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Pegvisomant-induced cholestatic hepatitis with jaundice in a patient with Gilbert's syndrome

¹ Endocrine Division, Departamento of Medicina, Complejo Hospitalario Universitario de Santiago, Hospital Clínico Universitario de Santiago, Universidad de Santiago de Compostela, Travesia Choupana s/n, 15706 Santiago de Compostela, La Coruña, Spain² Pathology Department, Complejo Hospitalario Universitario de Santiago, Universidad de Santiago de Compostela, Santiago de Compostela, Spain³ Instituto Salud Carlos III, Centro de Investigación Biomédica en Red (CIBER), Area Fisiopatología Obesidad y Nutrición (CiberObn), Santiago de Compostela, Spain⁴ Endocrine Division, Hospital Universitario de La Princesa, Universidad Autónoma de Madrid, Madrid, Spain

(Correspondence should be addressed to I Bernabeu; Email: ignacio.bernabeu.moron{at}sergas.es)

Abstract

We report on a patient with active acromegaly and Gilbert's syndrome who developed severe hepatic dysfunction during pegvisomant (PEGv) monotherapy. She was partially resistant to all previous therapies, including long-acting somatostatin analogs and cabergoline. Five months after starting PEGv therapy, with an already normalized IGF1, she developed cholestatic liver dysfunction with jaundice. Liver or biliary diseases including biliary sludge, cholelithiasis or liver steatosis were excluded. A liver biopsy was in keeping with drug-induced liver injury. The discontinuation of PEGv was followed by full clinical and biochemical recovery in 6 weeks. PEGv therapy was not resumed. Apart from a minimal increase of bilirubin levels, no liver function test abnormalities were found during the 4-year follow-up period after the PEGv was discontinued. Drug-induced liver injury is the most serious systemic adverse event resulting from PEGv therapy. Since patients with mild and asymptomatic liver disease could be at a higher risk of PEGv-induced hepatotoxicity, frequent monitoring of hepatic enzymes should be required in these cases.

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