Acute cholestatic liver injury due to hypothyroidism that reversed with intravenous levothyroxine: A rare case report

Liver dysfunction has been reported in patients with hypothyroidism, more commonly in myxedema coma, but acute cholestatic injury from less severe forms of hypothyroidism is rarely reported and is considered as an under-recognized complication of hypothyroidism. We describe a case of acute cholestatic liver injury that is possibly correlated with uncontrolled hypothyroidism, which was dramatically improved after intravenous levothyroxine. A 32-year-old woman with papillary thyroid carcinoma status post total thyroidectomy 13 years ago on levothyroxine (not complaint with standard administration technique), transferred from an outside institution for acute cholestatic liver injury work up. Patient initially presented with acute onset jaundice, pruritus, dark urine, and pale stools for about 1 week. Labs showed direct hyperbilirubinemia (total 10.1 mg/dL, direct 8.2 mg/dL) and elevated liver enzymes suggesting cholestatic liver injury. Viral, autoimmune, and metabolic workups were negative. Imaging including MRCP revealed hepatomegaly with steatosis and normal bile duct without obstruction. Despite cholestyramine and ursodiol treatment over a week, bilirubin rose to 12.8 mg/dL. Further workup in our institution showed TSH 24.5 mIU/L and Free T4 0.65 ng/dL. Without identifying other contributing factor to the cholestasis and failure of current treatment, patients received a trial of intravenous levothyroxine treatment, with rapid symptom relief and a 40% bilirubin drop in 24 hours. She transitioned to oral therapy three days later after her symptoms were fully resolved, with education of administration precautions. On one month follow up her liver function fully normalized. This case demonstrates that hypothyroidism without causing myxedema can still precipitate acute cholestasis, with underlying liver steatosis, history of gallbladder dyskinesia, co-administration of Glucagon-Like Peptide-1 receptor agonist ( GLP-1 receptor agonist) as a possible risk factor. Hypothyroidism should be considered in unexplained cholestatic liver injury. Prompt thyroid hormone replacement may enable rapid recovery and avoid unnecessary interventions.