Soleimanifar N, Shamsi A, Mami S, Zolfaghari M, Assadiasl S, Rostamian A, et al . Endocrine Dysregulation in Long-COVID Era. jmciri 2025; 43 (S1) :77-89
URL:
http://jmciri.ir/article-1-3453-en.html
Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran
Abstract: (86 Views)
Background: Beyond acute pneumonia and ARDS, COVID-19 due to SARS-CoV-2 induces persistent multi-systemic sequelae. The endocrine system is particularly vulnerable because endocrine tissues (pancreas, thyroid, adrenals, hypothalamus, and gonads) express high levels of ACE2, enabling direct viral entry, and are also prone to indirect injury via rich vascularization, systemic inflammation, and endothelial dysfunction. This review synthesizes molecular and immuno-inflammatory mechanisms underlying endocrine involvement in post-COVID, with emphasis on new-onset diabetes and worsening of pre-existing diabetes.
Results: Studies indicate a significantly elevated risk of incident diabetes post COVID infection. In the pancreas, viral binding to ACE2 and activation of TMPRSS2 facilitate entry; ACE2 down-regulation tilts Ang II/AT1R signaling impairment, activating NF-κB and amplifying pro-inflammatory cytokines. In parallel, glucocorticoid therapy—while clinically indicated in severe disease—exacerbates hyperglycemia via increased hepatic gluconeogenesis, impaired peripheral insulin signaling, and reduced β-cell insulin secretion.
Conclusion: Proactive endocrine screening during post-COVID follow-up is essential to mitigate individual and societal burden.
Type of Study:
Review |
Subject:
General