FRI573 Liver Enzyme Elevation In A Patient With Grave’s Disease; Could This Be Due To Anti-thyroid Drug Therapy?

Abstract

Abstract Disclosure: C.S. Park: None. J.L. Gilden: None. Introduction: Abnormal liver enzymes (LFTs) are often observed in patients with both hypothyroidism, as well as in 2.5% of patients with Grave’ s (GRAVES) Hyperthyroidism (HTH) treated with anti-thyroid medications (ATD). Furthermore, abnormal Liver function tests are reported within 6 months of untreated thyrotoxicosis in 39% of patients. The other common causes of abnormal LFTs in HTH are congestive hepatopathy with thyrotoxic heart failure, previous underlying liver disease, hypermetabolism of hepatocytes due to HTH with subsequent anoxia and free radical damage, hepatocyte degeneration due to glycogen and protein decomposition acceleration, and autoimmune-related liver injury. Case: A 52-year-old Mexican American female, with allergies, and recent COVID vaccine, was referred to the endocrine clinic for an unknown duration of GRAVES with unintentional weight loss and occasional tremors of three months duration, and some leg weakness, but denied other symptoms of hyperthyroidism, gastrointestinal disorders, or other autoimmune disorders. There was no known family history of HTH, or other autoimmune disorders. She presented after initiation of methimazole (MMI) 5 mg twice daily, prescribed by her primary care provider. VS BP 137/70 HR 94 BMI 25.32. Exam-slight tremor on outstretched arms, no ophthalmopathy, 35-40 gm thyromegaly, no onycholysis or pretibial myxedema. Labs: TSH <0.010 (0.27-4.20 mIU/mL); Free T4 1.84 (0.5-1.6 ng/dL); T3 Free 5.31 (2.52-4.34 pg/mL); TG AB 100 (0-4 IU/mL); Thyroid Peroxidase 1,425.00 (0.00-9.00 iu/Ml); TSI 27.10 (<=0.54 iu/l). LFT’s were elevated (AST 105, repeat 53, (13-39 U/L);ALT 272,repeat 150 (7-52U/L); Alkaline Phosphatase (AP) 305,repeat 290 (34-104 U/L); T.Bilirubin 0.4 (0.0-1.0 mg/dL)]. AP Bone 159 (0-55 U/L) AP liver 195 (0-94 U/L). ANA was positive with SCL-70 autoantibodies 5.0 (<1.0 AI). Thyroid US: slightly heterogenous thyroid gland of chronic thyroiditis. RUQ abdominal US-normal. MMI was stopped for 2 weeks, then restarted. 1 week later-TSH <0.10 uIu/mL, Free T4 1.79 ng/dL, Free T3 5.91 pg/mL and LFT’s improved over the next several weeks (AST 39 U/L; ALT 85 U/L; Alkaline Phosphatase 220 U/L. SCL-70 remained positive, and she remained asymptomatic. Conclusion: Although the etiology for LFT elevation is suggestive of MMI treatment, since it occurred with the initiation and titration of this therapy, this patient also had markedly elevated SCL-70, seen in 20% of patients with systemic sclerosis, which can also be associated with lupus erythematosus, and primary biliary cirrhosis. Furthermore, the elevation continued, even after MMI had been stopped and then when restarted, was lower. This case demonstrates that it is crucial to evaluate for other etiologies of elevated LFTS in any patient with HTH, and not just assume that it is due to GRAVES or ATD, and also to consider the possibility of other autoimmune conditions. Presentation: Friday, June 16, 2023