SUN-565 Do Over-the-Counter Energy Supplements Delay the Diagnosis of Graves' Disease?

Abstract

Introduction: Hashimoto’s thyroiditis (HT) and Graves’ disease (GD) are thyroid-specific autoimmune disorders with distinct pathological mechanisms. Conversion from hyperthyroidism to hypothyroidism have been reported, but conversion from hypothyroidism to hyperthyroidism is rare. We report a woman with HT, who then developed GD, but diagnosis was delayed due to hyperthyroid symptoms presumed to be from over-the-counter (OTC) energy supplements. Clinical Case: A 59-year-old postmenopausal woman was diagnosed with HT in June 2013. [(TSH = 16.75 IU/mL; nl 0.358-3.74), (FT4 = 0.70 ng/dl; nl 0.76-1.46), (peroxidase Ab = 2645.8 U/mL; nl 0-60), (thyroglobulin Ab = 216.2 U/mL; nl 0-60)]. Her son has GD. She was started on L-thyroxine 75 mcg daily, and was doing well until April 2014, when she reported lack of energy. Due to TSH of 3.81 IU/mL, the dose was then increased to 100 mcg. TSH was 0.096 IU/mL 6 months later, and L-thyroxine was reduced to 88 mcg. Three years later, she began taking the energy supplement ThyrominTM (porcine thyroid powder, pituitary powder and adrenal powder) for 7 months. Lab values showed a suppressed TSH <0.005 IU/mL and elevated FT4 =2.06 ng/dL. She also had clinical symptoms of hyperthyroidism (lid retraction, fine tremors of hands and sweaty palms with 18 lbs weight loss). She was then advised to stop this supplement and continue taking L-thyroxine 88 mcg. L-thyroxine dose was later reduced to 75 mcg due to continued low TSH <0.005 IU/mL. Seven months later, she was seen in ophthalmology clinic for double vision due to mild ocular muscle inflammation secondary to thyroid disease. L-thyroxine was then stopped due to evidence of clinical and biochemical hyperthyroidism with positive TSHrAb = 86% and TSI = 460%. RAI thyroid uptake scan showed diffuse increased uptake. She was then diagnosed with GD, although she claimed that she was “feeling fine”. Methimazole therapy was recommended, but she declined. Discussion: Although the most likely cause of hyperthyroidism in a patient with HT is over-replacement of thyroid hormone, it is crucial to include conversion to GD in the differential diagnosis, given the common autoimmune origin of both disorders. Even though the pathophysiology underlying the conversion of HT to GD remains largely unknown, it is possible that various autoantibodies interact leading to conversion, or severe autoimmune-induced tissue injury occurs with recovery or age-related changes in the immuno-modulatory state that drive the transformation between these disorders. By reporting this case, we hope to raise the physician awareness about this rare phenomenon, and illustrate the potential mechanisms behind such change. Improvement of recognition and identification of this conversion process between HT and GD, as well as the role of energy supplements, would allow clinicians to expeditiously implement appropriate treatment, thus increasing the quality of care.