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.
Subject(s)
Lead Poisoning/pathology , Liver/pathology , Opioid-Related Disorders , Opium , Abdominal Pain/etiology , Adult , Anemia/etiology , Anemia/pathology , Chelating Agents/therapeutic use , Chemical and Drug Induced Liver Injury/etiology , Chemical and Drug Induced Liver Injury/pathology , Cholangitis/etiology , Cholangitis/pathology , Drug Contamination , Fatty Liver/etiology , Fatty Liver/pathology , Hemosiderosis/etiology , Hemosiderosis/pathology , Humans , Lead/blood , Lead Poisoning/drug therapy , Lead Poisoning/etiology , Liver/drug effects , Male , Protoporphyrins/blood , Treatment OutcomeABSTRACT
Five cases of acute lead poisoning resulted from the self-injection of lead and opium pills which were crushed, heated and suspended in water. Two of the five patients died of illnesses in which hepatic failure and reversible acute tubular necrosis were prominent features. One of these two had a severe neuropathy, with flaccid quadriplegia and respiratory paralysis. The other three patients had relatively minor symptoms but unequivocal biochemical evidence of lead toxicity. Autopsy changes included hepatic degeneration with inclusion bodies, regenerating renal tubular epithelium and wasting of skeletal muscle. Hepatic lead content was extremely high in one case. Chelation therapy in the other fatal case resulted in a fall in blood lead to within normal limits and a clinical improvement, which was terminated by massive haemorrhage from a ruptured innominate artery.