Thyroiditis: A Potential Complication of COVID-19 Infection

ABSTRACT

Introduction: SARS-CoV-2 causes COVID-19 disease which can affect multiple organs including the lungs, heart, gastrointestinal tract, kidneys, central nervous system, and the endocrine system. Subacute thyroiditis is commonly caused by viral etiologies and is emerging as a potential complication of COVID-19. We report herein a case of subacute thyroiditis following COVID 19 infection. Case Description A 57-year-old gentleman known to have hypertension, hyperlipidemia, and reactive airway disease, presented to the Emergency Department (ED) 10 days after testing positive for SARS-CoV-2. He reported worsening shortness of breath, chest pain, increasing cough, generalized weakness, exercise intolerance, and decreased appetite. In the ED, he was hypoxemic (SpO2=93%), afebrile (T=36.9ºC) and hemodynamically stable (BP=120/76 mmHg, HR=88bpm). Otherwise, the rest of his physical exam was unremarkable. Chest X-Ray revealed COVID-19 associated pneumonia and his COVID PCR test was positive. He had elevated liver function tests (AST 588 U/L;ALT 933 U/L;AlkPhos 819 U/L) and electrolytes imbalance were noted. The patient was admitted and treated with a course of antibiotics and steroids. Labs also exhibited suppressed TSH at 0.164 mcUnits/mL (0.350 - 5.000 mcUnits/mL), elevated free T3 at 4.3 pg/mL (2.2 - 4.0 pg/mL) and free T4 at 2.2 ng/dL (0.8 - 1.5 ng/dL), and negative anti-thyroid peroxidase antibodies, anti-thyroglobulin and TSH receptor antibodies. Upon further investigation, he reported heat intolerance, excessive sweating, and occasional tremors. He denied any personal or family history of thyroid disease as well as any amiodarone consumption. Subacute thyroiditis was diagnosed. The home medication of Beta-blocker (metoprolol) was continued and cholestyramine 4g twice daily was added to his regimen. Symptoms and free T3 and T4 levels improved and were back to normal upon discharge. Four months later, in the outpatient setting, thyroid function tests remained normal. Discussion: COVID-19 can cause simultaneous inflammatory multi-organ damage. Our patient had COVID-19 associated pneumonia, liver injury and subacute thyroiditis. Non-thyroidal illness and steroid use may affect thyroid functions and lead to suppressed TSH. In such instances, we would expect the free T3 to be low, unlike our patient’s data. Due to the wide range of organ involvement and presenting symptoms associated with COVID-19, it is not uncommon to neglect some emerging conditions while focusing and treating the more life-threatening ones. Subacute thyroiditis is a commonly overlooked complication associated with COVID-19. Its presentation can range from being asymptomatic to a full-blown thyroid storm. Untreated hyperthyroidism can cause worsening hemodynamics in COVID-19 patients. Therefore, recognizing subacute thyroiditis in such patients may prevent more severe and serious sequelae.