Abstract

Abstract Introduction Postpartum thyroiditis is a form of destructive thyroiditis. It is thought to originate from an autoimmune mechanism that develops within one year of parturition. The condition results in inflammation of the thyroid resulting in damage to the thyroid follicles and release of previously stored thyroid hormone. There are only a handful of documented cases of postpartum thyroiditis associated with SARS CoV-2. Since the onset of COVID-19 a multitude of thyroid abnormalities have been associated with the virus. Case Summary A 33-year-old female, 5 months post-partum with a medical history significant for hypertension presents to the clinic for evaluation of hyperthyroidism. She tested positive for SARS-CoV-2 eleven days prior to delivering her child. Her pregnancy was only complicated by chronic hypertension. COVID-19 infection was symptomatic for mild respiratory symptoms. She had no history of hypo or hyperthyroidism prior to or during her pregnancy. At presentation, patient was largely asymptomatic with a physical exam significant only for sinus tachycardia. Laboratory tests done two weeks before her visit, were significant for a suppressed TSH <0.001 uIU/mL (reference range: 0.450- 4.50) and a mildly elevated Free T4: 1.84 NG/dL (reference range: 0.82-1.77) and T3: 139 NG/dL (reference range: 71-180). We repeated the tests and noted a recovering TSH of 0.110 uIU/mL; a low Free T4: 0.77 NG/dL and T3: 66 NG/dL. Thyroglobulin level was found to be elevated at 742.6 IU/mL (reference range 0.0-0.9). Thyroid Stimulating Immunoglobulin level was <0.10 IU/L (Normal- 0.00-0.55) and serum thyrotropin receptor Ab <1.10 IU/L (Normal- 0.00-1.75). Radioactive iodine uptake & scan was deferred as patient was breast-feeding at the time. As our patient was asymptomatic, she was prescribed only propranolol for her tachycardia. Discussion Documented cases of post-partum thyroiditis associated with SARS-CoV-2 infection are far and few. Post-partum thyroiditis is characterized by an initial thyrotoxic phase followed by hypothyroid phase and then a recovery period. Most patients are only mildly symptomatic during the initial hyperthyroid phase. At the time of referral to our clinic, the patient was already entering a hypothyroid state. She was asymptomatic at the time and therefore treated with expectant management only. COVID-19 has been identified as a cause of subacute post-infectious thyroiditis. It is known to be associated with a hyperinflammatory state characterized by a cytokine storm. Elevation of these cytokines can contribute to thyroid dysfunction. Conclusion It is hard to say whether our patient's acute thyroiditis was secondary to postpartum thyroiditis, subacute thyroiditis secondary to COVID-19 infection, or a combination of both factors. However, regardless of etiology it is important to note a possible correlation of post-partum thyroiditis in the setting of a SARS-CoV-2 infection. It is necessary to identify all cases of COVID-19 infection that can be associated with thyroid dysfunction. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

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