Potential impacts of SARS-CoV-2 on parathyroid: current advances and trends

Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection affects several important organs including endocrine glands. Experimental studies demonstrated that the virus exploits the ACE2, a transmembrane glycoprotein on the cell surface as a receptor for cellular entry. This entry process is exclusively facilitated by other intracellular protein molecules such as TMPRSS2, furin, NRP1, and NRP2. Recent findings documented the involvement of the SARS-CoV-2 in inducing various parathyroid disorders including hypoparathyroidism and hypocalcemia, which received significant attention. This review extensively describes rapidly evolving knowledge on the potential part of SARS-CoV-2 in emerging various parathyroid disorders due to SARS-CoV-2 infection particularly parathyroid malfunction in COVID-19 cases, and post-COVID-19 conditions. Further, it presents the expression level of various molecules such as ACE2, TMPRSS2, furin, NRP1, and NRP2 in the parathyroid cells that facilitate the SARS-CoV-2 entry into the cell, and discusses the possible mechanism of parathyroid gland infection. Besides, it explores parathyroid malfunction in COVID-19 vaccine-administered cases. It also explains the possible long-COVID-19 effect on parathyroid and post-COVID-19 management of parathyroid. A complete understanding of the mechanisms of SARS-CoV-2-triggered pathogenesis in parathyroid dysfunctions may curtail treatment options and aid in the management of SARS-CoV-2-infected cases.

Automated summary

Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection affects endocrine glands, with the virus using ACE2 as a receptor for cellular entry. This review explores the potential involvement of SARS-CoV-2 in parathyroid disorders, discusses the expression of ACE2 and other molecules in parathyroid cells, and examines the long-term effects on parathyroid function and post-COVID-19 management. Understanding the mechanisms of SARS-CoV-2-triggered pathogenesis in parathyroid dysfunction is crucial for effective treatment and management of infected cases.