Introduction
Diabetes mellitus (DM) is one of the most frequent comorbidities in individuals with SARS-CoV-2 infection [1, 2]. Evidence shows that individuals suffering from diabetes present a higher rate of hospital admission and a higher mortality as compared to non-diabetic subjects [1, 3, 4].
Analogue to the general population, pregnant women suffering from preexisting diabetes seem to present with a higher severity degree of SARS-CoV-2 infection [5, 6]. An international case control analysis comparing data stratified by the severity of maternal disease identified pulmonary comorbidities, hypertensive disease and DM as risk factors associated with a severe form of SARS-CoV-2 infection in pregnancy [5]. Furthermore, it has been previously suggested that hyperglycemia generally increases viral replication and decreases anti-viral response, making a causal relationship between diabetes and SARS-CoV-2 biologically plausible [7,8]. However, there is limited data so far whether these elaborations also apply to gestational diabetes (GDM).
GDM is a major public health issue, with an abrupt increase in prevalence in the last decade, as international committees report a so-called ‘metabolic pandemic‘ [9,10]. According to The Hyperglycemia and Adverse Pregnancy Outcome Study, the level of glycaemia during pregnancy is directly linked to the presence of adverse obstetrical outcomes [11].
Prevalence of GDM lies worldwide between 9,3% and 25,5% [11]. A British study described a 33.8% increase in GDM since the onset of the pandemic, attributing this mainly to reduced exercise levels and psychical stress [12].
SARS-CoV mediated pancreatic islet cell damage is not a newly described phenomenon, as earlier experiences with MERS and SARS teach us [9]. DM is a multifactorial disease, whose development is linked to genetic and environmental influences. Indeed, a causal relationship between viral infections and acute glycemic decompensation with onset of Type I diabetes has been previously described. To date, several viruses have been suggested as promoters for the development of Type I diabetes in humans, including Coronavirus [1, 10].
In this context, increasing evidence shows that SARS-CoV-2 can trigger severe diabetic ketoacidosis in persons with new-onset Type I diabetes, most probably due to high angiotensin converting enzyme 2 (ACE2) expression in the endocrine part of the pancreas [9]. The mechanism seems to involve cell apoptosis with decreased pancreatic insulin secretion [13, 14].
The aim of our study was to investigate a possible bidirectional association between GDM and SARS-CoV-2 infection during pregnancy, as well as to evaluate the plausibility of a physiopathological background, by using a case-control approach.