A 19-year-old male patient in Kiel, Germany, was diagnosed with insulin-dependent diabetes after recovering from an asymptomatic SARS-CoV-2 infection, according to a case study published in Nature Metabolism. Although this report does not establish a causal link between COVID-19 and diabetes, the findings suggest that SARS-CoV-2 infection might negatively affect the function of the human pancreas—the organ that controls blood sugar levels.
SARS-CoV-2 enters human cells through binding the ACE2 glycoprotein, which is also found on human pancreatic β-cells. Pancreatic β-cells play a key role in insulin production, and ACE2 is known to be important for β-cell function. Several recently published studies indicate possible links between COVID-19 and diabetes, but the data are insufficient to support that COVID-19 directly causes diabetes in humans.
Matthias Laudes and colleagues describe a 19-year-old white patient admitted to the emergency department of the University Medical Centre Schleswig-Holstein with abnormal fatigue, exhaustion, excessive thirst and frequent urination. He had also lost 12 kilograms of body weight within several weeks. Blood tests revealed a loss of β-cell function among other hallmarks of diabetes. The patient had no high-risk human leukocyte antigen genotype (which predisposes people to autoimmune diseases), but he did have a genotype associated with a slightly elevated risk of autoimmune type 1 diabetes. However, the patient did not have the auto-antibodies typically seen in patients with common forms of autoimmune type 1 diabetes. The patient tested positive for immunoglobin G but not immunoglobin M antibodies against SARS-CoV-2, thus indicating that he had become infected with SARS-CoV-2 between 5 and 7 weeks before entering the hospital. Around that time, his parents had returned from a skiing trip in Austria and developed typical symptoms of COVID-19.
The patient’s high levels of haemoglobin A1c (a marker indicating whether blood glucose levels have been higher than normal) at the time of diagnosis might suggest that the patient had recently developed type 1 diabetes before his SARS-CoV-2 infection. However, the authors note that diabetic ketoacidosis (a serious complication of type 1 diabetes when the body produces excess blood acids) can cause high haemoglobin A1c levels regardless of the duration of diabetes, and the patient experienced diabetic symptoms only after infection.
The authors conclude that this case study does not indicate that COVID-19 caused diabetes in this patient, and the possibility that he might have had a pre-existing rare form auto-antibody-negative type 1 autoimmune diabetes cannot be ruled out. However, they argue that SARS-CoV-2 infection might negatively affect pancreatic function through direct effects of the virus on β-cells. More epidemiological and experimental research is needed to investigate possible links between SARS-CoV-2 infection and the development of new-onset diabetes.
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