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A new global registry has been established to collect data on patients with COVID-19-related diabetes. Emerging evidence suggests that COVID-19 may actually trigger the onset of diabetes in healthy people.
A notice about the CoviDiab registry was published online June 12 in a letter to the editor in the New England Journal of Medicine by Francesco Rubino, MD, King’s College London, UK, and a panel of diabetes experts from Europe, Australia, and the United States.
“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 represents classic type 1, type 2, or possibly a new form of diabetes,” said Rubino in a press release from his institution.
Not everyone agrees, however, that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus triggers diabetes in people who did not have it before getting COVID-19.
“There is no robust data yet to indicate that COVID-19 causes new diabetes,” Riyaz Patel, MBBS, a cardiologist at University College Hospital, London, UK, told the UK Science Media Center.
Lora Heisler, PhD, of the University of Aberdeen, UK, agrees, but she said: “This registry is a great first step in trying to answer the question of…whether the diabetes is actually new…because some people may have [had] undiagnosed diabetes.”
Rubino and colleagues say their goal “is to establish the extent and phenotype of new-onset diabetes that is defined by hyperglycemia, confirmed COVID-19, a negative history of diabetes, and a history of a normal glycated hemoglobin level.”
Evidence for Potential Diabetogenic Effect of SARS-CoV-2 Virus
The authors point out that a bidirectional relationship has been observed between COVID-19 and diabetes. On the one hand, the presence of diabetes is associated with increased COVID-19 severity.
But in addition, new-onset type 1 and type 2 diabetes have been reported, as have severe metabolic complications of pre-existing diabetes, including diabetic ketoacidosis and hyperosmolarity requiring exceptionally high insulin doses.
One theory as to how the SARS-CoV-2 virus could trigger diabetes is through binding to angiotensin-converting enzyme 2 (ACE2) receptors in key metabolic organs and tissues, including pancreatic beta cells and kidneys.
There are also several precedents for viral triggering of ketosis-prone diabetes, including other coronaviruses.
“In the aggregate, these observations provide support for the hypothesis of a potential diabetogenic effect of COVID-19, beyond the well-recognized stress response associated with severe illness,” Rubino and colleagues say.
“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 risk of future diabetes,” added Paul Zimmet, MD, PhD, professor of diabetes at Monash University in Melbourne, Australia, and a co-lead investigator in the CoviDiab registry project.
“By establishing this global registry, we are calling on the international medical community to rapidly share relevant clinical observations that can help answer these questions,” Zimmet added.
“Given the very short history of human infection with SARS-CoV-2, an understanding of how COVID-19–related diabetes develops, the natural history of this disease, and appropriate management will be helpful,” say the researchers.
At a later point, the registry will be expanded to include patients with pre-existing diabetes who present with severe acute metabolic disturbance.
Rubino has reported receiving grants from Ethicon and Medtronic, personal fees from GI Dynamic, Keyron, Novo Nordisk, Ethicon, and Medtronic.
N Engl J Med. Published online June 12, 2020. Letter
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