SUN-370 Acute Cholestatic Liver Injury From Subtle Hypothyroidism That Responding to Intravenous Levothyroxine: A Case Report

Abstract Disclosure: Q. Li: None. P. Goparaju: None. Introduction: Thyroid hormones play a crucial role in regulating the hepatobiliary system. While acute hepatobiliary abnormalities are traditionally considered to be associated with hyperthyroidism, recent research suggests that hypothyroidism can also contribute to cholestatic liver injury through distinct mechanisms. Hypothyroidism’s impact on the hepatobiliary system was generally considered as mild and chronic, with acute overt liver injury being rare in the absence of myxedema.We present a case of acute cholestatic liver injury caused by uncontrolled hypothyroidism without reaching myxedema, which achieved full resolution following appropriate levothyroxine therapy. Case Description A 30-year-old woman with post-surgical hypothyroidism on levothyroxine therapy, nonalcoholic fatty liver disease (NAFLD) and morbid obesity, developed acute jaundice and pruritus within past week. Initial workup showed total bilirubin 10.1mg/dL, direct bilirubin 8.2 mg/dL, alanine aminotransferase (ALT) 237 U/L, aspartate aminotransferase (AST) 122 U/L, alkaline phosphatase (ALP) 281unit/L and gamma-glutamyl transferase (GGT) 349 U/L, calculated R factor 1.5 suggesting cholestatic liver injury. Other lab works, MRCP, abdominal US and CT scan ruled out biliary tract obstruction, viral or autoimmune hepatitis, acetaminophen intoxication, alcohol or other substance use, alpha-1 antitrypsin deficiency, Wilson disease, hemochromatosis, or progression of NAFLD. Standard cholestyramine and ursodiol treatment were ineffective. Further evaluation revealed elevated TSH as 24.564 mIU/L, low-normal free T4 as 0.65 ng/dl, low total T3 as 0.55 ng/mL and normal free T3 as 2.69 pg/mL. Experimental intravenous (IV) levothyroxine treatment led to rapid and dramatic improvement in bilirubin level and pruritus within 24 hours. Patient’s oral levothyroxine dose was adjusted on discharge. One-month follow up showed full resolution of her symptoms and liver panel abnormalities. Discussion: Hypothyroidism can contribute to cholestatic liver injury through mechanisms that are distinct from the liver injury seen in uncontrolled hyperthyroidism. Hypothyroidism correlates with reduction of biliary cholesterol secretion, dysfunction of the sphincter of Oddi, and bile flow impairment, which also possibly related to biliary tract stone formation and NAFLD in hypothyroidism patients. Our case manifested a rare scenario that mildly uncontrolled hypothyroidism, superimposed on NAFLD, triggered significant acute cholestatic liver injury, which was fully reversed with appropriate levothyroxine treatment. Notably, myxedema should not be considered as a prerequisite for diagnosing hypothyroidism-induced acute liver injury, as hypothyroidism can contribute to acute liver dysfunction even in its less severe forms. Presentation: Sunday, July 13, 2025