Impacts of COVID-19 on glycemia and risk of diabetic ketoacidosis
Abstract Background Reports indicate that COVID-19 may impact pancreatic function and increase type 2 diabetes (T2D) risk, although real-world COVID-19 impacts on HbA1c and T2D are unknown. We tested whether COVID-19 increased HbA1c, risk of T2D, or diabetic ketoacidosis (DKA).Methods We compared pre- and post-COVID-19 HbA1c, and risk of developing T2D in a large real-world clinical cohort of 8,755 COVID-19(+) patients and a matched control cohort of 11,998 COVID-19(-) patients. We investigated if DKA risk was modified in COVID-19(+) patients with type 1 diabetes (T1D) (N=704) or T2D (N=22,904), or by race and sex.Findings We observed a statistically significant, albeit clinically insignificant, HbA1c increase post-COVID-19 (all patients ΔHbA1c=0.06%,P<.001; with T2D ΔHbA1c=0.1%;P<.001), and no increase among COVID-19(-) patients (P>.05). COVID-19(+) patients were 40% more likely to be diagnosed with T2D compared to COVID-19(-) patients (P<.001) and 28% more likely to be diagnosed with T2D for the same HbA1c change as COVID-19(-) patients (P<.001). COVID-19(+) patients with T2D on insulin were 34% more likely to develop DKA compared to COVID-19(-) patients on insulin (P<.05), and COVID-19(+) Black patients with T2D displayed disproportionately increased DKA risk (HR:1.63,P=.007). There was no significant difference in DKA risk between COVID-19(+) and COVID-19(-) patients with T1D.Interpretation DKA risk is increased in T2D patients on insulin and in Black patients with T2D after COVID-19 infection.T2D risk is greater in COVID-19(+) patients for the same HbA1c increase in COVID-19(-) patients, indicating that T2D risk attributed to COVID-19 may be due to increased recognition during COVID-19 management.Funding No funding to report..
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Preprint| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
bioRxiv.org - (2023) vom: 18. Nov. Zur Gesamtaufnahme - year:2023 |
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| Sprache: |
Englisch |
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| Beteiligte Personen: |
Sharma, Anukriti [VerfasserIn] |
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| Links: |
Volltext [kostenfrei] |
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| doi: |
10.1101/2022.03.08.22272041 |
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XBI03546755X |
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| 520 | |a Abstract Background Reports indicate that COVID-19 may impact pancreatic function and increase type 2 diabetes (T2D) risk, although real-world COVID-19 impacts on HbA1c and T2D are unknown. We tested whether COVID-19 increased HbA1c, risk of T2D, or diabetic ketoacidosis (DKA).Methods We compared pre- and post-COVID-19 HbA1c, and risk of developing T2D in a large real-world clinical cohort of 8,755 COVID-19(+) patients and a matched control cohort of 11,998 COVID-19(-) patients. We investigated if DKA risk was modified in COVID-19(+) patients with type 1 diabetes (T1D) (N=704) or T2D (N=22,904), or by race and sex.Findings We observed a statistically significant, albeit clinically insignificant, HbA1c increase post-COVID-19 (all patients ΔHbA1c=0.06%,P<.001; with T2D ΔHbA1c=0.1%;P<.001), and no increase among COVID-19(-) patients (P>.05). COVID-19(+) patients were 40% more likely to be diagnosed with T2D compared to COVID-19(-) patients (P<.001) and 28% more likely to be diagnosed with T2D for the same HbA1c change as COVID-19(-) patients (P<.001). COVID-19(+) patients with T2D on insulin were 34% more likely to develop DKA compared to COVID-19(-) patients on insulin (P<.05), and COVID-19(+) Black patients with T2D displayed disproportionately increased DKA risk (HR:1.63,P=.007). There was no significant difference in DKA risk between COVID-19(+) and COVID-19(-) patients with T1D.Interpretation DKA risk is increased in T2D patients on insulin and in Black patients with T2D after COVID-19 infection.T2D risk is greater in COVID-19(+) patients for the same HbA1c increase in COVID-19(-) patients, indicating that T2D risk attributed to COVID-19 may be due to increased recognition during COVID-19 management.Funding No funding to report. | ||
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| 700 | 1 | |a Milinovich, Alex |4 aut | |
| 700 | 1 | |a Kattan, Michael W. |4 aut | |
| 700 | 1 | |a Pantalone, Kevin M. |0 (orcid)0000-0002-3840-4161 |4 aut | |
| 700 | 1 | |a Rotroff, Daniel M. |4 aut | |
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