Subacute thyroiditis after COVID-19

We now have a good understanding of the acute complications of COVID-19, but we know less about possible long-term sequelae. The aim of this case report is to raise awareness of subacute thyroiditis as a potential complication of COVID-19.

A previously healthy man in his forties who used no regular medications was diagnosed with SARS-CoV-2 infection after a positive polymerase chain reaction (PCR) test on a nasopharyngeal swab. The infection caused mild symptoms, with a few days of fever and cough, but required no specific treatment. The man then had three weeks of good health, before gradually developing reduced general condition with fever (38.3 °C), dysphagia, headache, a mild dry cough, dyspnoea and general myalgia. Paracetamol and ibuprofen had only a brief antipyretic effect. In the out-of-hours primary care centre, he was found to have an elevated C-reactive protein (CRP) level of 88 mg/L (reference range <5), but tested negative for COVID-19. He was admitted to hospital for assessment just under six weeks after first testing positive for SARS-CoV-2.

Upon arrival at hospital, the patient was breathing normally, but was subfebrile with reduced general condition. He had a regular heart rate of 95 beats/min, blood pressure 120/80 mmHg, temperature 37.7 °C, respiratory rate 18/min and oxygen saturation of 95 %. Diffuse tenderness to palpation was noted on both sides of the throat, but there was no enlargement of the thyroid. Clinical examination was otherwise unremarkable, including a normal pharynx and no tenderness over the temples. Blood tests showed a sedimentation rate of 92 mm/hr (<10), CRP 86 (<6) mg/L, and leukocytes 11.9 × 10⁹/L (3.5–11), but otherwise normal electrolytes, kidney function, liver enzymes, D-dimer, ferritin and procalcitonin.

During his first 72 hours of observation on the ward, he developed recurrent fever with a highest measured temperature of 38.9 °C. He also complained of a sore throat and myalgia. His heart rate was persistently slightly elevated (90–100/min), but his respiratory rate was normal and his peripheral oxygen saturation (SpO₂) was 95–98 % without supplemental oxygen.

All microbiological tests were negative, including another PCR test for COVID-19, a respiratory pathogen panel, and blood cultures. Serological testing suggested previous Epstein-Barr and cytomegalovirus infections, but results were negative for Hepatitis B and C. Chest X-ray and CT sinuses were also normal.

On the patient’s second day in hospital, we began to suspect subacute thyroiditis and therefore ordered a metabolic panel. This showed thyroid-stimulating hormone (TSH) 0.01 mIU/L (0.35–3.6), FT4 (tetraiodothyronine) 27.8 pmol/L (9–19), FT3 (triiodothyronine) 7.5 pmol/L (2.6–5.7), thyroperoxidase (P-TPO) <3 (<6) and TSH receptor antibodies (TRAb) <0.9 (<1.8). The biochemical findings were thus consistent with mild hyperthyroidism, but not autoimmune thyroiditis as TPO and TRAb were both negative. An ultrasound of the neck showed slight diffuse enlargement of the thyroid gland with discrete surrounding oedema and heterogeneous parenchyma, consistent with thyroiditis. There was no evidence to suggest a thyroid abscess.

While the ultrasound findings were consistent with thyroiditis, areas of mild hyperaemia were also described. In cases of subacute thyroiditis, vascularity in the gland is typically low to normal. On the basis of the hyperaemia, plus the persistent symptoms of fever, myalgia and sore throat as well as the elevated CRP and sedimentation rate, other diagnoses such as temporal arteritis and polymyalgia rheumatica were also considered. However, the fact that the patient was under 50 years of age made these diagnoses less likely, and treatment was therefore initiated for subacute thyroiditis (1). Non-steroidal anti-inflammatory drugs had had little to no effect when used for several weeks prior to admission, and it was therefore decided to begin peroral prednisolone at a moderate dose of 20 mg × 1 (2). A response to glucocorticoid therapy is typically expected after one to three days. Our patient showed significant improvement on day two, when his CRP level fell from 92 to 35 mg/L. A detailed plan was outlined in the discharge summary for tapering prednisolone over the course of a month.

At a follow-up appointment two months later, the patient was symptom-free with normal thyroid function and negative results in tests for infectious diseases. He was not taking any medications and his general health was good. He was advised to receive further follow-up by his general practitioner, with thyroid function tests every four weeks for a minimum of four months. An additional thyroid ultrasound was considered unnecessary.