Abstract

Permanent Hypothyroidism is the known consequence of Radioactive iodine (RAI) therapy and is one of the widely used therapy for Graves’ disease (GD). Relapse of Graves disease, within a few months is a well-known treatment failure either due to inadequate RAI dosage, rarely Marine-Lenhart syndrome. We present a case of GD which reappeared 15 years after successful RAI therapy, with a hypothyroid phase in the meantime. To the best of our knowledge, this is one of four cases reported with GD relapse after more than ten years, following RAI-induced hypothyroidism. Patient is a 58-year-old Hispanic female with a remote history of GD status post RAI treatment 15 years ago in Mexico. No further details were available at this time. During the interval, patient was treated with levothyroxine, for post-ablative hypothyroidism to date. Patient did well until recently when she presented to ER in Mexico with palpitations and unintentional weight loss of 30 pounds over 3 months. She was diagnosed with new onset Afib and hyperthyroidism. Patient was started on Eliquis and Amiodarone while levothyroxine was discontinued. After one month, Patient presented to the ED, in the USA with persistent Afib. Biochemical assessment of thyroid showed TSH < 0.005 (0.4-4.1 mIU/ml), free T4 > 7.70 (0.93-1.7 ng/dl), Total T3 321 (80-200ng/dl), TSI 20.10 (< 0.54 IU/L). Ultrasound thyroid showed enlarged heterogeneous hyper vascular thyroid gland consistent with Graves' disease. Amiodarone was discontinued since there was a concern for Amiodarone induced Type I thyrotoxicosis. Hence, treatment with beta-blocker and methimazole was initiated. While on Methimazole 30mg/day for 8 weeks, repeat labs showed TSH < 0.005 (0.4-4.1 mIU/ml), free T4 0.97 (0.93-1.7 ng/dl), Total T3 174 (80-200 ng/dl), TSI 10.30 (< 0.54 IU/L). There has been clinical and biochemical improvement. GD recurrence is extremely rare after successful treatment with therapeutic doses of RAI treatment. Once RAI treatment induces hypothyroidism, it is usually irreversible and requires thyroid replacement for life. Our Patient had a true recurrence that relapsed after a prolonged period following the achievement of hypothyroidism. Speculations may refer to the autoimmune nature of GD, in subjects with high elevations of antibody titer, inappropriate dose or non-adherence with levothyroxine, which may also contribute to an enlarged thyroid gland with increased production of endogenous thyroid hormones. As a result, complete ablation fails, and the disease may reoccur. This case illustrates the need for on-going monitoring of GD even after an effective RAI treatment.

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