The human multidrug resistance (MDR1) gene product P-glycoprotein is highly expressed in intestinal epithelial cells, where it constitutes a barrier against xenobiotics, bacterial toxins, drugs and other biologically active compounds, possibly carcinogens. In this study, an association of MDR1 gene polymorphism and the occurrence of colorectal cancer were evaluated. In this case-control-designed 118 unrelated colorectal cancer and 137 sex-and-ages matched healthy controls were enrolled. The C3435T MDR1 gene polymorphism was identified using the polymerase chain reaction-restriction fragment length polymorphism method. Significantly increased frequencies of the 3435T allele and the 3435TT were observed in patients with colorectal cancer compared with controls (P = 0.03; OR, 95% CI; 1.46 for 3435T allele and P = 0.003; OR, 95% CI; 2.2 for 3435TT genotype). In contrast, frequency of genotype TT was significantly higher in controls compared to colorectal cancer (P = 0.006; OR, 95% CI; 0.49 for TC genotype). In this study suggest that C3435T MDR1 polymorphism has an association with colorectal cancer. The results support that the presence of allele C results in decreased susceptibility to colorectal cancer.

IntroductionLead poisoning is a major public health risk which may involve major organs. Recently, there have been reports of opioid adulteration with lead in Iran. The following case report is the first of its kind in that intrahepatic cholestasis due to lead toxicity has been described.Case PresentationA 65-year-old man presented to the emergency department with abdominal pain, abnormal liver function tests (cholestatic pattern), and normocytic anemia. He had been an opium user for 20 years. Clinical and preclinical findings including the bluish discoloration of periodontal tissues, or Burton’s sign, and generalized ileus on abdominal x-ray led us to the possibility of lead poisoning. Lead levels were higher than normal (150 μg/dL). Magnetic resonance cholangiopancreatography (MRCP) and abdominal ultrasound were performed to rule out extra hepatic causes of cholestasis. To evaluate the possibility of lead-induced hepatotoxicity, a liver biopsy was performed. Histological features of lead-induced hepatotoxity have rarely been described in humans. In this patient, focal canalicular cholestasis and mild portal inflammation were confirmed. Thus, treatment with ethylenediaminetetraacetic acid (EDTA) and British anti-lewisite (BAL) were initiated and continued for five days. The patient’s liver function tests returned to their normal values, clinical findings including nausea, vomiting, and abdominal pain subsided, and the patient was discharged from the hospital in good condition.ConclusionsLead toxicity should always be taken into account in cases of intrahepatic cholestasis with an unknown etiology, especially in a setting where opium abuse is common.

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