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Resumen Introduccion La hemorragia digestiva alta por varices esofagogastricas (HDA por VEG) puede desencadenar una isquemia hepatica aguda (IHA). El objetivo de este estudio fue analizar la incidencia de IHA tras una HDA por VEG, los factores de riesgo y su mortalidad. Pacientes y metodos Estudio retrospectivo sobre pacientes cirroticos con HDA por VEG. Se clasificaron en 2 grupos, determinados por el desarrollo o no de una IHA. Definimos IHA como AST y ALT por encima de 10 veces el valor basal, descartando otras causas de hepatitis aguda. El tratamiento inicial estandar fue soporte hemodinamico, endoscopia urgente con ligadura con bandas y/o escleroterapia, somatostatina y antibioticos. En caso de fracaso de estas medidas, se recurrio a la implantacion de una derivacion portosistemcica percutanea intrahepatica (DPPI). Ambos grupos (IHA y no-IHA) fueron comparados. Resultados Durante un periodo de 5 anos, se recogieron 68 pacientes con HDA por VEG. La incidencia de IHA fue del 16,2%. Tras el analisis univariante, los factores asociados con IHA fueron la diabetes mellitus (OR: 7,5; IC: 1,9-29), shock (OR: 8,5; IC: 2,06-34) y la persistencia de la hemorragia (OR: 9, IC: 1,6-49, p = 0,03). En el analisis multivariante solo mostraron significacion estadistica la diabetes mellitus (OR: 8,61; IC: 1,4-52,5) y el shock (OR: 7,58; IC: 1,26-45,51). La mortalidad del grupo de IHA fue mayor (45%) que en el grupo no-IHA (10,5%) (p = 0,012). Conclusiones La IHA tras una hemorragia digestiva por VEG en el paciente cirrotico ocurrio en el 16,2%, asociandose con un peor pronostico y una mortalidad del 45%. Nuestros resultados sugieren que la diabetes mellitus y el shock hipovolemico son factores de riesgo para el desarrollo de IHA. La deteccion precoz de estos pacientes en riesgo podria por tanto ayudar a prevenir la IHA.

Resumen Introduccion El tratamiento de la hepatitis cronica B antigeno e negativa (HCB HBeAg negativa) con antiviricos orales (AO) suele prolongarse de forma indefinida debido a que la perdida del antigeno de superficie como objetivo para su suspension es un hecho infrecuente. Recientemente han aparecido las primeras evidencias que sugieren finalizar la terapia con AO en casos seleccionados. Objetivos Analizar la tasa de rebote virologico en pacientes con HCB Age negativa que suspendieron el tratamiento con AO. Material y metodos Estudio retrospectivo observacional que incluyo 140 casos de HCB HBeAg negativa. Veintidos pacientes, que recibieron exclusivamente AO, los suspendieron por diversos motivos realizandose un seguimiento posterior. Todos presentaban transaminasas normales, ADN indetectable y ausencia de cirrosis o comorbilidades importantes al finalizar el tratamiento. Resultados Doce pacientes presentaron rebote virologico (54,54%), transcurriendo una media de 6,38 meses (± 1,9) desde la suspension hasta el rebote (el 75% dentro de los 12 primeros meses tras la suspension). Cinco recibieron adefovir, uno lamivudina mas adefovir, uno tenofovir y 5 lamivudina. La duracion media del tratamiento, desde el inicio hasta la suspension, fue de 38,5 meses (± 4,5). El grupo con respuesta sostenida presentaba una edad media y duracion del tratamiento superior a los sujetos con rebote, si bien estas diferencias no resultaron estadisticamente significativas. Conclusiones Los resultados sugieren que es posible suspender la terapia con AO en casos seleccionados de HCB Age negativa, siempre que no exista cirrosis, se cumpla un tiempo minimo de tratamiento, las transaminasas sean normales y el ADN indetectable de forma mantenida. En estos casos, se debe realizar un seguimiento estrecho durante el primer ano y posteriormente de forma indefinida.

