the Asociación Mexicana de Endoscopia Gastrointestinal (AMEG) developed the first Mexican scientific position statement on said theme.

Introduction: The sofosbuvir-velpatasvir (SOF/VEL) combination is a direct-acting antiviral therapy that is authorized and available in Mexico, making the performance of a real-world multicenter study that evaluates the sustained virologic response at 12 weeks post-treatment a relevant undertaking. Methods: A retrospective review of the case records of 241 patients seen at 20 hospitals in Mexico was conducted to assess hepatitis C treatment with the SOF/VEL combination (n = 231) and the sofosbuvir/velpatasvir/ribavirin (SOF/VEL/RBV) combination (n = 10). The primary efficacy endpoint was the percentage of patients that achieved SVR at 12 weeks after the end of treatment. Results: Overall SVR was 98.8% (95% CI 97.35–100%). Only three patients did not achieve SVR, two of whom had cirrhosis and a history of previous treatment with peg-IFN. Of the subgroups analyzed, all the patients with HIV coinfection, three patients with genotype 3, and the patients treated with the SOF/VEL/RBV combination achieved SVR. The subgroups with the lower success rates were patients that were treatment-experienced (96.8%) and patients with F1 fibrosis (95.5%). The most frequent adverse events were fatigue, headache, and insomnia. No serious adverse events were reported. Conclusion: Treatments with SOF/VEL and SOF/VEL/RBV were highly safe and effective, results coinciding with those of other international real-world studies. Resumen: Introducción: La combinación de sofosbuvir-velpatasvir (SOF/VEL) es una terapia antiviral de acción directa que está autorizada y disponible en México. Esto hace que la evaluación de la respuesta virológica sostenida (RVS) 12 semanas después del tratamiento, por medio de la realización de una revisión multicentro en el mundo real, sea una tarea relevante. Métodos: Se efectuó una revisión retrospectiva de los registros de 241 casos de pacientes atendidos en 20 hospitales en México para evaluar el tratamiento contra la hepatitis C con la combinación SOF/VEL (n = 231) y sofosbuvir/velpatasvir/ribavirin (SOF/VEL/RBV) (n = 10). El objetivo de eficacia primario fue el porcentaje de pacientes que lograron la RVS 12 semanas posterior a la finalización del tratamiento. Resultados: En general, la RVS fue de 98.8% (IC 95% 97.35 a 100%). Solo tres pacientes no lograron la RVS, de los cuales dos padecían cirrosis y una tenía historia previa de tratamiento con interferón pegilado (peg-IFN). De los subgrupos analizados, todos los casos con infección de virus de la inmunodeficiencia humana (VIH), tres con genotipo 3 y aquellos tratados con la combinación SOF/VEL/RBV, lograron RVS. Los subgrupos con tasas menores de éxito fueron los pacientes que tenían experiencia con tratamiento (96.8%) y pacientes con fibrosis F1 (95.5%). Los eventos adversos más frecuentes fueron fatiga, cefalea e insomnio. No se reportaron eventos adversos graves. Conclusión: Los tratamientos con SOF/VEL y SOF/VEL/RBV fueron altamente seguros y efectivos y los resultados coinciden con los de otros estudios internacionales realizados en el mundo real.

The term cholestasis refers to bile acid retention, whether within the hepatocyte or in the bile ducts of any caliber. Biochemically, it is defined by a level of alkaline phosphatase that is 1.67-times higher than the upper limit of normal. Cholestatic diseases can be associated with an inflammatory process of the liver that destroys hepatocytes (hepatitis), withjaundice (yellowing of the skin and mucus membranes, associated with elevated serum bilirubin levels), or with both, albeit the three concepts should not be considered synonymous. Cholestatic diseases can be classified as intrahepatic or extrahepatic, depending on their etiology. Knowing the cause of the condition is important for choosing the adequate diagnostic studies and appropriate treatment in each case. A complete medical history, together with a thorough physical examination and basic initial studies, such as liver ultrasound and liver function tests, aid the clinician in deciding which path to follow, when managing the patient with cholestasis. In a joint effort, the Asociación Mexicana de Hepatología (AMH), the Asociación Mexicana de Gastroenterología (AMG) and the Asociación Mexicana de Endoscopia Gastrointestinal (AMEG) developed the first Mexican scientific position statement on said theme. Resumen: El término colestasis se refiere a la retención de ácidos biliares ya sea dentro del hepatocito o en los ductos biliares de cualquier calibre. Por laboratorio, se define por la elevación de fosfatasa alcalina arriba de 1.67 veces su valor normal. Las enfermedades colestásicas pueden asociarse a un proceso inflamatorio de la glándula hepática que provoca destrucción de los hepatocitos (hepatitis), a ictericia (coloración amarillenta de piel y mucosas asociada a elevación en niveles séricos de bilirrubinas) o ambas, aunque estos tres conceptos no deben considerarse sinónimos. Los padecimientos colestásicos pueden clasificarse como intra o extrahepáticos dependiendo de su etiología, y esto es importante para elegir los estudios diagnósticos adecuados y la terapéutica indicada en cada uno de los casos. Una historia clínica completa, aunada a exploración física exhaustiva y estudios iniciales básicos como el ultrasonido hepático y las pruebas de funcionamiento del hígado pueden ayudar al clínico a decidir el camino a seguir al enfrentarse al paciente con colestasis. La Asociación Mexicana de Hepatología, la Asociación Mexicana de Gastroenterología y la Asociación Mexicana de Endoscopia Gastrointestinal decidieron trabajar en el primer posicionamiento científico mexicano sobre este tema.

