Introduction
Subacute thyroiditis is a rare complication of the “novel” disease COVID-19, and it should be considered especially in the setting of persistent tachycardia without any suggestion of progression of COVID-19 and other common cardiorespiratory causes. Anterior neck pain, which can be taken as an upper respiratory tract symptom, especially in the setting of COVID-19, should not be dismissed and warrants further examination and investigation as required.
Case Description
Age 73: 2020 Nov: Referred to Samatvam Endocrinology Diabetes Center – Telemedicine Clinic for management of Thyrotoxicosis – “Supressed TSH”. Amidst the Covid pandemic in India, he developed fever and cough of 6 days duration [treated with Azithromycin, Oseltamir and Paracetamol – home care]. During the work up of this “viral” respiratory illness, he – scientist - himself “self” obtained a very wide battery of blood tests, which “incidentally” revealed suppressed TSH 0.03, next day repeat 0.02 uIU/ml with increased Free T4 1.96 ng/dl [0.89-1.76], increased Free T3 4.7 pg/ml [2.3-4.2], Total T4 9.43 ug/dl, Total T3 140 ng/dl, S Cortisol 18.2 ug/dl. Height 5 feet 5 Inches, Weight 66 Kg. PR 100/min; SPO2 95 to 98. ESR 55: There was no history of neck or throat pain or dysphagia. There was history of weight loss, palpitation and muscle cramps. Isotope Thyroid Scan was obtained, which was consistent with thyroiditis. Age 69: Prediabetes [FP Glucose 123 mg/dl; HbA1c 6.4%] and Dyslipidemia on statin and aspirin.
Assessment: Possible Covid Atypical Subacute Thyroiditis [Painless variant], with thyrotoxicosis transient.
Discussion
Retrospective data from Italy Intensive Care Units indicates that patients with COVID-19 commonly had low or suppressed serum thyroid stimulating hormone, with and without elevated free thyroxine concentrations. Possibilities included: (a) Critical illness related alterations of thyroid function tests [non-thyroidal illness syndrome] and (b) SARS-CoV-2 direct infection of the thyroid gland [unrelated to underlying thyroid autoimmunity]. Also, the mild “thyrotoxicosis” in these patients was not associated with neck pain (consistent with silent thyroiditis); they did not have leucocytosis, but had lymphopenia, as observed with COVID-19 infection. Besides this, classic subacute thyroiditis, characterised by a pathognomonic infiltration of giant cells (congregates of lymphocytes, histiocytes, and colloid), with swelling of thyroid follicles, stretching of the thyroid capsule, and consequent neck pain, has also been reported. Angiotensin-converting enzyme 2 (ACE2), the host-cell entry receptor for both SARS-CoV and SARS-CoV-2, might be partly responsible for a common pathogenic pathway. ACE2 is more highly expressed in thyroid cells than in lung cells, and in women such expression negatively correlates with signatures of immune cell enrichment. This expression profile has been suggested to explain why the most severe forms of COVID-19 pneumonia and associated thyroid dysfunction has been predominantly observed in men in the ICU retrospective study [but not in women, as in classic viral subacute thyroiditis].