BACKGROUND: Lenalidomide is an immunomodulatory drug frequently used for treatment of patients with multiple myeloma and myelodysplastic syndromes. This report presents a rare case of lenalidomide-associated hepatotoxicity and reviews the available literature. CASE REPORT: A 67-year-old male with multiple myeloma was hospitalized with nausea, vomiting and jaundice, while treated with a second three-week course of lenalidomide. The patient was found to have acutely elevated bilirubin, alkaline phosphatase, AST and ALT. He also had acute on chronic renal function impairment. Serology for viral hepatitis, abdominal ultrasound, magnetic resonance cholangiopancreatography and hepatobiliary scan revealed no abnormalities. Lenalidomide was stopped, resulting in subsequent (8 days) clinical improvement and normalization of the liver abnormalities. The RUCAM causality assessment score was 8, consistent with probable lenalidomide-associated hepatotoxicity. Literature review revealed four other published cases of lenalidomide-associated hepatotoxicity with clinical presentation varying between cholestatic-, hepatocellular- or mixed-pattern of liver injury. All patients had clinical and laboratory improvement soon after lenalidomide discontinuation. Renal function impairment was present in 3 of the 5 reported cases. The exact mechanism of lenalidomide-associated liver injury remains unclear as only 2 patients had liver biopsies without specific findings. CONCLUSION: Physicians should be aware of the potential for lenalidomide-associated hepatotoxicity, particularly in patients with underlying renal insufficiency.
BACKGROUND:Lenalidomide is an immunomodulatory drug frequently used for treatment of patients with multiple myeloma and myelodysplastic syndromes. This report presents a rare case of lenalidomide-associated hepatotoxicity and reviews the available literature. CASE REPORT: A 67-year-old male with multiple myeloma was hospitalized with nausea, vomiting and jaundice, while treated with a second three-week course of lenalidomide. The patient was found to have acutely elevated bilirubin, alkaline phosphatase, AST and ALT. He also had acute on chronic renal function impairment. Serology for viral hepatitis, abdominal ultrasound, magnetic resonance cholangiopancreatography and hepatobiliary scan revealed no abnormalities. Lenalidomide was stopped, resulting in subsequent (8 days) clinical improvement and normalization of the liver abnormalities. The RUCAM causality assessment score was 8, consistent with probable lenalidomide-associated hepatotoxicity. Literature review revealed four other published cases of lenalidomide-associated hepatotoxicity with clinical presentation varying between cholestatic-, hepatocellular- or mixed-pattern of liver injury. All patients had clinical and laboratory improvement soon after lenalidomide discontinuation. Renal function impairment was present in 3 of the 5 reported cases. The exact mechanism of lenalidomide-associated liver injury remains unclear as only 2 patients had liver biopsies without specific findings. CONCLUSION: Physicians should be aware of the potential for lenalidomide-associated hepatotoxicity, particularly in patients with underlying renal insufficiency.