Introduction and Objectives: IL-1β is a proinflammatory key cytokine that participates in the progression of liver disease. Its antagonist IL-1RA mediates damage limitation; its increase is associated with positive effects on chronic liver diseases. This study aimed to evaluate the concentration of IL-1β and IL-1RA in subjects with alcoholic liver disease (ALD), chronic hepatitis C (CHC) and non-alcoholic fatty liver disease (NAFLD). Materials and Methods: A cross-sectional and multicenter study was carried out, which included alcoholic subjects (OH), alcoholic cirrhosis (CiOH) and alcoholic hepatitis (HA); patients with CHC and NAFLD were compared against subjects without criteria for alcohol drinking habits (CT). IL-1β and IL-1RA were quantified by Multiplex-MERCK©. For statistical analysis, SPSS V.22 were used, Mann-Whitney U, p

Introduction and Objectives: We recently published that in the serum of patients with chronic Hepatitis C, there are high concentrations of inactive Matrix Metalloproteinases (MMP). However, the MMP has not been studied in other liver diseases. This study aimed to evaluate serum concentrations of MMP-7 in different hepatic etiologies and according to fibrosis stage. Materials and Methods: A cross-sectional and multicenter study was carried out, including subjects with alcoholism (WHO criteria), without (OH) and with liver injury (cirrhosis, CiOH); diagnosed by clinical, biochemical data, non-alcoholic fatty liver (NAFLD) and chronic Hepatitis C (CHC). Transitional elastography (Fibroscan) was performed in NAFLD and CHC, considering mild fibrosis (MF: F0, F1, F2) and advanced fibrosis (AF: F3, F4). As controls, subjects without alcohol consumption (CT) were recruited. For the quantification of MMP-7, Multiplex-MERCK© was used. Statistical analysis was performed using SPSS V.22 using Mann Whitney U, p

Introduction and Objectives: Malnutrition is a frequent complication in patients with cirrhosis, associated with greater disease progression, complication rate, and mortality. Sarcopenia is one of the main indicators of malnutrition, characterized by a general decrease in muscle mass and functional deterioration. CT determination of muscle mass is not easily accessible in routine clinical practice, so practical measurement tools are essential. It has been proposed to classify sarcopenia as severe when decreased muscle strength, muscle mass, and low physical performance coexist. The impact of severe sarcopenia on the risk of developing hepatic encephalopathy is currently unknown. Primary outcome: Determine if there is a significant correlation between the degree of sarcopenia and hepatic encephalopathy. Secondary outcomes: to determine the prevalence of sarcopenia in patients with cirrhosis, the association between sarcopenia and liver decompensation events, to determine the correlation between individual tests (battery of functional physical performance tests [SPPB], grip strength, and skeletal muscle mass) with hepatic encephalopathy. Materials and methods: Prospective, cross-sectional, observational, descriptive, and analytical study in patients with liver cirrhosis evaluated by outpatient consultation, with diagnosis confirmed by transitional elastography (Fibroscan® 502 ECHOSENS® equipment). The presence of sarcopenia was determined by measurement of grip strength with a hand-held hydraulic dynamometer (JAMAR® B001D7QDJG) and determination of muscle mass by tetrapolar electrical bioimpedance (OMRON® HBF 500). A positive case was considered when coexisting force ≤27 kg / ≤16 kg and skeletal muscle mass ≤20 kg / ≤15kg in men and women respectively, classifying it as severe sarcopenia with a score of ≤8 pts in SPPB. The presence of hepatic encephalopathy was determined by clinical evaluation and critical flicker rate (cut-off

