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Background: Although SARS-CoV-2 virus infection has been reported to cause subacute thyroiditis, the mRNA vaccine for SARS-CoV-2 is suspected to induce thyroiditis with thyrotoxicosis. Case Report: : We describe 3 patients with no history of thyroid disease who presented with symptomatic, biochemical, and radiological evidence of thyroiditis with thyrotoxicosis, 10 to 20 days after receiving either Pfizer Bio-NTech or Moderna COVID-19 mRNA vaccines. All patients presented with thyrotoxicosis but with negative thyroid-stimulating immunoglobulins for Graves disease and no autonomous nodules. Two patients underwent thyroid uptake scans that confirmed thyroiditis. One patient had significantly increased erythrocyte sedimentation rate and interleukin-6. All patients showed improvement in symptoms with nonsteroidal anti-inflammatory drugs, and 1 patient eventually required steroids for symptom control. Discussion: The mRNA vaccine for SARS-CoV-2 was associated with thyroiditis and led to thyrotoxicosis. Elevated proinflammatory markers and cytokines after vaccines may play a major role. Conclusion: Our case series report highlights a possible relationship between the COVID-19 mRNA vaccine and thyroiditis with thyrotoxicosis, which has not been recognized by health providers.
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Hypoparathyroidism is usually caused by postsurgical or autoimmune damage to the parathyroid gland. We present the case of a 46-year-old Hispanic male with no significant past medical history who was admitted to the hospital with hypoxic respiratory failure due to coronavirus disease 2019 (COVID-19) infection and had a prolonged hospital course. He was incidentally found to have hyperphosphatemia and low parathyroid hormone (PTH) levels. During the second month of hospitalization, his phosphorus levels rose to 6.9 mg/dL (normal range: 2.4-4.7 mg/dl). His PTH levels were found to be at 8 pg/mL. Vitamin D levels obtained were also low (7 ng/dL), phosphorus was at 5.8 mg/dL with albumin of 2.9 g/dL, and calcium level was normal at 9.2 mg/dl. Parathyroid hormone-related peptide (PTHrP) level was low at 10. Malignancy and genetic causes were ruled out. The patient was started on 50,000 units of ergocalciferol once a week. He was also started on calcium acetate 1,334 mg three times a day for hyperphosphatemia. Phosphorus levels remained elevated, and sevelamer was added on discharge after he was weaned off oxygen and cleared by physical therapy. No explanation for persistent hyperphosphatemia and hypoparathyroidism was found. To date, there have been some reports linking severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to widespread tissue injury; however, there have been no reports so far on the effect of the parathyroid gland. Further studies are necessary to elaborate and to confirm the causative relationship between SARS-CoV-2 and hyperphosphatemia.
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OBJECTIVE: The objective of this report was to emphasize the early recognition of thyrotoxicosis in the assessment of a pediatric patient with tachycardia. We present here the case of a 17-year-old female who presented with supraventricular tachycardia and was found to be in a state of severe thyrotoxicosis with borderline features of a thyroid storm. METHODS: A 17-year-old African American female presented to the hospital with complaints of nausea, vomiting, and diarrhea associated with palpitations for 1 week. Initial workup included electrocardiogram, total blood count, lipase, basic metabolic panel, and thyroid function tests. RESULTS: Initial vital signs were significant for a temperature of 100.1°F, and tachycardia with a heart rate (HR) of 180 beats per minute (bpm). Initial telemetry was significant for supraventricular tachycardia with a HR of 180 bpm. Vagal maneuvers including carotid sinus massage were attempted first followed by 6 mg intravenous (IV) push and then 12 mg IV push of adenosine. However, the patient remained tachycardic with a HR in the 150s. Laboratory evaluation confirmed the presence of thyrotoxicosis with a thyroid-stimulating hormone of 0.17 µIU/mL (normal, 0.5 to 4.7 µIU/mL) with a free thyroxine of 4.90 ng/dL (normal, 0.8 to 2.0 ng/dL) and free triiodothyronine >20 pg/mL (normal, 1.95 to 5.85 pg/mL). She was subsequently treated with propranolol, methimazole, and hydrocortisone, which resolved her symptoms in a few hours. CONCLUSION: Due to high mortality rates, severe thyrotoxicosis needs to be recognized and treated early. This case report highlights the importance of early recognition of thyrotoxicosis in the initial management of tachycardia in the pediatric population.