ABSTRACT Objective: To evaluate the association between HbA1c levels measured in the third trimester and the risk for large for gestational age (LGA) in neonates of mothers affected by gestational diabetes mellitus (GDM). Secondarily, we aimed to identify an ideal cut-off for increased risk of LGA amongst pregnant women with GDM. Materials and methods: Observational retrospective review of singleton pregnant women with GDM evaluated in a diabetes and pregnancy clinic of a tertiary and academic hospital. From January/2011 to December/2017, 1,085 pregnant women underwent evaluation due to GDM, of which 665 had an HbA1c test in the third trimester. A logistic regression model was performed to evaluate predictors of LGA. A receiver-operating-characteristic (ROC) curve was used to evaluate the predictive ability of third trimester HbA1c for LGA identification. Results: A total of 1,085 singleton pregnant women were evaluated during the study period, with a mean age of 32.9 ± 5.3 years. In the multivariate analysis, OGTT at 0 minutes (OR: 1.040; CI 95% 1.006-1.076, p = 0.022) and third trimester HbA1c (OR: 4.680; CI 95% 1.210-18.107, p = 0.025) were associated with LGA newborns. Using a ROC curve to evaluate the predictive ability of third trimester HbA1c for LGA identification, the optimal HbA1c cut-off point was 5.4% where the sensitivity was 77.4% and the specificity was 71.7% (AUC 0.782; p < 0.001). Conclusions: Few studies in the Mediterranean population have evaluated the role of HbA1c in predicting neonatal complications in women with GDM. A third trimester HbA1c > 5.4% was found to have good sensitivity and specificity for identifying the risk of LGA.

Objetivo Este artigo revê o estado da arte relativamente à associação entre as ações dos glicocorticoides e a obesidade e a resistência à insulina, dois dos principais componentes da síndrome metabólica. Métodos Uma revisão da literatura nas bases de dados PubMed e SciELO foi realizada usando os seguintes termos: estresse, síndrome metabólica, glicocorticoides, obesidade, resistência à insulina, eixo hipotálamo-hipófise-suprarrenal e 11β-hidroxiesteróide desidrogenase. Resultados O estresse crônico, principalmente através da desregulação do eixo hipotálamo-hipófise-suprarrenal, promove a acumulação de gordura visceral. Reciprocamente, a obesidade promove um estado inflamatório sistêmico de baixo grau, mediado por alterações na secreção de adipocinas, que cronicamente podem estimular e perturbar o sistema de estresse. Esse círculo vicioso, provavelmente iniciado pela disfunção do tecido adiposo visceral, pode ser o mecanismo primário que conduz ao desenvolvimento da síndrome metabólica. Conclusão Um conhecimento mais aprofundado sobre os mecanismos envolvidos na associação entre a liberação de glicocorticoides, a obesidade e o diabete tipo 2 pode ser útil na prevenção e tratamento da síndrome metabólica.

Objective This article reviews the state of the art regarding the association between glucocorticoid actions and both obesity and insulin resistance, two main features of the metabolic syndrome. Methods A methodological assessment of the literature on PubMed and SciELO databases was conducted by using the following terms: stress, metabolic syndrome, glucocorticoids, obesity, insulin resistance, hypothalamic-pituitary-adrenal-axis and 11β-hydroxysteroid dehydrogenase. Results Chronic stress, mainly through hypothalamic-pituitary-adrenal axis dysregulation, promotes the accumulation of visceral fat. Reciprocally, obesity promotes a systemic low-grade inflammation state, mediated by increased adipokine secretion, which can chronically stimulate and disturb stress system. This vicious cycle, probably initiated by visceral adipose tissue dysfunction, might be the trigger for the development of metabolic syndrome. Conclusion Given the strong evidences linking glucocorticoid release, obesity and type 2 diabetes, better understanding of the mechanisms underlying this connection might be useful for prevention and treatment of the metabolic syndrome.