Introduction and Objectives: Non alcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease (ALD) are the most common emergent causes of chronic liver disease; they evolve from simple steatosis, steatohepatitis, fibrosis/cirrhosis and hepatocellular carcinoma. Knowing the factors that influence their development and screening can improve the prognosis of these patients. Objective: To determine the prevalence of incidental findings of fatty liver in necropsies performed for all causes of mortality and to analyze the main characteristics of these patients. Materials and Methods: Type and design of the study: Observational, descriptive, transversal study. Procedure: All necropsy records for all causes of mortality registered at the Pathology Department in our center in the last 10 years were reviewed (January 2010 – December 2019). We search the following findings: “liver steatosis,” “steatohepatitis,” degree of fibrosis/cirrhosis, “atherosclerosis,” “heavy alcohol intake,” “diabetes, obesity, dyslipidemia, metabolic syndrome.” We used descriptive and analytical statistics: X2, exact Fisher´s test, univariate and multivariate logistic regression models. Results: 4557 necropsies were registered. Fatty liver was found in 6.4% of the cases. 53.3% were women; 51±15 years old; There was simple steatosis in 156 cases (53.6%) and steatohepatitis with necroinflammatory activity in 135 (46.4%). A 49.8% presented liver fibrosis (F1=38 [13.1%]; F2=48 [16.5%]; F3=15 [5.2%]; F4=44 [15.1%]). The etiology through clinical history and histological findings compatible with alcoholic liver injury occurred in 67 cases (23%), NAFLD in 98 (33.7%), mixed type (NAFLD+ALD) in 19 (6.5%), the etiology could not be identified in 107 (36.8%). The multivariate analysis showed alcohol intake as the main risk factor for necroinflammation (OR=2.58; ICal95%= 1.52-4.38; p

Introduction and Objectives: Liver cirrhosis is a highly prevalent worldwide disease and in the last decade, there has been an increase of 13%. Patients with advanced liver disease are at higher risk of developing life-threatening decompensations; one of these main complications is the presence of upper gastrointestinal bleeding, representing a frequent cause of hospital admission and mortality. Broad knowledge of these complications is essential to improve the diagnostic and therapeutic approach in these patients. Objectives: To compare the different complications related to upper gastrointestinal bleeding of variceal vs. non-variceal origin and the characteristics of these patients. Methods: Case-control study conducted in a cohort. The cohort was made up of cirrhotic patients due to any etiology who were admitted for hospitalization at our unit in a period from January 2017 to May 2021; two groups were extracted, those with variceal bleeding formed the cases group and, those with non-variceal hemorrhage the control group and a comparison between groups was made using X2 or Fisher's exact test or Student's test accordingly to the type and distribution of each variable, considering significant a value of p

Introduction and Objectives: Refractory ascites is an infrequent complication in patients with cirrhosis; it is considered in those who do not respond to diuretics or who have adverse effects with diuretics. Treatment is large-volume paracentesis, followed by plasma volume expansion to prevent paracentesis-induced circulatory dysfunction (PICD) to avoid deterioration in renal function and hyponatremia. Intermittent paracentesis could increase morbidity and mortality in these patients. Perhaps the classic prognostic scales, such as MELD, undervalue this factor that is not usually considered for prioritizing transplantation. The objective of this study is to assess the survival of patients with cirrhosis with refractory ascites. Material and methods: Observational, retrospective, descriptive and analytical study. Patients with cirrhosis and refractory ascites were included, who were subjected to intermittent paracentesis on several occasions from February 2019 to June 2021. Descriptive statistics were performed with central tendency and dispersion measures, baseline and final MELD were calculated, and mortality was evaluated. Results: Eleven patients were included, six men (54.5%) and five women (45.5%), aged 54 ± eight years. The patients had a range of paracentesis performed from 3 to 30 occasions (median five interventions), with a follow-up of 1 to 40 months (median of 8 months). The etiology of cirrhosis was alcoholic 63.6%, MALFD 9.1%, and 27.3% other causes. The total amount of fluid drained per patient was 37 to 439 L, 90% of the patients classified as Child-Pugh grade C, and 10% B. The median of the initial MELD was 15 (range = 13), and the median of the final MELD was 22 (range=17). There was no significant difference according to the Wilcoxon test p = 0.317. The renal function between the first and the last paracentesis decreased mildly by 24% and from 36% to 45% severely. Overall mortality was six patients (54.5%). The causes of death were spontaneous bacterial peritonitis (SBP) 9%, ACLF (Acute on Cronic Liver Failure) 27%, infarction 9%, and sepsis 9%. Median survival was 18 months (range 13-23) Discussion: Patients with refractory ascites have very high mortality (59%); Despite the amount of fluid drained, up to 439L in one patient (for example), it did not seriously affect kidney function overall. We found no statistically significant difference between the initial and final MELD values (Figure 1). However, the MELD score does not make them candidates for liver transplantation; therefore, refractory ascites should be considered with an additional score to enter them on the transplant list. Conclusions: Refractory ascites is uncommon, but it has high mortality; the MELD scale may not accurately predict the possibility of death, so they should be entered with an additional score to consider them candidates for liver transplantation.The authors declare that there is no conflict of interest

