Endocrine Abstracts

Background: Subacute thyroiditis (SAT) is typically a self-limiting condition, with patients usually returning to normal thyroid function after healing. However, very rarely, Graves’ disease (GD) may develop following SAT.

Case presentation: A 50-year-old female patient presented to an outside internal medicine outpatient clinic with anterior neck pain, fatigue, and subclinical fever symptoms. Her medical history included a diagnosis of psoriatic arthritis and she was receiving weekly methotrexate along with folate replacement. Firstly, the patient was given oral antibiotics that failed to relieve the symptoms. Laboratory tests revealed thyrotoxicosis [TSH: 0.096 uIU/ml (0.38-5.33 uIU/ml), fT4: 28.6 pmol/l (7.8-14.4 pmol/l), fT3: 7.9 pmol/l (3.8-6 pmol/l)]; and elevated acute phase reactants [eritrocyte sedimentation rate (ESR): 28 (0-20), C-reactive protein (CRP): 48 mg/l (0-5 mg/l)]. Both anti-thyroglobulin (Anti-Tg Ab, 602 IU/ml (0-40 IU/ml), and anti-thyroid peroxidase antibodies (Anti-TPO Ab, 28 IU/ml (0-9 IU/ml) were positive, while the thyroid stimulating immunoglobulin (TSI) was undetectable. She was then consulted to endocrinology outpatient clinic. On physical examination, she had a diffuse tender goiter and no symptoms of orbitopathy. Ultrasonographic examination revealed enlargement in the thyroid gland, and patchy heterogenous areas with decreased vascularization on color Doppler imaging, consistent with SAT. Treatment with methylprednisolone 16 mg/day was initiated, which led to instant symptom relief. The dosage was gradually reduced and the medication was eventually discontinued after 4 weeks. One month after cessation of treatment, thyroid function tests were normal. However, after an additional 2 months, the patient presented with complaints of anterior neck pain, palpitations, sweating and hair loss. Thyroid examination revealed mild tenderness, and thyroid function tests showed subclinical hyperthyroidism (TSH: 0.2 mIU/l, fT₄: 14.5 pmol/l, fT₃: 5.4 pmol/l). Both ESR and CRP levels were in normal range. However, TSI level was 1 IU/l (<0.1 IU/l), inciting a suspicion of GD. A thyroid scintigraphy was performed which demonstrated diffuse radioisotope uptake with reduced counting time. In addition, increased vascularity was observed on color Doppler imaging. The patient was therefore diagnosed with GD following SAT.

Conclusions: This case highlights the unusual onset of GD following subacute SAT. Although the pathogenic pathways have yet to be uncovered, the inflammatory environment of SAT might trigger an immunological response, resulting in the onset of GD. Clinicians must be mindful for GD in individuals with persistent hyperthyroidism after SAT remission, especially in patients with a history of other autoinflammatory disorders, as in our case.