COVID-19 may trigger Graves’ disease relapse, subacute thyroiditis
Approximately 15% of patients with mild to moderate COVID-19 have thyroid dysfunction, and SARS-CoV-2 may directly affect thyroid morphology and function, worsening preexisting autoimmune thyroid disease, data from a review show.
In a review of literature published from January 2019 to February 2021 assessing thyroid dysfunction and COVID-19, researchers also found that preexisting autoimmune thyroid disease appears unlikely to make adults more vulnerable to COVID-19; however, some reports documented relapse of Graves’ disease or newly diagnosed Graves’ disease about 1 month after SARS-CoV-2 infection.
“Mild COVID-19 infection is not, at present, thought to affect thyroid function; however, up to 10% of severe cases have been associated with thyroid disorders, primarily hyperthyroidism, both overt and subclinical forms,” Leonidas H. Duntas, MD, PhD, professor of endocrinology and internal medicine at Evgenideion Hospital and the University of Athens, Greece, told Healio. “Moreover, approximately 10% of patients admitted to intensive care showed atypical subacute thyroiditis characterized by transiently high free thyroxine, normal free triiodothyronine and low thyroid-stimulating hormone. The course of atypical subacute thyroiditis in the setting of COVID-19 is usually mild and only in a few cases is corticosteroid treatment needed.”
Duntas and colleagues found that COVID-19 may worsen autoimmune thyroid disease through its effects on the immune system and may result in the development of cytokine storm. However, it is still uncertain whether patients with autoimmune diseases are at increased risk for a worse disease outcome, although those receiving immune modulatory treatment appear not to be at greater risk.
“The possibility that thyroid dysfunction may also increase susceptibility to COVID-19 infection deserves further investigation,” the researchers wrote. “While COVID-19 is associated with nonthyroidal illness, it is not clear whether it also increases the risk of the development of autoimmune hypothyroidism. Recent data illustrate the importance of thyroid hormone in protecting the lungs from injury, including that associated with COVID-19.”
Thyroid function is not routinely assessed in the context of COVID-19 infection, and more frequent thyroid function testing is considered to be reasonable, the researchers wrote. Adults with Graves’ disease and COVID-19, particularly during the acute stage of their autoimmune disease, or who are receiving long-term treatment with antithyroid drugs, “should be carefully monitored,” as aggravation of either or both diseases is possible.
Duntas said relapsed Graves’ disease or Graves’ disease induced by the virus has been reported in temporal sequence with COVID-19. Hypothyroidism has been reported less frequently, at about 5%, and mainly occurs in those who are admitted to hospital but not to the ICU, he said. Liothyronine in an inhaled form was shown to speed recovery from severe acute respiratory syndrome in two patients hospitalized with COVID-19.
“Approximately 15% of patients with mild to moderate COVID-19 were observed to have thyroid dysfunction,” Duntas told Healio. “The more severe the infection, the lower the TSH and the T3 levels. The latter has been proposed as a biomarker of prognosis for COVID-19. Patients with thyroid diseases and comorbidities have worse outcome of COVID-19 infection, but not when the adjustment for the comorbidities was performed, clearly indicating that the underlining diseases may increase the risk rather than the thyroid disease, per se. Monitoring of thyroid function in moderate-severe COVID-19 patients is advisable.”
Duntas said more research is needed to identify vulnerable thyroid patient groups so that preventive measures, therapeutic intervention and long-term monitoring can be implemented.
“We must clarify whether the viral infection targeting the thyroid gland is influenced by patients’ susceptibility and disease history and further evaluate T3 as an inhaled medication for patients with severe lung injury,” Duntas said. “There is some hope that T3 can be applied as COVID-19 targeting drug.”
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Leonidas H. Duntas, MD, PhD, can be reached at firstname.lastname@example.org.