Introduction and Objectives: If direct antiviral agents (DAA) are related to the development of HCC is controversial; therefore, exploring risk factors are crucial. We aimed to determine factors related to the development of hepatocellular carcinoma (HCC) in patients with hepatitis c (HCV) and decompensated cirrhosis (DC) treated with DAA. Materials and Methods: A multicenter real-world cohort study including patients with HCV + DC treated with sofosbuvir (SOF) based on regimens free of inhibitors of protease (IPs). Results: 222 patients, 118 (53.2%) were women, mean age 57.2 ±11.5-year-old, 209 (94.1%) achieved sustained virological response (SVR). According to Child-Pugh 44(19.8%) were A with history of any clinical decompensation event, 147(66.2%) B, and 31 (14%) C. After DAA, 134 (60.4%) improve in MELD, 45 (20.3%) had no change, and 43 (19.4%) worse, this worse in MELD was related to non-SVR [SVR 37/209 (17.7%) vs. non-SVR 6/13 (46.2%); OR=2.6, 95%CI:1.4-5.0, p=0.02]. Nineteen (8.6%) developed HCC during the follow-up after therapy with DAA; however, when we compared basal laboratory values between those who developed HCC and those who did not only alfa-fetoprotein (AFP) levels were different (without HCC 14.3 [mean 95%CI: 10.6-18.1] ng/mL vs. HCC 55.7 [mean 95%CI: 28.4-83.0] ng/mL; p 20ng/mL, it is essential to note that patients in this cohort had no any suspicious lesion in ultrasonography (USG) previous to start DAA therapy in their semestral screening as most of the guidelines recommend. AASLD, for example, recommends semestral HCC screening with USG with or without AFP, giving more weight to the imagen study. However, based on our results, we recommend always determining AFP levels as a compliment to USG. Conclusions: In HCV patients with DC treated with DAA and with a negative basal screening USG for suspicious malignant lesions, basal AFP > 20ng/mL are the most critical factor related to the development of HCC and should be determined complementary to the USG study.The authors declare that there is no conflict of interest.

Introduction and Objectives: Upper gastrointestinal bleeding is a common complication among cirrhotic patients and holds high mortality and morbidity; the most common cause is variceal hemorrhage. Nonetheless, non-variceal hemorrhage is also frequent; this study aims to determine the prevalence of upper gastrointestinal bleeding complications among Mexican patients with cirrhosis. Methods: Retrospective, cross-sectional, an analytic study among patients with cirrhosis of all etiologies admitted to the Gastroenterology department of the Hospital General de Mexico “Dr. Eduardo Liceaga” with acute upper gastrointestinal bleeding of both etiologies (variceal and non-variceal hemorrhage) in the period comprised from January 2017 to May 2021. Complications associated with the bleeding events were evaluated. For statistical analysis, quantitative variables were described as mean and standard deviation for qualitative variables in frequencies and percentages. Results: A total of 295 patients were included, 55.3% male, mean age was 54.6 ± 11.8 years, 16.27% patients were staged as Child A, 49.15% Child B y 34.57% Child C, with and an average MELD score of 16. Main cirrhosis etiology was alcohol-related liver disease in 39.7%, viral hepatitis 6.4%, NASH 5.8% and others 3.4%; however, in 44.7% of patients, we were not able to determine the etiology of liver disease. The main cause of gastrointestinal bleeding was variceal hemorrhage in 71.1% and 28.9% non-variceal. The shock was identified in 5.76% (17) of patients, 9 of them required vasopressors, hepatic encephalopathy was present in 42.71% (126), Ascites in 18.64% (55), jaundice in 16.94% (50), acute kidney injury in 31.52% (93), bacterial infections in 24.06% (71), four patients (1.35%) died. Complications related to gastrointestinal bleed according to disease severity are depicted in table 1. Discussion and Conclusions: Complications associated with upper gastrointestinal bleeding among Mexican patients with cirrhosis are frequent. Encephalopathy is the most common (42.71%) followed by acute kidney injury (31.52%) preponderantly of high grade, patients with more advanced disease are more prone to present infections, mainly UTI and ascites. Therefore they must be monitored closely.The authors declare that there is no conflict of interest.