Resumen Introduccion La globalizacion y los movimientos migratorios hacen que la hepatitis cronica B Age+ (HCBe+) cobre cada dia mayor relevancia en nuestro entorno. Objetivo Analizar las caracteristicas epidemiologicas, evolucion y respuesta al tratamiento con antivirales orales (AO) de los pacientes con HCBe+. Material y metodos Se analizaron 436 casos de infeccion cronica por el virus de la hepatitis B atendidos en el Hospital Universitario Ramon y Cajal desde 1990 hasta junio del 2012. Resultados Sesenta y cinco (14,9%) presentaban HCBe+. Siete pacientes en fase de tolerancia inmune no fueron tratados; los 58 restantes, si. Fueron excluidos 4: 2 hepatitis agudas graves, una coinfeccion por VHC y otro por virus Delta. De los 54 restantes, 19 recibieron interferon con o sin AO y 35 solo AO. Dos tratados durante menos de un mes no fueron incluidos en el analisis. Este se realizo finalmente en 33 pacientes. Duracion media del tratamiento: 46,81 meses (6-138). Lamivudina fue el farmaco mas prescrito (39,39%), seguida de tenofovir (24,24%) y entecavir (21,21%). Edad media: 42,08 ± 14 anos; varones 75,75% (25/33). El 57,57% (19/33) seroconvirtio el antigeno e y el 27,27% (9/33) elimino el antigeno de superficie. No se objetivo la reaparicion de este ultimo tras un seguimiento medio de 35,6 meses. Resistencias: 8 casos en 7 pacientes, 7 a lamivudina y uno a adefovir. Conclusiones El 15% de las HCB en nuestro medio son e+. El tratamiento con AO logra una elevada tasa de seroconversion (57,57%) y un considerable porcentaje de perdida del antigeno de superficie (27,27%).

Para cualquier cli´nico, y ma´s au´n para aquellos dedicados a lahepatologi´a, no es infrecuente encontrarse en el di´a a di´a conconcentraciones elevadas de amonio en sangre. Esto es debido a laestrecha relacio´n existente entre la encefalopati´a hepa´tica y estamole´cula orga´nicaquesedescribedesdehacemuchotiempocomouno de los principales agentes etiolo´gicos en esta entidad

Acute hypertriglyceridemic pancreatitis is the third cause of acute pancreatitis in the Western population. There is usually an underlying alteration in lipid metabolism and a secondary factor. Clinical presentation is similar to that of pancreatitis of other etiologies, but the course of acute hypertriglyceridemic pancreatitis seems to be worse and more recurrent. Some laboratory data can be artefacts, leading to diagnostic errors. This is the case of amylase, which can show false low levels. Treatment is based on intense fluidotherapy and analgesia. When there is no response to conservative management, other methods to lower triglyceride levels should be used. Several options are available, such as plasmapheresis, insulin, and heparin. The present article provides a review of the current literature on this entity.

Chylous ascites is infequent after abdominal surgery. We describe the case of a 43-year-old man with portal cavernomatosis who underwent surgery to insert a splenorenal shunt, which was not placed due to the absence of signs of portal hypertension. On postoperative day 20, the patient developed abdominal distension and mild dyspnea and was diagnosed with chylous ascites, which was related to the surgery. The patient was initially treated with diet and diuretics, with no clinical response, and consequently octreotide therapy was started. Four days later, the ascites was almost resolved and an ultrasound scan at 4 months showed its complete disappearance. This article demonstrates the effectiveness of octreotide in the treatment of postsurgical chylous ascites.

Resumen La hepatitis B aguda es una enfermedad en descenso gracias a las mejoras socioeconomicas y los programas poblacionales de vacunacion. Sin embargo, es potencialmente grave, siendo responsable de aproximadamente el 30% de los casos de insuficiencia hepatica aguda en nuestro pais. El tratamiento farmacologico de la hepatitis B aguda es un tema que ha cobrado importancia en la ultima decada. En este texto se revisan los trabajos publicados, asi como las recomendaciones de las guias clinicas internacionales. La mayoria de los textos analizados son de baja calidad metodologica y en todos se empleo la lamivudina como tratamiento. Se ha observado un beneficio en la supervivencia con un inicio precoz del tratamiento en la insuficiencia hepatica aguda y probablemente en la hepatitis aguda grave (bilirrubina total > 10 mg/dl e INR > 1,5). Las guias internacionales coinciden en recomendar el tratamiento en estos casos, aunque existen discrepancias sobre el farmaco a emplear y la duracion.

The hepatitis E virus is an RNA virus with 4 genotypes. Genotypes 1 and 2 only affect humans and produce epidemic acute hepatitis in endemic regions (Asia and Africa). Genotypes 3 and 4 are considered a zoonosis and produce episodic acute hepatitis in non-endemic areas (America and Europe). However, in the last 3 years there have been cases of chronic HEV hepatitis, mainly in immunosuppressed patients. Here we review the known data of chronic hepatitis E in terms of evolution and treatment.

Portal cholangiopathy encompasses a group of abnormalities of the biliary system and gallbladder that occur secondary to chronic portal vein thrombosis and collateral venous circulation. Chronic obstruction of the portal vein is a frequent cause of gastrointestinal variceal bleeding, but data on biliary tract abnormalities are limited. We report the case of a male patient with obstructive jaundice secondary to portal cholangiopathy. We describe the pathogenesis of this entity, and the various diagnostic and therapeutic options available.

