Endocrine Abstracts

Introduction: Liver dysfunction during hyperthyroidism may be secondary to thyrotoxicosis, to an associated liver pathology, or to the medical treatment of hyperthyroidism posing a problem of etiological diagnosis. In this context, we report a demonstrative observation.

Case presentation: We report the observation of a 23-year-old female patient, followed for Basedow disease under carbimazole since 1 year, not controlled under medical treatment. During her follow-up, she presented cholestatic jaundice, associated with significant cytolysis and biological cholestasis, which persisted despite the discontinuation of synthetic antithyroid drugs. Biliary tract obstruction, viral or autoimmune hepatitis, and primary biliary cirrhosis were excluded. Liver biopsy showed lymphocytic infiltrate with discrete hepatic steatosis without stigma of autoimmune or toxic hepatitis. Our patient was treated only with Iodine 131. The post-iratherapy evolution was marked by the achievement of clinical and biological euthyroidism with normalization of the hepatic balance. This constitutes a major argument in favor of the thyrotoxic origin of this hepatopathy.

Discussion: Jaundice, during uncomplicated thyrotoxicosis, is rare and moderate (5-11%). Its exact etiopathogenesis remains poorly elucidated. An increased hepatic oxygen consumption due to hypermetabolic state not compensated by an increase in hepatic blood flow has been suggested. This imbalance leads to a decrease in oxygen tension in the centrilobular areas, which may lead to hepatocyte dysfunction with cholestasis. On anatomopathological examination, lymphocytic infiltrate in portal spaces, vacuolation and more rarely hepatic steatosis and intrahepatic cholestasis are often described, which was found in our patient.

Conclusion: Hyperthyroidism is an unusual cause of cholestatic jaundice that should be evoked in the absence of underlying liver disease.