Introduction and Objectives: Decompensation of liver cirrhosis represents a turning point in the prognosis of cirrhotic patients presenting more complex medical needs that can lead to a prolonged hospital stay and a significant risk of in-hospital death. Likewise, mean survival decreases from 12 years for compensated cirrhosis to almost two years for decompensated cirrhosis. Apica BS et al. (2013) reported ascites as the most frequent cause of decompensation in 95.3% cases in the African population. On the other hand, the Colombian study of Sanchez (2016) conducted with the Latin population indicates as the leading cause of decompensation ascites (36.1%), variceal bleeding (28.4%). Unfortunately, in Mexico, we do not have data indicating the most frequent cause of decompensation in hospitalized patients. Therefore, knowing the frequency and most common causes of decompensation will direct prevention and timely treatment strategies. Objective: To determine the cause and prevalence of liver cirrhosis decompensation in patients admitted to the Hospital General de México. Material and Methods: Observational, descriptive, retrospective study, Inpatients, hospitalized in the Gastroenterology Service of the General Hospital of Mexico ''Dr. Eduardo Liceaga'' with a diagnosis of liver cirrhosis, during the period from March 2019 to March 2021. The results were analyzed by descriptive statistics, frequency measures, and measures of central tendency (to obtain percentages, mean and average). Results: We reviewed 454 records of patients diagnosed with liver cirrhosis with an average age of 59 years with a range of 18-75 years, predominantly male 59.25%. The most frequent etiology was alcohol in 44.71%, followed by non-alcoholic steatohepatitis 9.91%, autoimmune causes 7%, and viral (hepatitis B and C) 3.30%; however, up to 31.7% the etiology cannot be determined. According to the Child-Pugh classification, the predominant one was C up to 53.96%. The most frequent decompensation was gastrointestinal bleeding with 52.64%, of which 47.57% were of variceal origin, acute kidney injury with 50%, hepatic encephalopathy 46.03%, and ascites 40.96%. It should be noted that 15.19% presented acute on chronic hepatic failure, and 11.23% toxic-alcoholic hepatitis: less frequently hyponatremia 8.37%, spontaneous bacterial peritonitis (SBP) 7.92%, hepatorenal syndrome 1.98%, and hepatopulmonary syndrome 1.10%. See table 1. Conclusions: In this study, the most frequent cause of decompensation was variceal bleeding, which differs from that reported in the literature in previous studies; however, this may be because the study population attends assessment in advanced stages of the disease and sometimes in the terminal phase to receive specialized care.The authors declare that there is no conflict of interest.

Introduction and Objectives: Metabolic syndrome and alcohol consumption are the two main causes of liver steatosis. Often, one of them predominates for its development and the other acts as a cofactor. The impact of these entities separately and their damage in synergy in the Mexican population is currently unknown. Our objective is to determine the prevalence of non-alcoholic liver steatosis, alcoholic liver steatosis, and dual damage in donors from the blood bank of the Hospital General de México “Dr. Eduardo Liceaga” (HGMEL) using transient elastography (TE). Materials and Methods: Pilot study. prospective, transversal, descriptive, and analytical. Healthy donors from the HGMEL blood bank who attended from June 8 to 29 2021 ≥18 years old, of any gender, will be included with a body mass index (BMI) ≥18.5. Donors with liver disease of any etiology and liver malignancy will be excluded. Donors who did not attend TE will be eliminated. The equipment used for TE was FibroScan® 502 Touch. Descriptive statistics will be used with measures of central tendency and dispersion. Results: 30 donors were recruited, four were eliminated for not having performed TE. The age of the subjects was 36.53 ± 12.13 years. There were 13 female subjects and 13 males. Seven (26.92%) donors were classified with non-alcoholic fatty liver disease (NAFLD), 2 (7.69%) with alcoholic fatty liver disease (ALD), and 1 (3.84%) subject with liver steatosis due to combined damage; the 16 (61.55%) remaining subjects corresponded to a healthy population. From the NAFLD group, S1 steatosis was documented in 1 subject (14.28%), S2 in 2 (28.56%), and S3 in 4 (57.16%); F0-F1 liver stiffness was found in 6 (85.72%) subjects, and F4 in 1 (14.28%); Of this group, 3 (42.86%) subjects were classified as overweight, 3 (42.86%) with grade 2 obesity, and 1 (14.28%) with grade 3 obesity. On the other hand, from the ALD group, one donor was found with steatosis S1, and 1 with S2; one of them had liver stiffness F0-F1 with an AUDIT score of 17 and a risk pattern for excessive alcohol consumption (117 g 2 to 4 times a month), while the other subject had F4 fibrosis with an AUDIT score of 7 and a pattern risk of excessive consumption (208 g 2 to 4 times per month), both consume beer. Finally, one donor had liver steatosis due to combined damage, with S3 for steatosis and F4 liver stiffness (27.4 kPa, the highest record in the study); He has grade 3 obesity (BMI 44.41), an AUDIT score of 4, and a pattern of excessive consumption (78 g 2 to 4 times a month) of distillates. Discussion: What is relevant about this work is that it studies an apparently healthy population and, according to our results, 38.45% (10) of the subjects already have a degree of liver steatosis and even 11.53% (3) showed advanced fibrosis. Our findings are similar to others about the prevalence of nonalcoholic liver steatosis, such as the work of the López-Velázquez group (26%) in 2014. Our study is novel in the investigation of alcoholic liver steatosis and the combined damage. Those issues are scarce addressed in our country. We also collect additional information, such as the identification of the consumption pattern of people with risky alcohol intake and the type of drink they consume. Conclusions: Our study shows that liver steatosis in this sample of the Mexican population is predominantly non-alcoholic; all subjects within this group have high BMI. Excessive risk consumption is prevalent in subjects with alcohol-related steatosis, and beer is the most frequent drink. In combined damage, obesity and excessive consumption of distillates seem to be the cause of severe steatosis. The only patient in this group already shows advanced fibrosis, which makes us suspect that dual damage accelerates the rate of fibrosis progression.The authors declare that there is no conflict of interest.

