S5534 Noncirrhotic Portal Hypertension in the Setting of Uncontrolled Graves’ Disease: A Diagnostic Challenge

Introduction: Hepatic dysfunction is a recognized but uncommon manifestation of Graves’ disease. Even more rarely, hyperthyroidism has been associated with noncirrhotic portal hypertension (NCPH)—portal hypertension in the absence of cirrhosis. We present a case highlighting the diagnostic complexity of NCPH in the setting of uncontrolled Graves’ disease. Case Description/Methods: A middle-aged man with history of Graves’ disease presented in thyroid storm after prolonged medication nonadherence. On admission, the patient reported abdominal pain and frequent vomiting, and exam was significant for abdominal distension. Imaging revealed a nodular liver contour with moderate ascites. Diagnostic paracentesis showed elevated polymorphonuclear cells (PMNs), suggestive of spontaneous bacterial peritonitis (SBP), though bacterial cultures were negative. Despite antibiotic treatment, his ascites persisted, and fluid studies continued to reveal elevated PMN counts. The serum-ascites albumin gradient (SAAG) was >1.1, consistent with portal hypertension. Despite a clinical picture suggestive of portal hypertension, further workup revealed discrepancies that made the etiology less straightforward. Hepatic venous pressure gradient (HVPG) measurement revealed a gradient of 4 mmHg, inconsistent with portal hypertension. Liver biopsy demonstrated stage 2–3 fibrosis without evidence of cirrhosis or hepatic venous outflow obstruction (HVOO). Echocardiogram showed reduced ejection fraction and right heart catheterization showed elevated pulmonary capillary wedge pressure, raising concern for cardiac ascites; however, lack of HVOO on biopsy made this etiology less likely. Discussion: After treatment of thyroid storm and adherence to his thyroid medication, his ascites resolved, and he no longer required frequent paracenteses. Although his clinical presentation, including ascites with high SAAG and recurrent SBP, was consistent with portal hypertension, the absence of elevated HVPG and preserved liver function pointed toward a noncirrhotic, likely prehepatic, etiology. Given his clinical improvement and stabilization of ascites following control of thyrotoxicosis, his NCPH was likely precipitated by uncontrolled Graves’ disease. This case adds to a limited but growing body of literature suggesting that thyrotoxicosis may contribute to portal hypertension through mechanisms unrelated to cirrhosis. Further study is needed to clarify the pathophysiology of thyroid-induced portal hypertension and to guide appropriate management.