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FRI565 Spontaneous Conversion Of Long-standing Hypothyroidism To Grave’s Disease: A Case Report
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Abstract
Disclosure: M. Dominic: None. M. Shakir: None. A. Kakkar: None. O.Z. Syed: None. A. Sood: None. D.A. Alvarez: None.
Introduction: Autoimmune thyroid diseases associated with IgG4 include Hashimoto’s thyroiditis (HT) and Graves’ disease (GD). HT involves a combination of antibody-mediated thyroid gland destruction and inhibition of thyroid hormone production through a predominance of TSH receptor-blocking antibodies (TBAb). GD is due to increased thyroid hormone production in response to thyroid-stimulating antibodies (TSAb). Although transition to hypothyroidism in patients with GD is commonly encountered in clinical practice, conversion of primary hypothyroidism to GD is a rare event and is described here. Clinical Case: We describe the case of an 81-year-old female with primary hypothyroidism diagnosed more than 10 years ago. She was briefly treated with desiccated thyroid which was later changed to levothyroxine, and she remained euthyroid for several years on Levothyroxine 88 mcg daily. In 05/2021 her routine blood test showed suppressed TSH of less than 0.01uIU/mL for the first time, and it remained consistently low with elevated free T4 & T3 levels despite gradually reducing levothyroxine dose. Patient also started to have tremors, weight loss and anxiety during this period. She was found to have a hypermetabolic thyroid nodule during a PET-CT for evaluation of newly diagnosed Gastrointestinal Stromal Tumor in 09/2022. Levothyroxine was stopped shortly thereafter, but the hyperthyroid labs persisted, following which TSAb levels were obtained and found positive. She was started on methimazole 10 mg twice daily, which resulted in symptomatic improvement and marked reduction of T3 & T4 levels in one month. Clinical lessons: Over-replacement is the most common cause of hyperthyroid symptoms in patients receiving thyroid hormone replacement. Primary hypothyroidism is usually a permanent condition requiring lifelong therapy. Conversion of this condition to GD is a rare entity and can be missed in clinical practice by being mistaken for levothyroxine over-replacement. Proposed mechanisms for conversion of long-standing hypothyroidism to hyperthyroidism include fluctuating levels of TBAbs and TSAbs, spontaneous development of autoimmunity and rarely, production of TSAbs in patients with established Hashimoto’s thyroiditis. Another proposed theory is initial hypothyroidism due to extensive autoimmune gland damage in patients with GD who later develop hyperthyroidism after tissue recovery. It should be noted that this transition to GD has been reported to occur even 30 years after the diagnosis of hypothyroidism. Thus in patients with well-established hypothyroidism requiring lower thyroid replacement doses than before, and labs showing persistent hyperthyroid picture with no evident cause, a careful evaluation is required to check for conversion to GD in order to start appropriate treatment at the earliest.
Presentation: Friday, June 16, 2023
Title: FRI565 Spontaneous Conversion Of Long-standing Hypothyroidism To Grave’s Disease: A Case Report
Description:
Abstract
Disclosure: M.
Dominic: None.
M.
Shakir: None.
A.
Kakkar: None.
O.
Z.
Syed: None.
A.
Sood: None.
D.
A.
Alvarez: None.
Introduction: Autoimmune thyroid diseases associated with IgG4 include Hashimoto’s thyroiditis (HT) and Graves’ disease (GD).
HT involves a combination of antibody-mediated thyroid gland destruction and inhibition of thyroid hormone production through a predominance of TSH receptor-blocking antibodies (TBAb).
GD is due to increased thyroid hormone production in response to thyroid-stimulating antibodies (TSAb).
Although transition to hypothyroidism in patients with GD is commonly encountered in clinical practice, conversion of primary hypothyroidism to GD is a rare event and is described here.
Clinical Case: We describe the case of an 81-year-old female with primary hypothyroidism diagnosed more than 10 years ago.
She was briefly treated with desiccated thyroid which was later changed to levothyroxine, and she remained euthyroid for several years on Levothyroxine 88 mcg daily.
In 05/2021 her routine blood test showed suppressed TSH of less than 0.
01uIU/mL for the first time, and it remained consistently low with elevated free T4 & T3 levels despite gradually reducing levothyroxine dose.
Patient also started to have tremors, weight loss and anxiety during this period.
She was found to have a hypermetabolic thyroid nodule during a PET-CT for evaluation of newly diagnosed Gastrointestinal Stromal Tumor in 09/2022.
Levothyroxine was stopped shortly thereafter, but the hyperthyroid labs persisted, following which TSAb levels were obtained and found positive.
She was started on methimazole 10 mg twice daily, which resulted in symptomatic improvement and marked reduction of T3 & T4 levels in one month.
Clinical lessons: Over-replacement is the most common cause of hyperthyroid symptoms in patients receiving thyroid hormone replacement.
Primary hypothyroidism is usually a permanent condition requiring lifelong therapy.
Conversion of this condition to GD is a rare entity and can be missed in clinical practice by being mistaken for levothyroxine over-replacement.
Proposed mechanisms for conversion of long-standing hypothyroidism to hyperthyroidism include fluctuating levels of TBAbs and TSAbs, spontaneous development of autoimmunity and rarely, production of TSAbs in patients with established Hashimoto’s thyroiditis.
Another proposed theory is initial hypothyroidism due to extensive autoimmune gland damage in patients with GD who later develop hyperthyroidism after tissue recovery.
It should be noted that this transition to GD has been reported to occur even 30 years after the diagnosis of hypothyroidism.
Thus in patients with well-established hypothyroidism requiring lower thyroid replacement doses than before, and labs showing persistent hyperthyroid picture with no evident cause, a careful evaluation is required to check for conversion to GD in order to start appropriate treatment at the earliest.
Presentation: Friday, June 16, 2023.
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