Introduction and Objectives: Clinical trials demonstrated the efficacy and safety of direct antiviral agents (DAA) to treat hepatitis C virus infection (HCV) in patients with decompensated cirrhosis (DC); however, very few real-world studies have been reported in this group. Moreover, predictive factors for non-achieving sustained virological response (SVR) in DC are not entirely understood. Therefore, the aim was to verify the efficacy and safety of DAA and to identify risk factors for failure to achieve SVR in DC. Materials and Methods: A real-world cohort study included HCV patients with DC [Child-Pugh B/C or A but with a history of previous clinical decompensation events like variceal bleeding (VB), hepatic encephalopathy (HE), or ascites]. All patients treated before transplant had MELD ≤ 20 and Child-Pugh ≤ 12 according to AASLD guidelines. Results: 222 patients, 118 (53.2%) were women, mean age 57.2±11.5 year-old, 61 (27.5%) were treated with Sofosbuvir(SOF)/Ledipasvir, 152 (68.5%) with SOF/Velpatasvir, and 9 (4.1%) with SOF/Daclatasvir, 175 (78.8%) used also ribavirin, 209 (94.1%) achieved SVR, despite non-significant difference, Child-Pugh C patients had a suboptimal response (SVR < 95%): A 42/44 (95.5%), B 140/147 (95.2%), C 27/31 (87.0%), p=0.2. Related adverse events were fatigue 60 (27%), nausea 44 (19.8%), headache 43 (19.4%), non-severe peripheral edema 10 (4.5%), anasarca 4 (1.8%), jaundice 6 (2.7%), 3 hemolytic anemia (1.4%), 1 dermatosis (0.4%), congestive cardiac failure 2 (0.9%), need to suspend therapy due to liver-related adverse events 2 (0.9%) they also died. In those who achieved SVR, MELD improved (basal 12.4±3.3 vs. post-SVR 10.9±3.5; p20 and Child-Pugh C >12 are related to non-SVR; however, our study also shows that additional clinical factors have a negative impact on SVR: history of recurrent VB and episodic and persistent HE; therefore, these criteria should also be considered to decide to treat previous or after liver transplantation. In addition, acute decompensation and mortality events are very high in those who do not achieve SVR. Conclusions: SOF based on regimens without PIs are effective and safe in VHC with DC. Additional to classic criteria (MELD >20, Child-Pugh > 12), recurrent VB and HE are predictors of failure to achieve SVR in VHC with DC.The authors declare that there is no conflict of interest.

