Fulminant hepatitis due to spontaneous reactivation of virus B in an immunocompetent patient

We present the case of a 52-year-old woman with a history of HBeAg-negative chronic hepatitis B virus (HBV) infection, viral load (VL) Z+<20,000U.l/ml with no evidence of liver fibrosis and, therefore, untreated. She presented to the emergency department with jaundice, epigastric pain, nausea, and vomiting. On admission, blood analysis revealed ALT 3982U/l, AST 3221U/l, Gamma-GT 80U/l, alkaline phosphatase 252U/l, LDH 960U/l, bilirrubin12.5mg/dl; no elevation of acute phase reactants, 141,000 platelets and coagulopathy with a prothrombin activity of 29%. Abdominal ultrasound showed no relevant findings. The serological profile revealed AgHBs+, anti-HBe+ y anti-HBc IgM+ and VL VHB>100 mills. Ul/ml, the remaining serology was negative and other causes of liver disease were ruled out. With the diagnosis of severe acute hepatitis (SAH) due to HBV reactivation (HBVR) treatment with entecavir was initiated. Given the analytical evolution (Table 1) and the appearance of encephalopathy grade I-II/IV, an urgent liver transplant was performed. The histological result of the explant was conclusive with intense interphase and lobular hepatitis with extensive areas of massive necrosis in both lobes, without hepatic fibrosis compatible with fulminant hepatitis (FH). (AU)

Fulminant hepatitis due to spontaneous reactivation of virus B in an immunocompetent patient.

We present the case of a 52-year-old woman with a history of HBeAg-negative chronic hepatitis B virus (HBV) infection, viral load (VL) Z+<20,000U.l/ml with no evidence of liver fibrosis and, therefore, untreated. She presented to the emergency department with jaundice, epigastric pain, nausea, and vomiting. On admission, blood analysis revealed ALT 3982U/l, AST 3221U/l, Gamma-GT 80U/l, alkaline phosphatase 252U/l, LDH 960U/l, bilirrubin12.5mg/dl; no elevation of acute phase reactants, 141,000 platelets and coagulopathy with a prothrombin activity of 29%. Abdominal ultrasound showed no relevant findings. The serological profile revealed AgHBs+, anti-HBe+ y anti-HBc IgM+ and VL VHB>100 mills. Ul/ml, the remaining serology was negative and other causes of liver disease were ruled out. With the diagnosis of severe acute hepatitis (SAH) due to HBV reactivation (HBVR) treatment with entecavir was initiated. Given the analytical evolution (Table 1) and the appearance of encephalopathy grade I-II/IV, an urgent liver transplant was performed. The histological result of the explant was conclusive with intense interphase and lobular hepatitis with extensive areas of massive necrosis in both lobes, without hepatic fibrosis compatible with fulminant hepatitis (FH).

Liver abscess as a atypical presentation of hepatocellular carcinoma.

We present the case of a 64-year-old male with a history of chronic liver disease due to hepatitis C virus, with a sustained viral response after oral antiviral treatment and without follow-up for 5 years. He was admitted after a one-month history of constitutional symptoms, low-grade fever, abdominal pain and a palpable epigastric tumor. Analysis showed marked elevation of acute phase reactants (48,000 leukocytes and C-reactive protein of 19mg/dl) and dissociated cholestasis. Two lesions were identified by abdominal CT.