Anticonvulsant hypersensitivity syndrome is an unpredictable, potentially fatal drug reaction to aromatic anticonvulsants such as carbamazepine, phenytoin and phenobarbital. The hallmark features include fever, eosinophilia, rash and involvement of one or more internal organs. Clearly established diagnostic criteria and treatment guidelines are lacking. A high index of suspicion is required to identify this syndrome, allowing early withdrawal of the drug and avoiding re-exposure. We report an illustrative case of anticonvulsant hypersensitivity syndrome and review the published literature.

Epiploic appendages are fat-filled, serosa-covered pediculated formations originating in the external wall of the bowel, toward the peritoneal cavity. Torsion of the epiploic appendages produces strangulation and infarction of the pedicle, initially venous and, when prolonged, ischemic, resulting in epiploic appendagitis. The main clinical manifestation is abdominal pain. Diagnosis is established through imaging techniques (ultrasound and computed tomography). Treatment is conservative and the prognosis is excellent.

Chronic abdominal pain is a common clinical problem in primary care, and is usually referred to gastroenterologists or general surgeons. Although up to 20% of cases of idiopathic abdominal pain arise in structures of the abdominal wall, this is frequently overlooked as a possible cause. It includes pain arising from structures of the abdominal wall including skin, parietal peritoneum, cellular subcutaneous tissue, aponeuroses, abdominal muscles and somatosensorial innervation from lower dorsal roots. The diagnosis is based on anamnesis and physical examination. Carnett's sign is a simple maneuver that discriminates between parietal and visceral pain. Management with topical anesthesia is effective in a majority of patients and can help to confirm the diagnosis.

There are multiple causes of hepatitis. The most frequent etiologies are viral, usually hepatitis A, B and C viruses. However, other, non-hepatotropic viruses can cause this disease, including parvovirus B19. We present a case of acute hepatitis due to parvovirus B19, as well as a review of the epidemiological, clinical, diagnostic and therapeutic features of this entity.

Hepatitis E virus (HEV) is a Herpesvirus, with four different genotypes. Genotypes 1 and 2 often cause acute hepatitis, which presents as outbreaks in endemic regions of Asia and Africa. Genotypes 3 and 4 cause sporadic cases of acute hepatitis in Europe and North America, where it is considered a zoonosis. Symptoms usually resolve spontaneously, but in recent years cases have been detected that progress to chronic liver disease mainly in immunocompromised patients (patients with solid organ transplants, lymphoma, human immunodeficiency virus, primary immunodeficiencies, and those under treatment with corticosteroids and immunosuppressive agents..). We report the case of a healthy, immunocompetent man who developed an episode of acute HEV hepatitis, which progressed to chronic liver disease with fibrosis grade III/IV in the liver biopsy within a year and half.

Introduction Variceal upper gastrointestinal bleeding (UGIB) can trigger acute hypoxic hepatitis (AHH). The aim of this study was to analyse the incidence, associated risk factors and mortality of AHH after variceal UGIB. Patients and methods Retrospective study of cirrhotic patients with variceal UGIB, classified into two groups according to the development of AHH. AHH was diagnosed when AST and ALT reached levels 10 times above the upper limit of normal, after ruling out other causes of hepatitis. The standard initial treatment consisted of haemodynamic support, emergency endoscopy with rubber band ligation, somatostatin and antibiotics. In the case of failure of primary haemostasis, a transjugular intrahepatic portosystemic shunt (TIPS) was implanted. Both groups (AHH and non-AHH) were compared. Results Sixty-eight cirrhotic patients with variceal UGIB admitted to the gastroenterology department of Hospital Ramon y Cajal between January 2007 and March 2012 were analysed. Eleven of these patients (16.2%) developed AHH. Univariate analysis showed the following items as risk factors: diabetes (OR: 7.5; CI: 1.9–29), shock (OR: 8.5; CI: 2.06–34) and persistent bleeding (OR: 9.0, CI: 1.6–49, p = 0.03). However, multivariate analysis confirmed only diabetes (OR: 8.61; CI: 1.4–52.5) and shock (OR: 7.58; CI: 1.26–45.51) as risk factors. Mortality rate in the AHH group was 45%, compared to 10.5% in the non-HAA group ( p = 0.012). Conclusions AHH after variceal UGIB occurred in 16.2% of cirrhotic patients and was associated with a poorer prognosis, with a mortality rate of 45%. Our findings suggest that diabetes and shock are risk factors for the development of AHH. Early identification of at-risk patients could therefore help prevent AHH.

