%0 Journal Article
%T Concurrent Liver Hodgkin Lymphoma and Nodular Regenerative Hyperplasia on an Explanted Liver with Clinical Diagnosis of Alcoholic Cirrhosis at University Hospital Fundaci車n Santa Fe de Bogot芍
%A R. L車pez
%A L. Barrera
%A A. Vera
%A R. Andrade
%J Case Reports in Pathology
%D 2014
%I Hindawi Publishing Corporation
%R 10.1155/2014/193802
%X Liver involvement by Hodgkin lymphoma (HL) is well documented. However, secondary liver failure to this neoplastic process is rare and usually presents late in the course of the disease. We present a case of a HL associated with nodular regenerative hyperplasia (NRH) diagnosed on an explanted liver from a 53-year-old patient with clinical diagnosis of alcoholic cirrhosis. Hematoxylin and eosin stain (H&E) showed abnormal liver architecture with hepatocytes nodules highlighted by reticulin stain with absent fibrosis on the trichrome stain. The portal spaces had diffuse infiltration by Reed-Sternberg cells positive for CD15, CD30, and latent membrane protein (LMP) on immunohistochemical studies. The patient also had a concurrent hilar lymph node biopsy that also showed HL involvement. Liver failure as the initial presentation of Hodgkin＊ lymphoma is rare. We believe that more research about the utility of performing liver biopsies in patients candidates for transplantation with noncirrhotic hepatic failure is needed in order to establish the etiology and the optimal treatment. 1. Introduction Liver involvement by Hodgkin＊s lymphoma (HL) is well documented [1] and secondary liver failure usually presents late in the course of the disease; however, there are some HL cases that present as a primary acute liver failure [2]. It is believed that hepatic failure by HL is due to bile duct destruction and direct tissue infiltration by the neoplastic cells [1, 2]. 2. Case Report The clinical history is that of a 53-year-old man who presented to our hospital with hepatic encephalopathy; his clinical history was positive for 18 years of alcohol abuse. He referred; recurrent ascites and six episodes of upper gastrointestinal bleeding from portal origin. Laboratory tests showed aspartate aminotransferase (AST) 35ˋU/L (5每34ˋU/L), alanine transaminase (ALT) 31ˋU/L (<55ˋU/L), alkaline phosphatase 215ˋU/L (woman >15 years old: 40每150), gamma-glutamyltransferase (GGTP) 368ˋU/L (Adult woman: 9每36), serum bilirubin 1.6ˋmg/dL (Total 0,2每1ˋmg/dL), direct bilirubin 0.76ˋmg/dL (0.10每0.5ˋmg/dL), indirect bilirubin 0.85ˋmg/dL, albumin 3.5ˋg/dL (3.4每5.4ˋg/dL), platelets 147ˋ(10)3/mm3 (150每450ˋ(10)3/mm3), creatinine 0.71ˋmg/dL (0.7每1.3ˋmg/dL), prothrombin time (PT) 14,4ˋsec (Control 11.1), partial thromboplastin time (PTT) 33.2ˋsec (Control 28,1), and INR 1.29. The patient was on propranolol 40ˋmgr once a day, gabapentin 600ˋmgr three times a day, and omeprazole 20ˋmgr once a day. Abdominal computed tomography (CT) showed diffuse hypervascular lesions on the liver parenchyma, portal
%U http://www.hindawi.com/journals/cripa/2014/193802/