Simultaneous occurrence of subacute thyroiditis and Graves' disease

Rare cases of Graves' disease occurring years after subacute thyroiditis (SAT) have been reported. Here, we present the first known case of simultaneous occurrence of Graves' disease and SAT.

A 41-year-old woman presented with 10 days of neck pain, dysphagia, and hyperthyroid symptoms. Neck pain had initially started at the base of the right anterior neck and gradually spread to her upper chest, the left side of her neck, and bilateral ears. Physical examination revealed a heart rate of 110 beats/minute and a diffusely enlarged tender thyroid gland without evidence of orbitopathy. There was a resting tremor of the fingers and brisk deep tendon reflexes. Laboratory values: thyrotropin<0.01 mcIU/mL (nL 0.39-5.33), free thyroxine 2.0 ng/dL (nL 0.59-1.60), free T3 6.6 pg/mL (nL 2.3-4.2), thyroglobulin 20.1 ng/mL (nL 2.0-35.0), thyroglobulin antibody 843 IU/mL (nL 0-80), thyroperoxidase antibody 130 IU/mL (nL 0-29), thyroid stimulating hormone receptor antibody 22.90 IU/L (nL<1.22), thyroid stimulating immunoglobulins 299 units (nL<140), erythrocyte sedimentation rate 120 mm/h (nL 0-20), and C-reactive protein 1.117 mg/dL (nL 0-0.5). Human leukocyte antigen (HLA) typing revealed DRB1, DR8, B35, B39, DQB1, DQ4, and DQ5. A thyroid ultrasound showed an enlarged heterogeneous gland with mild hypervascularity. Fine-needle aspiration (FNA) biopsies of both thyroid lobes revealed granulomatous thyroiditis. The thyroid scan showed a diffusely enlarged gland and heterogeneous trapping. There was a focal area of relatively increased radiotracer accumulation in the right upper pole. The 5-hour uptake ((123)I) was 6.6% (nL 4-15). The patient was symptomatically treated. Over the next several weeks, she developed hypothyroidism requiring levothyroxine treatment.

This case illustrates a rare simultaneous occurrence of Graves' disease and SAT. Previous case studies have shown that Graves' disease may develop months to years after an episode of SAT. A strong family history of autoimmune thyroid disorders was noted in this patient. Genetic predilection was also shown by HLA typing.

Although the occurrence of SAT with Graves' disease may be coincidental, SAT-induced autoimmune alteration may promote the development of Graves' disease in susceptible patients. Genetically mediated mechanisms, as seen in this patient by HLA typing and a strong family history, may also be involved.