It was previously determined that diabetic carriers are disproportionately affected by SARS-CoV-2 but new research indicates that the devastating virus might actually create more cases of type 1 and type 2 diabetes—two afflictions that evidence several key differences with one another.
For a start, type 1 diabetes sufferers cannot produce insulin, while type 2 diabetes sufferers fail to properly respond to insulin. This primary distinction is important to diagnosis, treatment, and prognosis. All of these factors heighten research devoted to the progression of COVID-19.
Evidence intimates that the coronavirus not only makes diabetes worse, but it also may cause people to develop the disorder.
“Diabetes is one of the most prevalent chronic diseases and we are now realizing the consequences of the inevitable clash between two pandemics. Given the short period of human contact with this new coronavirus, the exact mechanism by which the virus influences glucose metabolism is still unclear and we don’t know whether the acute manifestation of diabetes in these patients represent classic type 1, type 2 or possibly a new form of diabetes,” the researchers write.
The authors of the new report arrived at their conclusion after reviewing a registry established to track diabetes patients diagnosed with COVID-19.
Consistently, coronavirus transmission compounded outcomes associated with type 1 and type 2 diabetes and caused more people to develop either in addition to a potential new form of the disorder. Between 20 and 30 percent of all COVID-19 related mortalities were also found to have diabetes.
“Diabetes is one of the most prevalent chronic diseases and we are now realizing the consequences of the inevitable clash between two pandemics,” explained Francesco Rubino, a co-author from King’s College London, in a press statement.
Patients who do not produce sufficient amounts of insulin become susceptible to many of the illnesses linked to severe COVID-19 prognoses, like heart disease and renal failure.
This explains the exacerbated scenarios in previously diagnosed diabetic patients after infection. However, this does not explain the elevated diabetes cases that follow coronavirus contraction. Sadly, even researchers are halved over possible explanations.
One theory suggests the process by which the ACE-2 protein binds to SARS-Cov-2 allowing the virus to infect host cells dually sets off a chain reaction of dysfunctions in glucose metabolism. A similar pathology has been noted in other viral infections studied to facilitate type 1 diabetes.
“We don’t know whether the acute manifestation of diabetes in these patients represents classic type 1, type 2 or possibly a new form of diabetes,” Dr. Rubino continues.
“We don’t yet know the magnitude of the new-onset diabetes in COVID-19 and if it will persist or resolve after the infection; and if so, whether or not or COVID-19 increases the risk of future diabetes,” Prof. Paul Zimmet from Monash University in Melbourne added.
Already, academicians around the globe have expressed their intent to uncover the mechanisms staffing the bi-directional relationship shared between COVID-19 and diabetes.
The new letter published in The New England Journal of Medicine was signed by 17 medical experts.
CW Headley is a reporter for the Ladders and can be reached at firstname.lastname@example.org