ECE2022 Eposter Presentations Thyroid (219 abstracts)
Charles Nicolle Hospital, Endocrinology, Tunis, Tunisia
Introduction: Thyrotoxicosis is an uncommon cause of cholestasis. Its a diagnostic challenge considering the broad differential diagnosis. Herein we report a case of Graves disease revealed by severe cholestatic jaundice.
Observation: A 46 old male with a history of Sickle cell disease complained of diarrhea and significant weight loss for eight months, followed the last month by palpitations, heat intolerance, anxiety, insomnia and progressive jaundice. He had no family history of autoimmune disease. He denied hepatotoxic drugs, alcohol use or high-risk sexual behavior. On physical examination his body mass was 21.23 kg/m2, his blood pressure was 110/50 mm Hg and his heart rate was 93 beats per minute. He had jaundice of sclerae and skin with mild hepatomegaly. His thyroid was symmetrically enlarged. Biochemical findings showed: total bilirubin 183.6 µmol/l (3.420), direct bilirubin 135 µmol/l (<8.6), alkaline phosphatase 143 U/l (40129), AST 69 U/l (138), ALT 23 U/l (141), TSH 0.005 µUI/l (0.27-4.2) and FT4 61.07 pmol/l (12-22). Hepatitis A, B, and C testing were negative and autoimmune screen was unremarkable except positive hyroid-stimulating hormone receptor antibodies. Abdominal ultrasound, computed tomography and MRI revealed hydatic cystis in the VI and VII segment without biliary ductual dilatation. Thyroid ultrasound showed a symmetrically diffuse enlarged, hyper vascular, heterogeneous gland without nodules. Regarding the severity of the thyrotoxicosis, methimazol, propranolol and corticoids were administrated before radioiodine treatment with a close monitoring of liver function. By day 40 bilirubin fell by 50% (91.4).
Conclusion: This case highlights the merit of considering thyrotoxicosis as a cause of cholestasis as attaining a euthyroid state is critical for hepatic recovery.