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Disclosures: The authors report no relevant financial disclosures.
October 12, 2020
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Antibody response in COVID-19 similar in adults with and without diabetes

Source/Disclosures
Disclosures: The authors report no relevant financial disclosures.
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Antibodies in adults with diabetes hospitalized with COVID-19 in Italy had a similar positive response to the SARS-CoV-2 spike protein as those without diabetes, according to findings published in Diabetologia.

Lorenzo Piemonti

“The antibody response against multiple SARS-CoV-2 antigens in patients with diabetes is superimposable, as for timing, titers and classes, to that of nondiabetic patients and is not influenced by glucose levels,” Lorenzo Piemonti, MD, professor of endocrinology and director of the San Raffaele Diabetes Research Institute in Milan, told Healio. “Glycemia is strongly associated with an increased mortality for COVID-19 pneumonia even in patients without diabetes. Positivity for immunoglobulin G against the SARS-CoV-2 spike receptor-binding domain is predictive of survival both in the presence and in the absence of diabetes.”

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Piemonti and colleagues conducted a study in 509 adults who tested positive for COVID-19 and were admitted to the emergency or clinical departments at San Raffaele Hospital in Milan from Feb. 25 to April 19. Patients with diabetes had been diagnosed before hospitalization (n = 90) or were diagnosed with diabetes during hospitalization (n = 49). Health information was collected from medical charts or interviews, and routine blood tests were conducted on all participants. Researchers used a novel assay based on the luciferase immunoprecipitation system format to detect the presence of three antibodies: IgG, IgM and IgA. The response of the antibodies was measured against multiple antigens of SARS-CoV-2.

Individuals with diabetes had worse lung and kidney function than the nondiabetic group. Those with diabetes also had a higher white blood cell count, worse inflammation, more tissue damage and more markers of coagulatory cascade than individuals without diabetes. After adjusting for age, sex and comorbidities, the diabetes cohort was at higher risk for COVID-19 mortality (HR = 2.32; 95% CI, 1.44-3.75) than individuals without diabetes.

“Diabetes was associated with increased levels of inflammatory biomarkers and hypercoagulopathy, as well as leukocytosis and neutrophilia,” Piemonti said. “This could explain why diabetes was independently associated with 2.3 times increased risk of death, even after adjustment for age, sex and other relevant comorbidities. The comprehension of the molecular mechanisms of this associations could provide specific pharmacological target to reduce the mortality in subject with diabetes and COVID-19.”

In the diabetes group, the risk for death increased by 13% with each 1.1 mmol/L increase in mean fasting plasma glucose (HR = 1.13 x 1.1 mmol/L; 95% CI, 1.01-1.26) and each 0.6 mmol/L increase in glucose variability (HR = 1.13 x 0.6 mmol/L; 95% CI, 1.03-1.24). For individuals without diabetes, there was also an association between mean FPG and an increased risk for death (HR = 2.39 x 1.1 mmol/L; 95% CI, 1.49-3.81).

In antibody analysis, the development of IgG antibodies to the SARS-CoV-2 spike receptor-binding domain was associated with improved survival rate for individuals with COVID-19 (HR = 0.4; 95% CI, 0.23-0.71). The effect was present in adults with (HR = 0.37; 95% CI, 0.17-0.81) and without diabetes (HR = 0.43; 95% CI, 0.19-0.95).

“Hyperglycemia does not impair the antibody response against SARS-CoV-2,” Piemonti said. “The evidence that the presence of IgG antibodies against the so-called ‘spike protein’ is associated with a remarkable protective effect — about a 60% reduction — in COVID-19 mortality in patients with diabetes allows for cautious optimism on the efficacy of future vaccines against SARS-COV-2 in people with diabetes, who are particularly vulnerable in this deadly pandemic.”

Piemonti said more research is needed to better understand the relationship between glycemia and the activation of innate immunity.

For more information:

Lorenzo Piemonti, MD, can be reached at piemonti.lorenzo@hsr.it. Twitter: @PiemontiL.