Introduction and objective: Chronic alcohol consumption can induce Alcoholic Liver Disease (ALD) promoting biological alterations and liver damage; however, the immunological changes usually are underestimated. It has been reported, the increase of leucocytes in alcoholic hepatitis patients1, but the regulation of other cell lineages has not fully evaluated. Objective: To evaluate the leukocyte profile in patients with liver damage induces by chronic and acute alcohol consumption. Material and methods: A Cross-sectional study. Patients were classified as follow: (1) Controls with alcohol consumption 8, without clinical or biochemical data of liver damage (OH, alcoholism); (3) Cirrhotic patients due to alcohol (CiOH) and (4) Patients with alcoholic hepatitis (AH). Leukocytes, lymphocytes, monocytes, neutrophils, eosinophils, and basophils were determined by hematic biometry. U-Mann Whitney was used for statistical analysis, p

Introduction and Objectives: Diagnosis of liver disease (LD) is essential for the treatment and management of patients. The use of non-invasive methodologies is necessary despite the availability of direct-acting antivirals, some reports has been showed that treated patients can progress to cellular hepatocarcinoma (HCC). Continuous sampling that will evaluate liver tissue before and after treatment are essential for the prognosis of LD. Objective: To determine the sensitivity and specificity of insulin-like growth factor binding proteins (IGFBP) in the different stages of fibrosis in hepatitis C Material and methods: A prospective, cross-sectional, observational study. The study included patients with CHC that were treatment naïve. The stages of fibrosis were classified as F0, 16 F1, F2, F3, or F4, according to international guidelines, through the FibroTest® and/or FibroScan® Patients with at-risk alcohol consumption (AUDIT>8), and without concordance between fibrosis diagnostic methods employed, and comorbidities were not included. Serum was obtained and multiple suspension array technology (Millipore®) was used to evaluated IGFBP-1,2, 3, 4, 5, 6, 7. Chi-square test, Mann-Whitney U test. Logistic regression models, odds ratios (ORs) and 5% confidence intervals were determined. Results: A total of 128 patients diagnosed with CHC and 123 CT were included. Fibrosis stages were classified as follows: F0 (n=18), F1 (n=16), F2 (n=20), F3 (n=25), and F4 (n=48). IGFBP-1 to -7 showed an evident increment in patients mainly at F3 and F4. IGFBP-7 allows discriminate F3 vs F4 (72% sensibility, 62.5% specificity and cut of value of 2.74), whereas IGFBP-4 discriminates F3 vs F4 (83% sensibility, 68% specificity and cut of value of 14.68). P

Introduction and Objectives: The virus of hepatitis C (HCV) and alcoholic liver disease (ALD), are of the main causes of liver disease mortality. There is a need to determine biomarkers, serum cytokines are candidates since they participate in the immunopathogenesis of these diseases by activating the inflammatory process. Increased serum levels of IL-10 and TNF-α have been reported in cirrhosis and have been associated with progression to hepatocellular carcinoma. While TNF-α has become a key factor in the inflammatory process with high circulating levels in alcoholic hepatitis (HA). The objective of this work is to evaluate the serum levels of IL-10 and TNF-α in patients with chronic hepatitis C and ALD. Materials and methods: A cross-sectional and multicenter study. Patients with chronic Hepatitis C (CHC) and CiOH (cirrhotic by alcohol) and alcoholic hepatitis (HA) with criteria for alcoholism (WHO) were included, personalized survey, clinical and biochemical evidence of ALD was recorder. The groups were compared with subjects with a negative viral panel obtained from the CT blood bank (controls). IL-10 and TNF-α from serum was quantified using the multiple suspension arrangement method (Milliplex®-MERCK ©). Statistical analysis was performed using SPSS software version 22 using Mann Whitney U test. It was considered statistically significant p

Introduction and Objectives: Several mechanisms participate in the physiopathology of chronic alcohol consumption and Alcoholic Liver Disease (ALD), such as deregulation in the immune system. Aim: To analyze the lymphocyte subpopulations from patients with chronic and acute alcohol consumption. Material and methods: A Cross-sectional study that included: G1: Controls with alcohol consumption

Introduction and objective: Hepatitis C virus and alcoholism are the main causes of Chronic Liver Disease. (1) The increase of CXCL-8 has been correlated with mortality in alcoholic hepatitis (AH), while in Chronic Hepatitis C (CHC) with the disease severity. (2) The IFN-γ has an anti-viral and anti-fibrotic function. There are few comparative studies in patients regarding the production of these mediators and their possible implication in liver damage. The objective is to evaluate the concentrations of CXCL-8 and IFN-γ in the serum of AH, alcoholic cirrhosis (CiOH) and CHC patients. Materials and methods: A multicenter cross-sectional study was carried out. Four participant groups were included: AH, CiOH, CHC and control group (CT). For the quantification of CXCL-8 and IFN-γ a multiple suspension array assay (Milliplex®-MERCK©) was used. Statistical analysis was performed by the SPSS V.22 software using Mann-Whitney-U-test. A p-value

