03 August 2022
2 minutes reading
disclosures: The authors report no relevant financial disclosures.
Adults with a genetic susceptibility to COVID-19 infection may be at 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 an increased risk of overt and subclinical hypothyroidism”, Ching-Lung Cheung, PhDassociate professor in the Department of Pharmacology and Pharmacy of the Li Ka Shing Faculty of Medicine at the University of Hong Kong, and Gloria Hi Yee Li, PhD, assistant professor in the department of health technology and computer science at Hong Kong Polytechnic University, Healio told me. “Conversely, we see no evidence that genetic predisposition to thyroid-related traits could alter liability for SARS-CoV-2 infection and COVID-19 outcomes.”
Researchers gathered data from the largest meta-analyses of genome-wide association studies. A bidirectional Mendelian randomization study was conducted to assess the relationship of liability for COVID-19 phenotypes with thyroid-related traits. Moving forward, researchers assessed whether COVID-19 phenotypes had a causal effect on thyroid characteristics. In the reverse direction, researchers analyzed whether genetically determined thyroid characteristics were causally associated with COVID-19 phenotypes. The main analysis was performed using the conventional inverse variance weighted method. Sensitivity analyzes were performed 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 of hypothyroidism (OR = 1.335; 95% CI, 1.167-1.526). Susceptibility analyzes using the median weight, Mendelian randomization-Egger regression, contamination mixture, and the outlier test of Mendelian randomization pleiotropy residual sum and outlier methods also found an increased risk of hypothyroidism with each doubling of genetic susceptibility to SARS-CoV-2 infection.
“Host genetic liability for SARS-CoV-2 infection may increase lifetime risk of overt and subclinical hypothyroidism,” said Cheung and Li. “It may be helpful for physicians to be aware of this possibility so that thyroid function monitoring and timely treatment can be arranged for individuals previously infected with SARS-CoV-2. This may reduce 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 collect additional data on long-term thyroid function in adults infected with COVID-19.
“In addition, long-term COVID and hypothyroidism have some common symptoms, such as fatigue, cognitive and mood problems,” Cheung and Li said. “Long-term studies are needed to investigate the possible link between long-term COVID and thyroid function.”
For more information:
Ching-Lung Cheung, PhDcan be reached at firstname.lastname@example.org.
Gloria Hoi-Yee Li, PhDcan be reached at email@example.com.