Chylous ascites is infequent after abdominal surgery. We describe the case of a 43-year-old man with portal cavernomatosis who underwent surgery to insert a splenorenal shunt, which was not placed due to the absence of signs of portal hypertension. On postoperative day 20, the patient developed abdominal distension and mild dyspnea and was diagnosed with chylous ascites, which was related to the surgery. The patient was initially treated with diet and diuretics, with no clinical response, and consequently octreotide therapy was started. Four days later, the ascites was almost resolved and an ultrasound scan at 4 months showed its complete disappearance. This article demonstrates the effectiveness of octreotide in the treatment of postsurgical chylous ascites.

The incidence of acute B hepatitis is decreasing due to socioeconomical changes and the implementation of vaccination programs. Nevertheless it is potentially severe, causing approximately 30% of acute liver failures in Spain. Pharmacological treatment of acute B hepatitis has become a matter of issue over the last decade. This text offers a review of the published data and international guidelines. Most published studies have a low methodological quality and lamivudine was used as treatment in all of them. A survival improvement with prompt treatment has been shown in acute liver injury and probably in severe acute hepatitis (total bilirubin10mg/dl and INR1.5). International guidelines support treatment in these cases, but there is no consensus on the drug to use or the length of treatment.

Portal cholangiopathy encompasses a group of abnormalities of the biliary system and gallbladder that occur secondary to chronic portal vein thrombosis and collateral venous circulation. Chronic obstruction of the portal vein is a frequent cause of gastrointestinal variceal bleeding, but data on biliary tract abnormalities are limited. We report the case of a male patient with obstructive jaundice secondary to portal cholangiopathy. We describe the pathogenesis of this entity, and the various diagnostic and therapeutic options available.

The hepatitis E virus is an RNA virus with 4 genotypes. Genotypes 1 and 2 only affect humans and produce epidemic acute hepatitis in endemic regions (Asia and Africa). Genotypes 3 and 4 are considered a zoonosis and produce episodic acute hepatitis in non-endemic areas (America and Europe). However, in the last 3 years there have been cases of chronic HEV hepatitis, mainly in immunosuppressed patients. Here we review the known data of chronic hepatitis E in terms of evolution and treatment.

Hepatitis E virus (HEV) is a Herpesvirus, with four different genotypes. Genotypes 1 and 2 often cause acute hepatitis, which presents as outbreaks in endemic regions of Asia and Africa. Genotypes 3 and 4 cause sporadic cases of acute hepatitis in Europe and North America, where it is considered a zoonosis. Symptoms usually resolve spontaneously, but in recent years cases have been detected that progress to chronic liver disease mainly in immunocompromised patients (patients with solid organ transplants, lymphoma, human immunodeficiency virus, primary immunodeficiencies, and those under treatment with corticosteroids and immunosuppressive agents..). We report the case of a healthy, immunocompetent man who developed an episode of acute HEV hepatitis, which progressed to chronic liver disease with fibrosis grade III/IV in the liver biopsy within a year and half.

Anticonvulsant hypersensitivity syndrome is an unpredictable, potentially fatal drug reaction to aromatic anticonvulsants such as carbamazepine, phenytoin and phenobarbital. The hallmark features include fever, eosinophilia, rash and involvement of one or more internal organs. Clearly established diagnostic criteria and treatment guidelines are lacking. A high index of suspicion is required to identify this syndrome, allowing early withdrawal of the drug and avoiding re-exposure. We report an illustrative case of anticonvulsant hypersensitivity syndrome and review the published literature.

Epiploic appendages are fat-filled, serosa-covered pediculated formations originating in the external wall of the bowel, toward the peritoneal cavity. Torsion of the epiploic appendages produces strangulation and infarction of the pedicle, initially venous and, when prolonged, ischemic, resulting in epiploic appendagitis. The main clinical manifestation is abdominal pain. Diagnosis is established through imaging techniques (ultrasound and computed tomography). Treatment is conservative and the prognosis is excellent.

Chronic abdominal pain is a common clinical problem in primary care, and is usually referred to gastroenterologists or general surgeons. Although up to 20% of cases of idiopathic abdominal pain arise in structures of the abdominal wall, this is frequently overlooked as a possible cause. It includes pain arising from structures of the abdominal wall including skin, parietal peritoneum, cellular subcutaneous tissue, aponeuroses, abdominal muscles and somatosensorial innervation from lower dorsal roots. The diagnosis is based on anamnesis and physical examination. Carnett's sign is a simple maneuver that discriminates between parietal and visceral pain. Management with topical anesthesia is effective in a majority of patients and can help to confirm the diagnosis.