Endocrine Abstracts

Graves’ disease is one of the multiple autoimmune diseases that have been reported in HIV-infected patients. With the upsurge of highly active anti-retroviral therapy (HAART) the incidence of autoimmune diseases in HIV-infected patients is increasing, especially after immune reconstitution. We present a male, 51-year-old, who started complaining with anxiety, sudoresis and palpitations. The laboratory workout revealed hyperthyroidism: TSH <0.02 μU/ml (0.46–4.68), FT4 28 pmol/l (10.0–28.2), FT3 13.7 pmol/l (4.26–8.10). The patient started propylthiouracilo 100 mg per day and was referred to the Endocrinology Department. He had Mitral Insufficiency and HIV-1 infection. He was on HAART since 2007 with emtricitabin, tenofovir, atazanavir and ritonavir. The etiologic study disclosed Graves disease with TRAbs level 45.3 U/l (<1). We changed propylthiouracilo for thiamazole. During follow-up most of the time it wasn’t possible to achieve euthyroidism. We offered other therapeutic options (Iodine-131 or surgery) but the patient rejected them. On the 23^rd month of thiamazole therapy the patient was icteric and blood workout revealed hyperbilirubinemia (total bilirubin 8.1 mg/dl), FT4 48.1 pmol/l and FT3 18.7 pmol/l. We discussed these results with the Infectiology Department and hyperbilirubinemia was interpreted as an atanavir adverse effect. Boosted atazanavir (with ritonavir) was replaced by rilpivirine and we maintained the same dosis of thiamazole (15 mg per day). 6 weeks later he had normal total bilirunin (0.64 mg/dl) and normal/low thyroid hormones: FT4 9.45 pmol/l and FT3 6.05 pmol/l. Both atazanavir, ritonavir and thiamazole are metabolized in cytochrome P450. In this case the interaction resulted in decreased benefit of thiamazole and explains why it was so difficult to attained euthyroidism. To the best of our knowledge this is the first time the interaction between atazanavir and thiamazole is reported.