Abstract
BACKGROUND Thyrotoxicosis is associated with well-recognized and clinically significant complications, including congestive heart failure and cardiac arrhythmias. The relationship between hyperthyroidism and hepatic dysfunction is complex, with several proposed pathophysiological mechanisms; however, direct cholestatic injury is frequently overlooked. Although mild liver enzyme elevation is common in hyperthyroidism, clinically overt jaundice is rare. Nevertheless, increasing evidence from case reports and case series suggests that thyrotoxicosis, especially Graves disease, can result in cholestatic-pattern jaundice. This temporal association is supported by substantial improvements in jaundice and liver biochemistry after antithyroid therapy. CASE REPORT A 62-year-old woman presented with a 1-month history of right upper quadrant abdominal pain, unintentional weight loss, and jaundice. Laboratory evaluation demonstrated cholestatic-pattern liver injury, and abdominal ultrasound revealed a solitary gallstone without evidence of acute or chronic cholecystitis. Abdominal computed tomography demonstrated right-sided heart failure with pericardial and bilateral pleural effusions and congestive hepatopathy. Endoscopic retrograde cholangiopancreatography showed no filling defects, excluding biliary obstruction. Because the patient had persistent sinus tachycardia, thyroid function tests were performed. The findings were consistent with primary hyperthyroidism and elevated thyroid-stimulating hormone receptor antibodies); thyroid ultrasound and scintigraphy results supported toxic multinodular goiter. Treatment with methimazole led to dramatic improvement of the jaundice. Given the possibility of competing etiologies, thyrotoxicosis was considered the most likely contributing factor to cholestatic jaundice onset. CONCLUSIONS This case highlights the importance of considering hyperthyroidism in the differential diagnosis of jaundice, particularly in diagnostically challenging cases.