Thyroiditis: A Potential Complication of COVID-19 Infection

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.

Persistent Primary Hyperparathyroidism Secondary to Unusual Location of an Ectopic Parathyroid Adenoma

Introduction: Persistent hyperparathyroidism (PHPT) is diagnosed by persistent hypercalcemia in the 6 months following primary parathyroidectomy. With a success rate of roughly 95%, failure of initial surgical exploration points to the possibility of an ectopic gland. High cervical parathyroid adenomas, known as undescended adenomas, occur with a frequency of less than 0.1% and account for 7% of failed parathyroidectomies. Case Description: A 33-year-old female presented with anxiety, panic attacks, fatigue, insomnia, joint pain, constipation, palpitations, polyuria and polydipsia. She had previous history of COVID-19, hyperlipidemia, vitamin D deficiency, and prediabetes. Vital signs were stable. Her physical exam was unremarkable with no thyromegaly, thyroid nodules or palpable neck masses. Initial labs were significant for elevated serum calcium (SCa) at 11.9 mg/dl, 24 hour urine calcium at 318 mg/24 hr and parathyroid hormone (PTH) at 284 pg/ml. All indicative of primary hyperparathyroidism. Preoperative SPECT-CT and ultrasound showed an enlarged right-sided nodule inferior to the thyroid gland. During the initial parathyroidectomy, the suspicious nodule was resected along with three presumed parathyroid glands and cervical lymph nodes. Intraoperative PTH was 234 and 1001 pg/ml. Pathology indicated bilateral benign inferior parathyroids, benign thyroid tissue, and fibroadipose tissue. The patient continued to have persistently elevated SCa at 11.1 mg/dl. Repeat parathyroid scintigraphy was equivocal to the initial scan. A second cervical exploration with right thyroid lobectomy and carotid sheath exploration failed to treat the persistent hypercalcemia. CT neck with contrast performed shortly after second exploration demonstrated an active lymph node versus undescended parathyroid gland inferior to the right submandibular gland. During a follow up appointment, a fine needle aspiration showed parathyroid tissue. After this intervention, the SCa returned to a normal level of 9.1mg/dl and patient’s symptoms resolved. Interestingly, the submandibular adenoma biopsy led to resolution of PTH secretion. This adenoma was eventually removed surgically and pathology confirmed necrosis, likely secondary to the biopsy. Discussion: Ectopic parathyroid adenomas above the carotid bifurcation are a rare cause of PHPT. This case is both unique due to the etiology and resolution of this patient’s PHPT. Recent literature focuses on the multimodal imaging approach to identify cervical ectopic adenomas;however, this case illustrates there may be a role for biopsy in both the diagnosis and potential treatment of submandibular parathyroid adenomas.