Diagnostic accuracy of liver and spleen stiffness measured by fibroscan® in the prediction of esophageal varices in HCV-related cirrhosis patients treated with oral antivirals / Evaluación de la rigidez hepática y esplénica mediante Fibroscan® para la predicción de varices esofágicas en pacientes con cirrosis hepática por VHC tratados con antivirales orales

Introduction: The aim of this study was to investigate the accuracy of liver and spleen stiffness measurement by transient elastography for the prediction of gastroesophageal varices in patients with HCV-associated cirrhosis treated with new direct-acting antiviral agents. Patients and methods: This cross-sectional observational study included patients with compensated HCV-related cirrhosis and sustained virological response after direct-acting antiviral therapy. Patients underwent liver and spleen stiffness measurement, abdominal ultrasound and oesophago-gastroduodenoscopy. Clinical and laboratory data and non-invasive markers such as the liver stiffness–spleen diameter to platelet ratio score, variceal risk index and platelet count to spleen diameter ratio were analyzed. Results: Ninety-seven consecutive patients were included. Liver stiffness measurement (12.2 vs 16; p=0.02), spleen stiffness measurement (39.4 vs 46.05; p=0.04), liver stiffness–spleen diameter to platelet ratio score (1.21 vs 2.02; p=0.008), platelet count to spleen diameter ratio (1102.19 vs 829.7; p=0.04) and variceal risk index (−3.4 vs −1.02; p=0.01) showed significant differences between patients without/with gastroesophageal varices. The best cut-off value to discard the presence of gastroesophageal varices was 12.3kPa for liver stiffness measurement and 27kPa for spleen stiffness measurement. However, diagnostic accuracy was moderate (AUROC: 0.671 and 0.624 respectively). Combining different non-invasive parameters did not significantly improve the overall performance. Discussion: Liver and spleen stiffness measurement showed suboptimal results for non-invasive assessment of gastroesophageal varices in HCV cirrhotic patients treated with direct-acting antiviral agents. Our results suggest that non-invasive methods cannot substitute standard procedures for predicting gastroesophageal varices in this population.(AU)

Introducción: El objetivo de este estudio fue evaluar la rigidez hepática y esplénica medidas con Fibroscan® para la predicción de várices esofágicas (VE), en pacientes con cirrosis hepática por VHC tratados con antivirales orales. Pacientes y métodos: Estudio observacional y transversal que incluyó pacientes con cirrosis hepática por VHC compensada y respuesta virológica sostenida tras tratamiento. Se recogieron datos clínico-analíticos, ecográficos y endoscópicos y marcadores no invasivos como el Fibroscan® hepático y esplénico, el modelo predictivo «Liver stiffness-spleen diameter to platelet ratio score» (LSPS), el «Varices Risk Index» (VRI) y el índice n° plaquetas/diámetro mayor del bazo. Resultados: Se incluyeron 97 pacientes consecutivos. Los valores del Fibroscan® hepático (12,2 vs. 16; p = 0,02), esplénico (39,4 vs. 46,05; p = 0,04), LSPS (1,21 vs. 2,02; p = 0,008), índice n.° plaquetas/diámetro mayor del bazo (1.102,19 vs. 829,7; p = 0,04) y VRI (-3,4 vs. -1,02; p = 0,01) mostraron diferencias significativas entre pacientes sin/con VE. El mejor punto de corte del fibroscán hepático y esplénico para descartar la presencia de várices fue 12,3 y 27 kPas, respectivamente, con precisión diagnóstica moderada (AUROC: 0,671 y 0,624, respectivamente). La combinación de los parámetros no invasivos no mejoró el rendimiento global de estas pruebas. Discusión: Los valores del Fibroscan® hepático y esplénico mostraron resultados subóptimos para la evaluación no invasiva de VE en pacientes cirróticos por VHC tratados con antivirales orales. Nuestros resultados sugieren que estas pruebas no pueden sustituir a los procedimientos estándar para predecir la presencia de várices en esta subpoblación.(AU)

Diagnostic accuracy of liver and spleen stiffness measured by fibroscan® in the prediction of esophageal varices in HCV-related cirrhosis patients treated with oral antivirals.

