Hypothyroidism Preceding Hyperthyroidism in a Patient with Continuously Positive Thyroid Stimulating Antibody.

Abstract

A 62-year-old womanwas initially hypothyroid and then developed hyperthyroidism with continuously positive thyroid-stimulating antibody (TSAb). Whenshe visited our hospital with the complaint of the feel of skipping beats, her serum free T4 level was initially low and thyrotropin (TSH) level was slightly elevated. One month after starting the supplement therapy with 1-T4, she developed hyperthyroidism with increased 123I-thyroid uptake. TSH-binding inhibitor immunoglobulin (TBII) was slightly elevated only during the hypothyroid stage. Throughout the whole course, TSAbwas continuously positive, while thyroid stimulation-blocking antibody (TSBAb) was not detectable. Primary hypothyroidism with TSAbmay suggest the possibility of subsequent development of hyperthyroidism. (Internal Medicine 34: 247-250, 1995)

Primary Hyperparathyroidism Presumably Caused by Chronic Parathyroiditis Manifesting from Hypocalcemia to Severe Hypercalcemia

“…All five cases presented clinically as primary hyperparathyroidism. The clinical course of our case is considered to have initially started as hypofunction, as in Hashimoto's disease, then to gradually have changed to hyperfunction as in Graves' disease, similar to autoimmune abnormalities often observed in the thyroid gland (5)(6)(7)(8)(9)(10)(11)(12)(13). Further similar case reports are required to analyze the details of the pathogenic mechanism of the parathyroid dysfunction associated chronic parathyroiditis.…”

Conversion of Primary Hypothyroidism to Hyperthyroidism: A Case Report

“…Alternatively, TBAb activity falls below the activity of TSAb, and a 'switch' occurs, often mediated by diminishing thyroid autoantibody levels secondary to antithyroid medications. 9 It is well-documented in literature that the incidence rate of agranulocytosis with thionamides is 0.1-0.5%. 10 Thionamides remain the first-line treatment option for hyperthyroidism, and their mechanism of action involves inhibiting the thyroid peroxidase enzyme which decrease the production of T3 and T4.…”

“…7 It is important to note that treatment with thyroxine can lead to an increase in ongoing antibody action or induce the production of TSAb in patients who may or may not have thyrotropin receptor blocking antibodies (TBAb). 9 It has been proposed that this could be due to a rise in serum T4 with replacement therapy, leading to an increased expression of stimulatory molecules that initiate antibody production. Alternatively, TBAb activity falls below the activity of TSAb, and a 'switch' occurs, often mediated by diminishing thyroid autoantibody levels secondary to antithyroid medications.…”

Thyrotrophin receptor antibody characteristics in a woman with long‐standing Hashimoto's who developed Graves' disease and pretibial myxoedema

“…The basis for an immunological paradigm shift in this subject is still unclear. The reports of patients with HT converting to GD do not provide a clear explanation as to the mechanism involved . However, immunological paradigm shifts do occur in pregnancy and iatrogenic immune modulatory states such as the ‘immune reconstitution syndrome’ seen with lymphocyte depleting agents like Alemtuzumab .…”

“…Hashimoto's thyroiditis (HT) and Graves' disease (GD) are two ends of the spectrum of autoimmune thyroid disease (AITD) – immune‐cell‐mediated thyroid follicular destruction primarily causing HT and antibody‐mediated TSH receptor (TSHR) activation causing GD . Reports of the two diseases occurring sequentially in the same patient are rare . The paucity of such reports probably reflects the uncommon nature of this conversion, publication bias notwithstanding.…”