Received:30.03.2008 Accepted: 08.04.2008 J Gastrointestin Liver Dis June 2009 Vol.18 No 2, 225-227 Address for correspondence: Dr. Joanne Verheij Department of Pathology VU University Medical Center 1081 HV Amsterdam, The Netherlands E-mail: J.Verheij@vumc.nl Hepatic Morphopathologic Findings of Lead Poisoning in a Drug Addict: a Case Report Joanne Verheij 1 , Jens Voortman 2 , Carin M.J. van Nieuwkerk 2 , S. Vijay A. Jarbandhan 2 , Chris JJ Mulder 2 , Elisabeth Bloemena 1 1) Department of Pathology; 2) Department of Gastroenterology and Hepatology, VU University Medical Center, Amsterdam, The Netherlands Abstract We describe the case of a 40-year old Iranian man who was admitted to our hospital with severe abdominal pain, abnormal liver function tests and normocytic anemia. Suffering from multiple sclerosis, he was a regular user of opium for pain relief. Basophilic stippling of erythrocytes pointed towards the diagnosis of lead intoxication, the most likely source being contaminated Iranian opium. Serum lead and zinc protoporphyrin levels were strongly elevated. To assess the hepatotoxic effects of lead poisoning a liver biopsy was performed. Pathomorphologic findings of hepatotoxicity, rarely reported in humans, included active hepatitis together with extensive microvesicular and macrovesicular steatosis, hemosiderosis and cholestasis, and a lymphocytic cholangitis. Whilst treated with chelating therapy, liver enzymes returned to normal, suggesting reversibility of the histological findings. Key words Liver biopsy – opium – Iran – hepatotoxicity. Introduction Lead poisoning is a medical condition also known as saturnism or plumbism. It is caused by occupational or environmental exposure to sources of (in)organic lead. The most common sources are lead-containing paint, water, leaded pipes from public water supply, Asian herbal remedies, lead-glazed ceramics, and lead shot game [1]. Prevalence in the general adult population is unclear and especially children are at risk for impaired neurological development upon chronic exposure [2]. It is estimated that nearly half a million of children in the United States have blood lead levels high enough to cause irreversible damage to their health, lead paint being the major source of lead toxicity in children [1]. Typically, lead-intoxicated patients present with neurological complaints and neurobehavioral disorders. However, toxic levels of lead do not only affect the nervous system but also hematopoiesis and renal function [2-5]. Lead-induced liver damage is an uncommon finding and has anecdotally been reported [6]. The resulting histopathological changes have rarely been described in humans. However, descriptive animal studies have been reported [4]. Clinical presentation We describe the case of a 40-year-old man, an immigrant from Iran, who presented himself at the emergency department of our hospital with severe, constant, upper abdominal pain. His complaints had started a few weeks before presentation, following a short stay in Iran. However, over one day his pain had progressed. His medical history included exacerbating-remitting multiple sclerosis, for which he received weekly interferon-beta injections. Due to chronic pain he also used Iranian opium regularly. There was no history of alcohol abuse. Physical examination revealed a sweating, afebrile, hemodynamically stable, non-icteric patient in evident pain. Upon examination of the abdomen, bowel sounds were decreased and especially the right upper abdominal quadrant was tender to palpation. No involuntary guarding or abnormal abdominal masses were observed. The initial differential diagnosis of the symptoms included biliary dyskinesia associated with the use of opium, chole(cysto)lithiasis, peptic ulcer disease, gastric perforation, nephrolithiasis, mesenterial ischemia and possibly porphyria. Laboratory findings included a normocytic anemia (hemoglobin 5.7 mmol/L; hematocrit 0.27, MCV 84 fl) and elevated liver function tests: AST 66 U/L (N 0-35), ALT 92 U/L (N 0-45), gamma-GT 729 U/L (N 0-40), without an acute-phase response. Renal function was normal. Ultrasonography and CT imaging of the abdomen did not