Post-Acute-COVID-19-Illness-Induced Endocrinological Sequelae
Editorial
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].
In conclusion, new or incident diagnosis in the post- acute-COVID-19-illness phase for a specific condition, such as endocrinological sequelae might be due to an exacerbation of a pre-existing condition in patients who did not receive medical care within the months of window period created by the continuous enrollment criteria in the studies, whereas the group with no-pre-existing comorbidities might have been misclassified. Some physicians might have underestimated some clinically significant outcomes during early COVID-19 pandemic.
References
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Gentile S, Strollo F, Mambro A, Ceriello A (2020) COVID-19 ketoacidosis and new-onset diabetes : Are there possible cause and effect relationships among them ? Diabetes Obes Metab 22(12): 2507-2508.
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Salvio G, Claudio G, Francesca F, Stefano L, Giancarlo B et al. (2020) Bone metabolism in SARS-CoV-2 disease: possible osteoimmunology and gender implications. Clin Rev Bone Miner Metab.
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Yang JK, Lin SS, Ji XJ, Guo LM (2010) Binding of SARS coronavirus to its receptor damages islets and causes acute diabetes. Acta Diabetol 47(3): 193-199.
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Di Meglio LA, Evans Molina C, Oram RA (2018) Type 1 diabetes. Lancet 391(10138): 2449-2462.
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Ruggeri RM, Campenni A, Siracusa M, Frazzetto G, Gullo D (2021) Subacute thyroiditis in a patient infected with SARS-CoV2 : an endocrine complication linked to the COVID-19 pandemic. Hormones (Athens) 20(1): 219- 221.
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