Endocrine Abstracts

Introduction: Hashimoto thyroiditis (HT; with anti-thyroid peroxidase antibodies (TPOAb)) and Graves’ disease (GD; with TSH receptor antibodies (TRAbs)) are frequent autoimmune disorders responsible for thyroid dysfunction. There are two types of TRAbs, the ones that stimulate the thyroid (TSAb) causing Graves’ hyperthyroidism and those that block thyrotropin action (TBAb) being occasionally responsible for hypothyroidism. Unusual patients switch from TSAb to TBAb (or vice versa) with concomitant thyroid function changes.

The progression from a HT to GD is not frequent and there are only a few cases described in the literature.

Case report: A 63-year-old woman with history of obesity and depressive syndrome was referred to our department in 2006 due to increasing weigh, with a BMI 39 kg/m².

Neck ultrasonography (US) revealed thyroid nodular disease and the laboratory confirmed a HT (TPOAA +) with normal thyroid function.

After 1 year follow-up, the patient presented with subclinical hypothyroidism (TSH 11.0), initiating treatment with levothyroxine 50 μg/day. Fine needle aspiration biopsy (FNAB) of thyroid nodule was benign. During 4 years, the patient maintained a stable thyroid function under levothyroxine.

Five years after diagnosis of hypothyroidism, the patient presented a subclinical hyperthyroidism (TSH=0.01). Despite levothyroxine withdrawal, she maintained hyperthyroidism complains, with weight loss, palpitations, tremor and heat intolerance, initiating treatment with methimasol and β-blockers. After scintigraphy and TRAbs titration, the diagnosis of GD was confirmed.

Discussion: The distinction between an evolution from HT to GD or from TBAb to TSAb is very difficult. Although the presence of TPOAb suggested HT diagnosis, the concomitant presence of these antibodies with TRAbs is also frequent. Nevertheless, considering the prevalence of both condition, the first option seemed most likely. Patients with thyroid function fluctuation should be closely monitored.