Lapatinib is an inhibitor of the tyrosine kinases of human epidermal growth factor receptor type 2 (HER2) and epidermal growth factor receptor type 1, with clinical activity in HER2-positive metastatic breast cancer. We present here a 60 year-old patient with metastatic breast cancer who presented with jaundice and increased serum aminotransferase levels and who had been treated with lapatinib for the previous 14 days. Laboratory tests excluded other causes of acute liver injury. Liver biopsy revealed lesions compatible with drug-induced hepatotoxicity. Bilirubin and liver enzymes returned to normal within three months of lapatinib discontinuation. Lapatinib should be included among the causes of drug-induced hepatitis.
Aim: It was the aim of this study to test the hypothesis that the voltage-gated sodium channel gene SCN2A R19K polymorphism confers liability to oxaliplatin-induced peripheral neuropathy (OXLIPN). Methods: Sixty-two patients with advanced colorectal cancer were genotyped, using allele-specific primers and SYBR green in real-time polymerase chain reaction. All patients had received adjuvant oxalipla-tin-based chemotherapy. The severity of OXLIPN was defined by means of the clinical total neuropathy score. Following the discontinuation of treatment, 36/62 patients (58.1%) developed OXLIPN. Grade I neurotoxicity was revealed in 14 (38.9%) patients and grade II neurotoxicity in 22 (61.1%) patients. Results: From patients without OXLIPN (n = 26), 80.8% (n = 21) were homozygous for G, 19.2% (n = 5) were heterozygous (AG) and none was homozygous for A. The corresponding percentages for patients developing any grade of OXLIPN (n = 36) were similar. Likewise, among patients experiencing OXLIPN, insignificant differences in R19K genotypes were revealed between those with grade I versus grade II neurotoxicity. Conclusion: Our study failed to provide evidence to support a causal relationship between the SCN2A R19K polymorphism and OXLIPN.
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