Introduction and Objectives: The damage caused by alcohol consumption generates liver fibrosis, which is characterized by the accumulation of extracellular matrix (ECM); To limit the liver damage, MMP-2 and MMP-9 gelatinases are produced as mediators to degrade ECM products. Their importance in liver damage proposes them as possible markers and target molecules in the diagnosis of alcohol consumption, as well as in alcoholic liver disease [1]. The objective of this work is to evaluate the serum concentrations of MMP-2 and MMP-9 gelatinases in subjects with different patterns of alcohol consumption and in alcoholic liver disease patients. Materials and methods: A cross-sectional study was carried out in which subjects with different patterns of alcohol consumption were included. The inclusion was according to the AUDIT, DSM-IV, and clinical and biochemical data of liver disease: risk (Ri), abuse (Ab), dependence (OH), cirrhosis due to alcohol (CiOH) and alcoholic hepatitis (HA). A group without alcohol consumption (TC) was also included for comparison. For the quantification of MMP-2 and MMP-9, a multiple suspension assay (Milliplex®-MERCK ©) was used. Statistical analysis was performed using SPSS V.22 software using Mann Whitney U. P

Introduction and Objectives: Primary biliary cholangitis (PBC), an immune-mediated disease, is characterized by destroying the intrahepatic bile ducts, leading to progressive damage to the biliary tree, cholestasis, and development of progressive fibrosis leading to cirrhosis with all its complications. The development of fibrosis is multifactorial and includes connective tissue growth factor (CTGF). in a mouse model of cholestasis by bile duct ligation, the hepatic and serum increase in CTGF associated with the progression of fibrosis was demonstrated. Our goal was to determine the relationship between CTGF levels and their association with the development of fibrosis in patients with PBC. Material and methods: Prospective, cross-sectional, and analytical study, including patients with PBC. The degree of fibrosis was determined by transient elastography (Fibroscan). Serum concentrations of FCTC-8pg/ml were quantified, for statistical analysis, the SPSS version 25.0 software was used; the medians (Q3, Q1) of CTGF, alkaline phosphatase, gamma-glutamyl-transpeptidase, and degree of fibrosis were compared with the Mann-Whitney U test with significantly less than 0.05. Results: We included 30 patients, 29 women (96.6%) and 1 man (3.4%), with a mean age of 55.5±12.4 years. Overexpression of CTGF protein was shown in 28 subjects (93.3%). Regarding the degree of fibrosis, all patients were categorized into one of two stages: Significant fibrosis (F2) and cirrhosis (F4). The F2 group had 11 patients with a median and standard deviation for CTGF of 915.9 and 522.9, respectively; The F4 group had 19 patients who showed a median: 945.7 (1313.85-738.32); p:0.025. In relation to the differences between fibrosis levels and markers of alkaline phosphatase cholestasis, the median and interquartile ranges F2: 79 (180.60) F4: 169(266-5.84) p: 0.066; GGT: F2: 1.51(7.7-1,04); F4: 1.2(2-1.92) p:0.746 In (Figure 1) The difference in medians of patients with different degrees of fibrosis and different concentration of CTGF is shown, confirming the association between peptide and the development and progression of fibrosis. Discussion: According to the results obtained in patients with CBP and chronic cholestasis, the increase in CTGF showed significant differences between the degree of fibrosis and its levels; this could perhaps be interpreted as if it were an important factor for the development and progression of liver fibrosis, taking into account the antecedent of the initial study in mice with bile duct ligation and secondary cholestasis, where this factor was overexpressed at the hepatic and serum level in subjects with advanced fibrosis. It will be important to add more samples to this work and compare it with healthy controls to have better evidence. Conclusions: Connective tissue growth factor (CTGF) probably participates directly in the processes of synthesis of extracellular matrix and therefore in the progression of fibrosis in subjects with primary biliary cholangitis, which makes it a possibility of a therapeutic target to develop in future studies.The authors declare that there is no conflict of interest.

Introduction and objective: Alcohol hepatitis (AH) is a clinical syndrome in patients with excessive and chronic alcohol consumption. Ethanol metabolism produces free radicals: reactive oxygen species (ROS) and reactive nitrogen species (RNS). This contributes to cellular damage in AH. The malondialdehyde (MDA) and carbonylated proteins are markers of oxidative damage in lipids and proteins. Our objective is to evaluate the levels of serum MDA and carbonylated proteins in AH patients with. Materials and methods: This transversal study included 147 individuals divided into two groups: the control group (n=100), which consists of individuals with alcohol consumption ≤ 10 g/day and AUDIT score ≤ 7, and the group with AH patients (n=47). We measured the serum levels of MDA (thiobarbituric acid method) and carbonylated proteins (DNPH reaction). The statistical analysis was performed by the Windows SPSS v22 software. Data were expressed as mean values ± SEM. Comparisons were carried out by analysis of variance (ANOVA). A p-value