Heterogeneity at diagnosis

Abstract

Gestational diabetes emerges in the context of pregnancy, in most cases, during the last trimester in which insulin sensitivity decreases between 40 and 60% due to the physiological changes inherent to pregnancy. However, there are some pregnant women who have hyperglycemia in the first trimester, which raises the question of whether it is a previously undiagnosed prediabetes or diabetes or a diabetes that begins during pregnancy.

The development of gestational diabetes is associated with the interaction of genetic, epigenetic and environmental factors whose clinical manifestation is hyperglycemia. The most important genetic factors are represented by the genes that affect the function of the pancreatic beta cell and, as a consequence, the secretion of insulin. There are also epigenetic mechanisms involved, such as modification of histones and non-coding RNA that contribute to altering the carbohydrate metabolism, leading to the development of gestational diabetes. Environmental factors such as obesity, previous insulin resistance and a sedentary lifestyle are determinants in the development of gestational diabetes.

From the etiopathogenic point of view, it is a heterogeneous group with a common denominator, which is hyperglycemia. Most of them share phenotypic characteristics and risk factors with type 2 diabetes. However, there are other pregnant women who also make up this population whose etiopathogenesis is similar to type 1 diabetes, LADA (Latent Autoimmune Diabetes in Adults) or monogenic diabetes (MODY). In most cases, there are diagnostic elements that guide us to establish the etiopathogenesis; such as the patient's phenotype, certain biochemical parameters and also family history. Precision medicine applied to gestational diabetes minimizes errors and contributes to making better decisions, which are considered of utmost importance for the future of the mother-child binomial.