Reactions Weekly | 2021

Lenvatinib

 

Abstract


Acute cholecystitis: 5 case reports In a retrospective series involving 15 patients who had been receiving lenvatinib in April 2020, 5 patients (three women and two men) aged 40–79 years were described, who developed acute cholecystitis during treatment with lenvatinib for differentiated thyroid cancer (DTC) [routes not stated]. A 79-year-old woman (patient A from table 1 of the article), who had DTC, was initially treated with iodine radioactive [radioiodine]. However, her DTC was noted to be refractory. Thereafter, she started receiving lenvatinib 24 mg/day. However, 2 months after initiation of lenvatinib therapy, she developed abdominal pain, anorexia and weight loss. Laboratory investigation revealed elevated levels of gamma-glutamyl transpeptidase and alkaline phosphatase. CT scan demonstrated gallbladder distension with wall thickening and oedema. She was diagnosed with acute cholecystitis secondary to lenvatinib. Lenvatinib therapy was interrupted for 2 weeks. A repeat CT scan performed after 3 months showed resolution of the gallbladder abnormalities. Two weeks later, lenvatinib was re-initiated at a lower dose. A 45-year-old woman (Patient B from table 1 of the article), who had DTC, was initially treated with iodine radioactive [radioiodine]. However, her DTC was noted to be refractory. Subsequently, she started receiving lenvatinib 24 mg/day. Her concomitant therapy consisted of estrogen. However, 3 months after initiation of lenvatinib therapy, she developed vomit, nausea, anorexia and weight loss. Laboratory investigation revealed elevated levels of bilirubin, alanine aminotrasferase, aspartate aminotrasferase, gamma-glutamyl transpeptidase and alkaline phosphatase. CT scan demonstrated dilation and thickening of the gallbladder wall without stones. She was diagnosed with acute cholecystitis secondary to lenvatinib. She was treated with hydration and unspecified nonsteroidal anti-inflammatory drugs. Thereafter, her symptoms resolved and laboratory indices improved. However, repeat CT scan at 12 months showed persistence of mild gallbladder injury. A 40-year-old woman (Patient C from table 1 of the article), who had DTC, was initially treated with iodine radioactive [radioiodine]. However, her DTC was noted to be refractory. Subsequently, she started receiving lenvatinib 20 mg/day. However, 2 months after initiation of lenvatinib therapy, she developed postprandial abdominal pain, anorexia and weight loss. Laboratory investigation revealed elevated levels of bilirubin, alanine aminotrasferase, gamma-glutamyl transpeptidase and alkaline phosphatase. CT scan demonstrated dilated gallbladder and hyper dense bile (sludge). Gallbladder stone (<1 cm) was observed in the infundibulum of gallbladder. She was diagnosed with acute cholecystitis secondary to lenvatinib. Lenvatinib dose was reduced to 14 mg/day. She was treated with ursodeoxycholic acid. Thereafter, her symptoms resolved and laboratory findings normalised. A 66-year-old man (Patient D from table 1 of the article), who had DTC, was initially treated with iodine radioactive [radioiodine]. However, his DTC was noted to be refractory. Subsequently, he started receiving lenvatinib 24 mg/day. However, 3 months after initiation of lenvatinib therapy, he developed vomit, nausea, postprandial abdominal pain, anorexia and weight loss. Laboratory investigation revealed elevated levels of gamma-glutamyl transpeptidase and alanine aminotrasferase. CT scan demonstrated tense and dilated gallbladder with sludge, pericholecystic fluid. He was diagnosed with acute cholecystitis secondary to lenvatinib. He was treated with ursodeoxycholic acid. Lenvatinib dose was reduced to 20 mg/day after 4 months of treatment. Further increase in gamma-glutamyl transpeptidase level along with nausea and vomiting was observed. Therefore, lenvatinib dose was further reduced to 14 mg/day at 8 months of treatment. He was treated with ursodeoxycholic acid. Thereafter, his gallbladder abnormalities resolved and he achieved clinical stabilisation. Lenvatinib therapy was progressively re-established and maintained at a final dose of 20 mg/day. A 60-year-old man (Patient E from table 1 of the article), who had DTC, was initially treated with iodine radioactive [radioiodine]. However, his DTC was noted to be refractory. Subsequently, he started receiving lenvatinib 20 mg/day. However, 2 months after initiation of lenvatinib therapy, he developed vomit, nausea, anorexia, jaundice, weight loss and fever. He was hospitalised. Laboratory investigation revealed elevated levels of bilirubin, alanine aminotrasferase, aspartate aminotrasferase, gamma-glutamyl transpeptidase and alkaline phosphatase. CT scan demonstrated gallbladder wall thickening and oedema with sludge. Common bile duct dilatation without stones was also noted. Contrast-enhanced CT also showed a neo-enlargement of the pancreas head, with no malignant findings at cytology [aetiology not stated]. He was diagnosed with acute cholecystitis secondary to lenvatinib. Lenvatinib therapy was interrupted for 4 weeks. He was treated with ursodeoxycholic acid. Thereafter, his symptoms and laboratory findings normalised. A repeat CT scan performed after 3 months showed resolution of the gallbladder abnormalities. After 4 weeks, lenvatinib therapy was re-initiated at a lower dosage.

Volume 1877
Pages 218 - 218
DOI 10.1007/s40278-021-03788-4
Language English
Journal Reactions Weekly

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