PSAT348 Falsely Elevated TSI Antibody Without Causing Hyperthyroidism, in a Hypothyroid Patient

INTRODUCTION: Hashimoto's thyroiditis and Graves’ disease are the most common causes for Hypothyroidism and Hyperthyroidism respectively. There are case reports of co-existence of these two disorders in the same patient (1) which causes an alternating clinical course of both hypothyroidism and hyperthyroidism. The Graves’ disease specific Thyroid Stimulating Immunoglobulin (TSI) antibody is reported to have a very high sensitivity and specificity. However, the presence of TSI antibody in a long-standing hypothyroid patient without developing hyperthyroidism, is of extreme rare occurrence. CASE DESCRIPTION: Our patient is a 58-year-old Caucasian female who has a history of hypothyroidism that was diagnosed in 1990. She was initiated on levothyroxine and had maintained a stable dose of 100 mcg daily for many years. During the initial visit at our endocrinology clinic in December 2020, the patient's labs were consistent with iatrogenic thyrotoxicosis due to a low TSH 0.233 (0.30-4.00 uIU/ml), normal Free T4 1.33 (0.80-1.80 ng/dl) and normal Free T3 2.28 (2.0-4.40 pg/ml). TPO antibody was negative at 11 (0-34 IU/mL). The levothyroxine dose was reduced to 88 mcg daily, but patient did not obtain follow-up labs for many months. In August 2021, the TSH was noted to be normal at 2.29. Patient was also diagnosed with multinodular goiter with the presence bilateral sub centimeter thyroid nodules which had remained stable over the years. However, thyroid ultrasound in December 2020 showed a 1.8 cm left mid to lower pole nodule that was biopsied and reported to be Bethesda category III with benign Afirma Genomic sequencing classifier. Subsequently, patient reported experiencing swelling and pain of bilateral fingers and underwent evaluation by rheumatologist who ordered a panel of blood tests to assess for autoimmune conditions. Interestingly, thyroid antibodies were also assessed, and it came back remarkable for elevated the Graves’ disease specific TSI antibody level 221% (< 140%) and elevated anti-thyroglobulin (TG) antibody 40.6 (<4.1). Patient's medication list was verified, and she was not on any high-dose biotin supplementation, and she denied experiencing any hyperthyroid symptoms. The corresponding thyroid labs were unremarkable with normal TSH 2.2, normal free T4 1.33 and normal free T3 2.28. Patient was reassured about the normal thyroid labs and advised that her symptoms are not thyroid related. The repeat TSH level continues to remain normal and was 2.18 in December 2021. CONCLUSION: Although the presence of TSI antibody has a high positive predictive value for diagnosing Graves’ disease, a falsely elevated TSI antibody, can rarely occur without causing any clinical consequences. REFERENCE: (1) Alvin Mathew A, Papaly R, et al. Elevated Graves’ Disease-Specific Thyroid-Stimulating Immunoglobulin and Thyroid Stimulating Hormone Receptor Antibody in a Patient With Subacute Thyroiditis. Cureus 13(11): e19448. doi: 10.7759/cureus.19448 Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.