ECE2023 Eposter Presentations Diabetes, Obesity, Metabolism and Nutrition (355 abstracts)
1Farhat Hached Hospital, Endocrinology Department, Sousse, Tunisia; 2Farhat Hached Hospital, Community Medecine, Sousse, Tunisia
Introduction: COVID-19 has been incriminated directly and indirectly in the increase of patients presenting with diabetic ketoacidosis.
Aim: The aim of this study is to compare diabetic ketoacidosis precipitating factors in the pre-pandemic and during the pandemic.
Methods: This is a retrospective comparative study between patients hospitalized in the diabetology department in the university hospital Farhat Hached of Sousse for diabetic ketoacidosis in the pre-pandemic (between March 2018 until March 2020) (G1) and during pandemic period (between March 2020 until March 2022) (G2).
Results: A total of 340 patients were included in this study, with 137 patients admitted in the pre-pandemic period (G1) and 203 admitted during pandemic period (G2). The overall distribution of diabetic ketoacidosis precipitating factors differed significantly in the pre-pandemic compared to the pandemic period (P=0.028) with a significant increase of psychological stress (31.2% in G2 vs 22.4% in G1 with an adjusted residual (AR) of 1.98) and excessive food intake notably hypertonic drinks (6.5% vs 2.2%, AR=2) at the expense of corticosteroid use as its accountability in precipitating DKA significantly decreased in G2 (1.5% in G2 vs 6.5% in G1, AR=2.2). In contrast, overall infections accountability did not differ between the two groups (28.6% in G2 vs 29.1% in G1, AR=0.1). The same was noticed regarding cardiovascular events. No identifiable precipitating factor was found in 40.3% in G1 vs 31.7% in G2 (AR=1.6). More specifically, infectious precipitating factors had a significantly different distribution between the two groups (P<0.001) with COVID-19 becoming the first infectious precipitating factor of DKA in G2 (37.04% vs 0% in G1, AR=4.2) with a decrease of pulmonary and other influenza like illness. The accountability of cutaneous, urinary, profound and other specific infections remained the same in the two groups with a respective AR of 1.8, 0.6, and 0.9.
Conclusion: COVID-19-like any other infection- is directly responsible for triggering diabetic ketoacidosis. COVID-19 seems to decompensate diabetes also indirectly through different mechanisms with an increased accountability of psychological stress and excessive food intake as precipitating factors due probably to periods of lockdown and restricted social activities. The accountability of corticosteroid use seems to decline as most of patients in this study who developed COVID-19 had minor symptoms and therefore did not require corticosteroids.