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Year : 2020  |  Volume : 17  |  Issue : 2  |  Page : 97-98

COVID-19 and thyroid

1 Department of Endocrinology, Sri Ramachandra Medical College and Research Institute, Chennai, Tamil Nadu, India
2 Dr. Chauhan's Clinic, Jabalpur, Madhya Pradesh, India
3 Consultant Endocrinologist, Sri Gokulam Medical College, Trivandrum, Kerala, India

Date of Submission22-Mar-2020
Date of Acceptance23-Mar-2020
Date of Web Publication01-Jul-2020

Correspondence Address:
Dr. Karthik Balachandran
Department of Endocrinology, Sri Ramachandra Medical College and Research Institute, Porur, Chennai, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/trp.trp_15_20

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How to cite this article:
Balachandran K, Chauhan VS, Shenoy M. COVID-19 and thyroid. Thyroid Res Pract 2020;17:97-8

How to cite this URL:
Balachandran K, Chauhan VS, Shenoy M. COVID-19 and thyroid. Thyroid Res Pract [serial online] 2020 [cited 2022 Aug 14];17:97-8. Available from: https://www.thetrp.net/text.asp?2020/17/2/97/290005

The coronavirus (CoV) (severe acute respiratory syndrome [SARS]-CoV-2) has taken the world by storm. From humble origins in China's wet meat markets, the virus has crashed even the biggest stock markets. Every special group has only one question in mind “What does this virus mean to me?” From a thyroid point of view, little is known about the virus at this juncture; however, useful information can be parsed from the existing literature[1] to answer two important questions – the effect of the thyroid on virus (susceptibility) and the effect of the virus on the thyroid.

Patients with thyroid disease, either hyperthyroidism or hypothyroidism, are not at increased risk of contracting the virus or developing complications. Neither thyroxine nor antithyroid drugs alter this risk, as they are not immunomodulators.

While autopsy studies of patients with COVID-19 (the recognized term for CoV infection) are lacking, autopsy studies of SARS-CoV-1-affected patients show no involvement of thyroid follicular cells.[2] The virus is confined to the blood vessels that course through thyroid and has no predilection for thyroid cells per se direct viral effect on the thyroid, therefore seems unlikely. However, this does not rule out the indirect effects of the cytokine storm that a serious viral illness like COVID-19 can cause. Unfortunately, the looming threat of mortality, the difficulty in distinguishing thyroid illness from nonthyroidal illness, and the lack of even intermediate-term follow-up data make it hard to predict the indirect effect of systemic inflammatory response or the treatment. However, like any other viral illness, postviral thyroiditis is possible, which the treating physician should bear in mind.

Favipiravir is another drug tried in the treatment of SARS-CoV-2 infection. Its effects on thyroid are not known. Remdesivir, a nucleotide analog used for the treatment of Ebola and Marburg viruses, has also been tried in SARS-CoV-2 infection. Its effect on thyroid is not known. Chloroquine, hydroxychlroquine, and azithromycin have been tried in COVID-19 with varying results. Chloroquine can potentially accelerate the metabolism of thyroxine and thus elevate thyroid-stimulating hormone.[3] However, this effect is likely to be modest. [Table 1] summarizes the effect of various drugs used to treat SARS-CoV-2 on thyroid.
Table 1: Effect of medications tried for COVID19 on Thyroid

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The more important issue is whether a thyroid function assessment is indicated at all for suspected viral respiratory illnesses during the COVID-19 pandemic. Indiscriminate thyroid function testing only serves to add to the confusion and should therefore be eschewed. The SARS-CoV-2 virus itself may be novel (as evidenced by the initial moniker nCoV-novel CoV), but the approach to this virus with respect to thyroid is likely same as any other virus. Sound clinical judgment should form the basis of testing and treatment.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Desailloud R, Hober D. Viruses and thyroiditis: An update. Virol J 2009;6:5.  Back to cited text no. 1
Gu J, Korteweg C. Pathology and pathogenesis of severe acute respiratory syndrome. Am J Pathol 2007;170:1136-47.  Back to cited text no. 2
Munera Y, Hugues FC, Le Jeunne C, Pays JF. Interaction of thyroxine sodium with antimalarial drugs. BMJ 1997;314:1593.  Back to cited text no. 3


  [Table 1]


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