Abstract
The devastating global pandemic Coronavirus disease 2019 (COVID 19) isolated in China in January 2020 is responsible for an outbreak of pneumonia and other multisystemic complications. The clinical picture of the infection has extreme variability: it goes from asymptomatic patients or mild forms with fever, cough, fatigue and loss of smell and taste to severe cases ending up in the intensive care unit (ICU). This is due to a possible cytokine storm that may lead to multiorgan failure, septic shock, or thrombosis.
Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV -2), which is the virus that causes COVID 19, binds to angiotensin-converting enzyme 2 (ACE2) receptors, which are expressed in key metabolic organs and tissues, including pancreatic beta cells, adipose tissue, the small intestine and the kidneys. Therefore it is possible to state that newly-onset diabetes is triggered by COVID 19 infection.
Although many hypotheses have clarified the potential diabetogenic effect of COVID 19, a few observations were reported during this pandemic. Two male patients admitted to us with devastating hyperglycemia symptoms were diagnosed with type 1/autoimmune diabetes mellitus within 3 months following COVID 19 infection. Autoantibodies and decreased C peptide levels were detected in these patients. We speculated that several mechanisms might trigger autoimmune insulitis and pancreatic beta-cell destruction by COVID 19 infection. We aim to raise awareness of the possible link between SARS-CoV-2 and newly onset type 1 diabetes mellitus. Further studies are needed to determine a more definitive link between the two clinical entities.
Keywords: covid 19, autoimmune diabetes mellitus, inflammation, pandemia, betacell destruction, c-peptide
Graphical Abstract
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