Abstract
Infantile hepatic hemangioma can be associated to consumptive hypothyroidism due to overexpression of type 3 deiodinase in the endothelium of vascular tumor, which catalyzes the conversion of T4 to reverse T3 (rT3) and of T3 to T2, both of which are biologically inactive. Here, we report an infant with a massive biopsy-proven infantile hepatic hemangioma who developed thyroid dysfunction without a typical biochemical profile consistent with severe consumptive hypothyroidism, despite the large tumor burden. Our patient was treated with propranolol that rapidly resolved both hepatic hemangioma and thyroid dysfunction. We propose propranolol as a first-line therapy of thyroid dysfunction associated with infantile hepatic hemangioma, in order to avoid interference with neurological development caused by hypothyroidism in the first months of life.