INTRODUCTION: The aim of this study was to investigate the accuracy of liver and spleen stiffness measurement by transient elastography for the prediction of gastroesophageal varices in patients with HCV-associated cirrhosis treated with new direct-acting antiviral agents. PATIENTS AND METHODS: This cross-sectional observational study included patients with compensated HCV-related cirrhosis and sustained virological response after direct-acting antiviral therapy. Patients underwent liver and spleen stiffness measurement, abdominal ultrasound and oesophago-gastroduodenoscopy. Clinical and laboratory data and non-invasive markers such as the liver stiffness-spleen diameter to platelet ratio score, variceal risk index and platelet count to spleen diameter ratio were analyzed. RESULTS: Ninety-seven consecutive patients were included. Liver stiffness measurement (12.2 vs 16; p=0.02), spleen stiffness measurement (39.4 vs 46.05; p=0.04), liver stiffness-spleen diameter to platelet ratio score (1.21 vs 2.02; p=0.008), platelet count to spleen diameter ratio (1102.19 vs 829.7; p=0.04) and variceal risk index (-3.4 vs -1.02; p=0.01) showed significant differences between patients without/with gastroesophageal varices. The best cut-off value to discard the presence of gastroesophageal varices was 12.3kPa for liver stiffness measurement and 27kPa for spleen stiffness measurement. However, diagnostic accuracy was moderate (AUROC: 0.671 and 0.624 respectively). Combining different non-invasive parameters did not significantly improve the overall performance. DISCUSSION: Liver and spleen stiffness measurement showed suboptimal results for non-invasive assessment of gastroesophageal varices in HCV cirrhotic patients treated with direct-acting antiviral agents. Our results suggest that non-invasive methods cannot substitute standard procedures for predicting gastroesophageal varices in this population.

Varices estomales: una causa infrecuente de sangrado por hipertensión portal / No disponible

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Stomal varices: an unusual cause of bleeding in liver cirrhosis.

Stomal varices are an unusual cause of bleeding in liver cirrhosis. Diagnosis and treatment should be individualized according to the experience and resources of the hospital. Percutaneous embolization can provide a therapeutic option for patients with severe comorbidities.

Hipertensión portal secundaria a hemangiomatosis hepática múltiple / Portal hypertension secondary to multiple hepatic hemangiomatosis

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Esteatohepatitis no alcohólica y adenomatosis hepática: ¿asociación casual o causal? / Nonalcoholic steatohepatitis and hepatic adenomatosis: casual or causal relationship?

La adenomatosis hepática es una enfermedad benigna definida por la aparición de múltiples adenomas en un hígado normal. Se trata de una entidad poco frecuente y de causa no conocida, de la que existen menos de un centenar de casos publicados en la literatura médica y que se ha relacionado con la toma de anticonceptivos orales o esteroides anabolizantes, con enfermedades por depósito y con mutaciones genéticas asociadas a la diabetes mellitus tipo MODY (maturity onset diabetes of the young). En los últimos años se ha comunicado la coexistencia de adenomatosis hepática con lesiones de esteatohepatitis no alcohólica en dos pacientes con síndrome metabólico, una asociación de interés por la creciente prevalencia de la enfermedad hepática grasa no alcohólica en los países desarrollados y por la posibilidad de que compartan un mecanismo causal. Comunicamos el caso de una mujer joven con fructosemia familiar y esteatosis hepática durante cuyo seguimiento aparecieron múltiples adenomas hepáticos asociados a lesiones de esteatohepatitis y discutimos el posible significado de dicha asociación (AU)

Hepatic adenomatosis is a benign disease defined as the presence of multiple adenomas in a normal liver. It is an uncommon condition and there are less than a hundred reported cases in the literature. The etiology is unknown, although it has been associated with the use of oral contraceptives, anabolic steroids, certain storage diseases and some genetic mutations linked to maturity onset diabetes of the young. The coexistence of hepatic adenomatosis and nonalcoholic steatohepatitis has been recently described in two patients suffering from metabolic syndrome. This association is particularly interesting due to the growing prevalence of nonalcoholic fatty liver disease in developed countries and the possibility of a common causal pathway. We report the case of a young woman with fructosemia and hepatic steatosis; multiple hepatic adenomas associated to steatohepatitis lesions were also found during clinical follow-up. The possible implications are discussed (AU)

