Attapon Cheepsattayakorn^1,2*, Ruangrong Cheepsattayakorn³ and Prajak Boonjitpimol¹

¹Faculty of Medicine, Western University, Pathumtani Province, Thailand
²10^th Zonal Tuberculosis and Chest Disease Center, Chiang Mai, Thailand
³Department of Pathology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand

*Corresponding Author: Attapon Cheepsattayakorn, 10^th Zonal Tuberculosis and Chest Disease Center, Chiang Mai, Thailand.

Received: June 28, 2021 ; Published: July 09, 2021

Endocrinological sequelae in post-acute-COVID-19 phase may be caused by iatrogenic complications, immunological and inflammatory damage, and direct SARS-CoV-2 (COVID-19) invasion, including apparently pre-existing diabetes mellitus during acute COVID-19 phase and can be long-term treated with antidiabetic agents other than insulin, although initially related to diabetic ketoacidosis (DKA) [1]. Primary deficit in insulin production may be mediated by several factors, such as infection stress response accompanying peripheral insulin resistance or inflammation [1]. Thus, reversion of COVID-19-related diabetes, nor that its outcomes difference in COVID-19 long haulers is not confirmed [2]. Lasting damage of the pancreatic β cells is still not confirmed although demonstrated ACE 2 and TMPRSS2, involving in SARS-CoV-2 (COVID-19)-cell-entry expression in pancreatic β cells [3]. Interruption of anabolic or antiresorptive agents, vitamin D insufficiency, exposure to corticosteroids, immobilization, and bone demineralization associated with systemic inflammation are also the COVID-19 risk factors [2]. Patients with newly diagnosed diabetes mellitus in the absence of traditional risk factors for type 2 diabetes should be performed serologic testing for type 1 diabetes-related autoantibodies repeated post-prandial C-peptide measurements at the follow-up, while patients with such risk factors can be similarly treatable to ketosis-prone type 2 diabetes [4]. New-onset Graves’ disease should be excluded before treating post-acute-COVID-19-illness patients with incident hyperthyroidism with corticosteroids due to SARS-CoV-2 (COVID-19)-associated destructive thyroiditis [5].

References

1. Gentile S., et al. “COVID-19, ketoacidosis and new-onset diabetes : are there possible cause and effect relationships among them?” Diabetes, Obesity and Metabolism 22 (2020): 2507-2508.
2. Salvio G., et al. “Bone metabolism in SARS-CoV-2 disease: possible osteoimmunology and gender implications”. Clinical Reviews in Bone and Mineral Metabolism (2020).
3. Yang JK., et al. “Binding of SARS coronavirus to its receptor damages islets and causes acute diabetes”. Acta Diabetologica 47 (2010): 193-199.
4. DiMeglio LA., et al. “Type 1 diabetes”. Lancet 391 (2018): 2449-2462.
5. Ruggeri RM., et al. “Subacute thyroiditis in a patient infected with SARS-CoV2: an endocrine complication linked to the COVID-19 pandemic”. Hormones (Athens) 20 (2021): 219-221.

Citation

Citation: Attapon Cheepsattayakorn., et al. “Endocrinological Sequelae-Associated Post-Acute-Covid-19-Illness ”. Acta Scientific Microbiology 4.8 (2021): 17-18.

Copyright

Copyright: © 2021 Attapon Cheepsattayakorn., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.