Genetic susceptibility to COVID-19 may increase risk for hypothyroidism
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Adults with a genetic susceptibility to COVID-19 infection may have an increased risk for hypothyroidism, according to findings from a Mendelian randomization published in Thyroid.
“Host genetic susceptibility to SARS-CoV-2 infection is associated with increased risk of overt and subclinical hypothyroidism,” Ching-Lung Cheung, PhD, associate professor in the department of pharmacology and pharmacy in the Li Ka Shing Faculty of Medicine at the University of Hong Kong, and Gloria Hoi-Yee Li, PhD, assistant professor in the department of health technology and informatics at The Hong Kong Polytechnic University, told Healio. “In the reverse direction, we do not observe any evidence supporting genetic predisposition to thyroid-related traits could alter the liability to SARS-CoV-2 infection and COVID-19 outcomes.”
Researchers collected data from the largest meta-analyses of genome-wide association studies. A bidirectional Mendelian randomization study was conducted to assess the relationship of liability to COVID-19 phenotypes with thyroid-related traits. In the forward direction, researchers assessed whether COVID-19 phenotypes had a causal effect on thyroid traits. In the reverse direction, researchers analyzed whether genetically determined thyroid traits were causally associated with COVID-19 phenotypes. The main analysis was conducted using the conventional inverse-variance weighted method. Sensitivity analyses were conducted using weight median, Mendelian randomization-Egger regression, contamination mixture and the outlier test of Mendelian randomization pleiotropy residual sum and outlier methods.
In the main analysis, having a genetic susceptibility to SARS-CoV-2 infection increased the risk for hypothyroidism (OR = 1.335; 95% CI, 1.167-1.526). Sensitivity analyses using the weight median, Mendelian randomization-Egger regression, contamination mixture and the outlier test of Mendelian randomization pleiotropy residual sum and outlier methods also found an increased risk for hypothyroidism with each doubling of SARS-CoV-2 infection genetic susceptibility.
“Host genetic liability to SARS-CoV-2 infection may increase the lifelong risk of overt and subclinical hypothyroidism,” Cheung and Li said. “It may be beneficial if physicians are aware of this possibility, such that monitoring of thyroid function and timely treatment may be arranged for individuals previously infected with SARS-CoV-2. This may alleviate the risk of undiagnosed hypothyroidism.”
No associations were observed between genetic susceptibility to hyperthyroidism, hypothyroidism and autoimmune thyroid disease and COVID-19 phenotypes. Genetically determined thyroid-stimulating hormone and free thyroxine levels in the reference range, and TSH in the full range were not associated with COVID-19 phenotypes.
Cheung and Li said prospective studies are needed to gather additional data on long-term thyroid function in adults infected with COVID-19.
“Moreover, long COVID and hypothyroidism have some common symptoms, such as fatigue, cognitive and mood problems,” Cheung and Li said. “Long-term studies are required to investigate the possible link between long COVID and thyroid function.”
For more information:
Ching-Lung Cheung, PhD, can be reached at lung1212@hku.hk.
Gloria Hoi-Yee Li, PhD, can be reached at gloria-hy.li@polyu.edu.hk.
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