Endocrine Abstracts

Introduction

Thyroid autoimmunity comprises a dynamic entity and may manifest with different forms over the course of time at the same patient, thus causing fluctuations in thyroid functionality. Hereby, we present the case of a patient treated for hypothyroidism of autoimmune etiology, who developed hyperthyroidism accompanied by an excess of thyrotropin receptor autoantibodies (TRAb) and was followed by multiple swings in the thyroid state over an 1.5-year period of time.

Case report

A 36-year old smoking female patient receiving supplementation therapy with levothyroxine 88 µg in terms of chronic hypothyroidism presented for endocrinological evaluation due to newly detected symptomatic hyperthyroidism. She reported no signs/symptoms of orbitopathy. The neck ultrasound revealed a pattern typical of autoimmune thyroiditis with diffuse heteroechogenicity and inhomogeneity accompanied by elevated blood flow; the adjunctive laboratory evaluation showed an excess of thyroid autoantibodies and TRAb-titers of 23 IU/l (reference range <2). As a diagnosis of thyrotoxicosis due to Graves’ disease seemed to be confirmed, levothyroxine was paused and the patient was started on methimazole 15 mg daily but developed in 6 weeks overt hypothyroidism. Due to the rapid manifestation of iatrogenic hypothyroidism a switch of diagnosis to a possible rare variant of late-onset hashitoxicosis with elevated thyrotropin-receptor blocking autoantibodies was presumed. The thyrostatic therapy was paused and the patient became euthyroid in one month. The euthyroid state persisted over the next 5 months, but a relapse of subclinical hyperthyroidism with partially suppressed TSH and a new onset of hyperthyroid symptoms were manifested and a low dose of methimazole (2.5 mg daily) was prescribed. Euthyroidism was restored in one month and mild subclinical hypothyroidism developed 2 months later. A cessation of methimazole led to moderate subclinical hyperthyroidism relapse without thyroid specific symptoms. The patient underwent thyroid scintigraphy, which showed a pattern typical of Graves’ disease. As euthyroidism was automatically restored after scintigraphy performance the patient remained without thyroid specific medication and is actually clinically and biochemically euthyroid.

Conclusion

Thyroid dysfunction due to autoimmunity has a potential of multiple swings and manifestations, possibly due to the switch of relative activity of thyroid related autoantibodies, thus causing unexpected fluctuations from hypo- to hyperthyroidism and vice versa. Although these swings do not represent the typical pattern of autoimmune thyroid disorders they should always be taken into account as they may trigger rapid changes in the thyrometabolic state and influence the path to diagnosis confirmation and subsequent choice of medical treatment.