Palpitations and Fatigue Post COVID: A Harbinger of Silent Thyroiditis!

Background: Subacute thyroiditis is a self-limiting condition brought about by an inflammatory reaction often linked to a recent viral infection. SARS-COV2 (COVID-19), an RNA coronavirus that started a global pandemic in December 2019 has been linked mostly to severe acute respiratory distress syndrome. However, there have been increasing reports of its effect on other organ systems. We present a case of a 32-year-old female recovering from COVID-19, only to develop silent thyroiditis afterwards. Clinical Case: A 32-year-old female with anxiety disorder but otherwise in excellent health was diagnosed with COVID-19 via nasal swab RT-PCR after experiencing low grade fever and cough. She quarantined at home and was on her way to recovery when, a few weeks later, she began to experience increasing bouts of chest pain with no relation to activity, intermittent headaches and lower extremity edema. This prompted her to visit the emergency department. Work-up done at that time was unremarkable and her symptoms were attributed mostly to anxiety. She was advised to follow-up as an outpatient with a cardiologist. One month later, due to the persistence of her fatigue, low exercise tolerance and tremors, she decided to seek consult with a cardiologist. An electrocardiogram done during that visit showed normal sinus rhythm with poor-R wave progression and early repolarization changes. Both the echocardiogram and 24-hour Holter monitoring, which were subsequently done, were unremarkable. Blood work-up, however, revealed a significantly low thyroid stimulating hormone (TSH) level of 0.17 mU/L, for which she was referred to an endocrinologist. A month later, she sought consult with an endocrinologist. Thyroid gland was non-tender on palpation. Repeat blood work-up showed an elevated TSH level (23.50 mU/L) with a low Free T4 (0.42 ng/dL) and an elevated thyroid peroxidase antibody (TPO-Ab) level (900 mU/mL), indicative of subacute thyroiditis, but without associated neck pain. Thyroid sonography done showed diffusely heterogeneous thyroid lobes with no evidence of a dominant mass or nodule. A decision was made to start her on low dose levothyroxine. Two months into treatment, she underwent repeat thyroid hormone levels. Normal TSH and normal free T4 were observed. However, TPO-Ab was still elevated. It was decided to continue her therapy for one more month before gradually tapering her levothyroxine dose. She was told to follow-up in a month for further monitoring. Conclusion: Subacute thyroiditis associated with COVID-19 infection has become a more common occurrence as more cases of COVID-19 are noted worldwide. Our patient followed the usual course of subacute thyroiditis, initially presenting with a thyrotoxicosis phase which typically lasts 4-10 weeks, then subsequently developing hypothyroidism, inadvertently needing thyroid hormone replacement. What made this case more intriguing was that she did not have severe anterior neck pain, the classic clinical presentation of subacute thyroiditis. While there is a very strong association between COVID-19 and respiratory failure, there is paucity of evidence linking COVID-19 to dysfunction of other body systems. This case of thyroiditis presenting post COVID-19 illness, buttresses the versatility of COVID-19. Physicians should keep this in mind when evaluating a COVID-19 survivor who continue to present with persistent tachycardia or palpitations with or without anterior neck pain even after a month or two from infection. Routine follow-up TSH assay on COVID-19 survivors may be a valuable consideration.