Progressive visceral leishmaniasis misdiagnosed as cirrhosis of the liver: a case report

Abstract

Introduction:
Visceral leishmaniasis is a potentially life-threatening infectious disease which is caused by parasites of the genus Leishmania and characterized in most cases by the presence of fever as well as signs and symptoms similar to those found in liver cirrhosis.

Case presentation:
In this case report we describe the history of a 50-year-old Caucasian man incorrectly diagnosed as having hepatitis C virus-associated liver cirrhosis, with a massive weight loss of around 100 kg during the previous 2 years. However, suspecting a lymphoproliferative disorder, we were able to make a correct diagnosis of visceral leishmaniasis by bone marrow examination. After a course of therapy with Liposomal Amphotericin-B the patient recovered and now, 20 months post-treatment, he is well and has regained a good part of the lost weight.

Conclusions:
This case taught us that patients with massive splenomegaly, even with a diagnosis of liver cirrhosis, should be investigated for infectious or lymphoproliferative diseases.

Introduction
Liver cirrhosis (LC), associated with the hepatitis C virus (HCV), is very common in the Mediterranean area and is characterized by enlargement of the liver and spleen and signs of portal hypertension and pancytopenia, leading to liver failure or hepatocellular carcinoma 1. Visceral leishmaniasis (VL) is an endemic protozoal disease of the Mediterranean area which, in its chronic course, presents signs such as liver and spleen enlargement and pancytopenia that are similar to those found in LC. Here we report the case of a patient who presented clinically with these signs, together with serologic anti-HCV positivity, who had been labeled with a diagnosis of LC which dramatically masked a picture of progressive VL.

Case presentation
A Sicilian male patient, 50 years of age, was admitted to our ward for the first time in February 2006 following a dramatic weight loss (roughly 100 kg) and a presumptive diagnosis of liver cirrhosis related to hepatitis C virus (HCV). He was a thalassemia trait carrier and had smoked 20 to 30 cigarettes per day until 6 months previously andhis past history, apart from marked familial obesity (around 150 kg), did not indicate any particular problems. However, following the appearance of asthenia and abdominal tenderness 6 years ago, laboratory analyses were performed which showed high serum levels of alanine aminotransferase (ALT). Liver cirrhosis was diagnosed on the basis of anti-HCV seropositivity (ELISA 2nd generation) with negative hepatitis B surface antigen (HBsAg) and the presence of hepato-splenomegaly associated with pancytopenia. He had no history of traveling, alcohol consumption, blood transfusion, jaundice or anything else of note and, as his HCV-RNA assay wasand remains negative, he has never been treated with antiviral therapy. He was followed up for many months in a city hospital and had been receiving therapy with vitamin K and spironolactone until recently, and he has never reported having a high temperature.He presented at our outpatient clinic with asthenia, fatigue, pedal edema, difficulty in walking, cough, hoarseness and considerable weight loss, which had started 2 years earlier. On physical examination his general condition was very poor, with loose skin folds, muscle flabbiness, dryness of the skin and mucosa, mycosis of the tongue with areas of thickening and massive hepatosplenomegaly.