https://diabetes.acponline.org/archives/2021/11/12/2.htm

No long-term disruption of glycemic control seen after COVID-19, study finds

The authors of a small Italian study of hospitalized COVID-19 patients speculated that reversible transient factors, such as inflammation-induced insulin resistance, may cause the hyperglycemia that occurs in some patients with and without diabetes during infection.


Hyperglycemia in patients hospitalized with COVID-19, with and without diabetes, generally resolved after the infection did, a small Italian study found.

Researchers studied an adult cohort of patients with suspected COVID-19 pneumonia at one hospital in Milan, comparing their glucose levels at admission with fasting blood glucose (FBG) levels in the year prior to their COVID-19 infection and during postdischarge follow up. They classified participants according to American Diabetes Association criteria as having pre-existing diabetes, newly diagnosed diabetes, hyperglycemia not in the diabetes range, or normoglycemia. FBG prior to admission and during follow-up was classified as normal, impaired, and or in the diabetes range. Results were published Oct. 29 by the Journal of Clinical Endocrinology & Metabolism.

Among 586 patients with confirmed COVID-19, the proportion with pre-existing diabetes was 19.6%; 6.7% had newly diagnosed diabetes, 43.7% had hyperglycemia not in the diabetes range, and 30.0% had normoglycemia. Patients with dysglycemia associated with COVID-19 had increased markers of inflammation and organ injury. Abnormal blood glucose levels were also strongly associated with worse clinical outcomes, defined by a composite endpoint of admission to ICU or death (respective hazard ratios for diabetes and hyperglycemia not in the diabetic range, 3.28 [95% CI, 2.04 to 5.30] and 2.16 [95% CI, 1.35 to 3.4); P<0.001 for both relative to normoglycemia).

Of the 115 patients with pre-existing diabetes, FBG levels from before admission were available for 43.5% and during follow-up for 82.1%. None of these patients required drug treatment escalation during follow-up, and their FBG did not change significantly from before infection to afterward. Of the 295 patients with newly diagnosed diabetes or hyperglycemia not in the diabetes range, FBG was available from before hospitalization for 28.5% and during follow-up for 74.8%, and these data showed an overall increase in glycemia during hospitalization, followed by a return to baseline. Among the 176 patients with normoglycemia during hospitalization, FBG was available from before admission for 36.9% and after for 69.6%. Their FBG did not change significantly from before COVID-19 to afterward.

Dysglycemia associated with COVID-19 resolved in the majority of patients after the infection waned, the authors noted. Because this trend occurred in a small comparison group of patients found not to have COVID-19, the authors speculated that reversible transient factors, such as inflammation-induced insulin resistance, may cause dysglycemia.

“It is clear from our study that patients with COVID-associated dysglycaemia had increased levels of inflammatory markers and indicators of organ injuries and showed a poorer clinical outcome,” the authors wrote. “This strongly support[s] the need to screen all patients [with] COVID-19 pneumonia for hyperglycemia at the time of admission, despite a mute personal or family history of diabetes, and treat their hyperglycemia promptly in order to achieve and maintain a good glycemic control during hospitalization. … [A]t this time any alarmist claim on an increased risk of diabetes after SARS-CoV-2 infection should be interpreted with caution.”