(16.02) A Case of Conversion from Hypothyroidism to Hyperthyroidism after 30 years?

Conversion of Hypothyroidism to Hyperthyroidism is an uncommon occurrence. We present a case of a patient with a 30-year history of autoimmune hypothyroidism who presented with overt Grave’s disease after 30 years.

Case(s) Description :

A 78-year-old Caucasian male with a 30-year history of hypothyroidism, coronary artery disease, hypertension, active tobacco use referred to endocrine clinic with symptoms of weight loss, palpitations, fatigue, resting tremor, heat intolerance and exophthalmos. On initial presentation 30-years ago, he presented with classic symptoms of weight gain, dry skin and generalized weakness. At the time, he was diagnosed with autoimmune hypothyroidism and started on levothyroxine. Given this clinical change in signs and symptoms consistent with hyperthyroid state, he was tapered off levothyroxine. Despite discontinuation of levothyroxine, the patient continued to have significant clinical symptoms. Labs revealed suppressed TSH, Free thyroxine (FT4) 2.2, Free triiodothyronine (FT3) 11.5, anti-thyroglobulin >1000, anti-microsomal >900, Thyroid stimulating immunoglobulin 327. Thyroid ultrasound showed enlarged gland with an increase in vascularization consistent with Grave’s disease. Patient was started on methimazole 20mg daily with subsequent improvement in symptoms, FT4 and FT3. His eye disease was treated with a course of teprotumumab.

Discussion :

Conversion from chronic autoimmune thyroiditis to Grave’s disease is rare. The first reported case of conversion was from Joplin and Fraser in 1959. Although many cases have been reported over the last several decades, it remains unclear why this phenomenon takes place. Several theories have been postulated. Moriarty et al. describe a similar case of conversion; they theorize that interaction between TRAB with the TSH receptor is responsible for the conversion from hypothyroidism to hyperthyroidism. Environmental or infectious trigger has been well-documented as a possible explanation as well, which works by altering the thyroid state by disrupting the balance in activity of blocking and stimulating antibodies. Furgan et al. reported three similar cases and theorize the possibility of thyroid damage from an autoimmune process, which initially causes thyroid hypofunction, but once enough thyroid tissue has recovered, it is stimulated by the stimulating autoantibodies and hyperthyroidism develops. Finally, it has been suggested that this conversion between blocking and stimulating antibodies occurs in some patients after using antithyroid drug treatment for Grave’s disease and levothyroxine for hypothyroidism.

It is rare for patients to convert from hypothyroidism to hyperthyroidism, especially with such a large interval of time of 30-years as seen in this patient. This case highlights that a diagnosis of primary hypothyroidism does not mean lifelong thyroid hormone supplementation will always be indicated. When presented with a patient with a history of hypothyroidism who develops persistent symptoms of hyperthyroidism, early differentials should include conversion to hyperthyroidism rather than assuming over replacement of thyroid hormone only.