Colestasis tras la colocación de un TIPS en paciente con colangitis esclerosante primaria; una complicación infrecuente / Cholestasis after TIPS placement in a patient with primary sclerosing cholangitis: an uncommon complication

Presentamos el caso de un paciente con colangitis esclerosante primaria que presentó un síndrome colestásico de rápida evolución, con hiperbilirrubinemia grave tras colocar un TIPS que se resolvió con una prótesis biliar mediante CPRE. Hasta la fecha no se han descrito casos similares en la literatura, ya que se trata de una complicación rara y, por otro lado, la experiencia con el TIPS en pacientes con CEP es limitada. Las causas de hiperbilirrubinemia tras realizar un TIPS son muy variadas y es crucial realizar un diagnóstico diferencial para instaurar un tratamiento precoz (AU)

We present the case of a patient with primary sclerosing cholangitis who presented a rapidly evolving cholestatic syndrome, with severe hyperbilirubinemia after placing a TIPS. It was resolved with a biliary prosthesis inserted by ERCP. To date, no similar cases have been described in the literature, as it is a rare complication and, on the other hand, the experience with TIPS in patients with PSC is limited. The causes of hyperbilirubinemia after TIPS placement are very varied and it is crucial to perform a differential diagnosis to establish an early treatment (AU)

Nonalcoholic steatohepatitis and hepatic adenomatosis: casual or causal relationship?

Hepatic adenomatosis is a benign disease defined as the presence of multiple adenomas in a normal liver. It is an uncommon condition and there are less than a hundred reported cases in the literature. The etiology is unknown, although it has been associated with the use of oral contraceptives, anabolic steroids, certain storage diseases and some genetic mutations linked to maturity onset diabetes of the young. The coexistence of hepatic adenomatosis and nonalcoholic steatohepatitis has been recently described in two patients suffering from metabolic syndrome. This association is particularly interesting due to the growing prevalence of nonalcoholic fatty liver disease in developed countries and the possibility of a common causal pathway. We report the case of a young woman with fructosemia and hepatic steatosis; multiple hepatic adenomas associated to steatohepatitis lesions were also found during clinical follow-up. The possible implications are discussed.

Cholestasis after TIPS placement in a patient with primary sclerosing cholangitis: an uncommon complication.

We present the case of a patient with primary sclerosing cholangitis who presented a rapidly evolving cholestatic syndrome, with severe hyperbilirubinemia after placing a TIPS. It was resolved with a biliary prosthesis inserted by ERCP. To date, no similar cases have been described in the literature, as it is a rare complication and, on the other hand, the experience with TIPS in patients with PSC is limited. The causes of hyperbilirubinemia after TIPS placement are very varied and it is crucial to perform a differential diagnosis to establish an early treatment.

Fallo hepático agudo en paciente consumidora de productos de Herbalife y zumo de Noni / Fallo hepático agudo en paciente consumidora de productos de Herbalife y zumo de Noni

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Cytomegalovirus myopericarditis and hepatitis in an immunocompetent adult: successful treatment with oral valganciclovir.

Primary infection by cytomegalovirus (CMV) commonly occurs subclinically or manifested by a self-limited mononucleosis-like syndrome in immunocompetent subjects. Severe clinical pictures are uncommon. We present a case of acute myopericarditis and hepatitis in a previously healthy 32-year-old man with primary CMV infection, assessed by serology and positive pp65 antigenemia. He was successfully treated with a course of oral valganciclovir therapy, with an immediate clinical response and normalization of laboratory tests. The literature on simultaneous presentation of CMV pericarditis and hepatitis in immunocompetent hosts, as well as the role of oral valganciclovir in this clinical setting, is reviewed.

Pancreatitis aguda como presentación inicial de la enfermedad inflamatoria intestinal / Acute pancreatitis as the form of presentation of inflammatory bowel disease

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