Early second trimester maternal serum markers in the prediction of gestational diabetes mellitus

Abstract

Aims/IntroductionTo determine whether maternal serum markers in the early second trimester are useful for prediction of gestational diabetes mellitus (GDM).Materials and methodsA total of 876 singleton pregnancies were recruited in the present study. Blood samples were collected during 16–20 gestational weeks. GDM women were diagnosed by an oral glucose tolerance test during 24–28 gestational weeks. A total of 56 women with GDM and 73 healthy pregnant women were selected. Maternal serum concentrations of placental protein 13 (PP13), pentraxin 3 (PTX3), soluble fms‐like tyrosine kinase‐1 (sFlt‐1), myostatin and follistatin (FST) were detected at 16–20 weeks’ gestation. All of these markers concentrations were expressed as multiples of the medians. The Mann–Whitney U‐test was used for comparison of the multiples of the medians of different concentrations of these five serum markers between the GDM group and the control group. Receiver operating characteristic curve analysis was applied to assess the sensitivity and specificity of significant serum markers from a Mann–Whitney U‐test comparison.ResultsCompared with healthy pregnancies, the serum levels of PP13, PTX3, sFlt‐1, myostatin and FST in the early second trimester were significantly increased in patients who had developed GDM late. In screening for GDM by PP13, PTX3, sFlt‐1, myostatin and FST, the detection rates were 92.3, 94.9, 94.9, 92.5 and 92.3%, respectively at 80% specificity. PTX3 and sFlt‐1 were the most sensitive markers.ConclusionsMaternal serum markers including PP13, PTX3, sFlt‐1, myostatin and FST increase in the early second trimester of women with GDM. These five markers, especially PTX3 and sFlt‐1, could have the value of prediction for those patients who would develop GDM in the late second trimester.

A simple model to predict risk of gestational diabetes mellitus from 8 to 20 weeks of gestation in Chinese women

“…Only following early detection can risk stratification and early intervention for GDM become possible, but still it is difficult. The available models suffer from one or more of the limitations including applying only to sub-populations [24], involving complicated algorithms [23], requiring specific laboratory tests [21, 22, 24] or applying in specific periods before GDM diagnosis [21, 22, 41]. The model derived in the present study did not have AUC, sensitivity or specificity as high as some previous models but it was simple, applicable to the Chinese population and covered a broad period before GDM diagnostic tests, and therefore has the potential to be widely used in less developed jurisdictions.…”

“…However, in a prospective cohort study in Brazil, levels of these lipids increased from the first trimester to the third trimester [14]. Despite the difficulties in risk prediction of GDM due to by these dynamic changes, efforts have been made to develop risk prediction models for GDM incorporating factors such as maternal age, ethnicity, BMI [15], family history of diabetes, personal history of GDM, fasting plasma glucose (FPG), vitamin D3, macrosomia and chronic hypertension, high-sensitive C-reactive protein, placental protein 13, pentraxin 3, myostatin, follistatin, and soluble fms-like tyrosine kinase-1 [15, 16, 17, 18, 19, 20, 21].…”

Myostatin as a Biomarker of Muscle Wasting and other Pathologies-State of the Art and Knowledge Gaps

“…Furthermore, myostatin expression in muscles and adipose tissue was demonstrated to be influenced by dysglycemia and insulin sensitivity [ 134 ]. Higher serum myostatin levels were found in pregnant (16–20 gestational week) women, who later developed gestational diabetes mellitus, indicating a possible usage of myostatin as a gestational diabetes biomarker [ 153 ]. As mentioned before, earlier research found that myostatin might induce insulin resistance via NF-κB and SMAD3 [ 60 , 61 ], and recent animal studies on myostatin function and mechanism brought insight into its role in adipogenesis, communication between adipose tissue and skeletal muscles as well as neural control over insulin sensitivity [ 154 , 155 , 156 ], yet many aspects remain unknown, and are awaiting in-depth studies.…”

Pregnancy Galectinology: Insights Into a Complex Network of Glycan Binding Proteins

“…In this regard, recent studies suggest that the kinetics of Lgals13 expression in PE would result from the concerted actions of this protein and antiangiogenic factors as sFlt-1 on the maternal vascular system, with a dual role for Lgals13: first in low levels acting as a priming insult promoting endothelial activation and angiogenic imbalance, and increasing later in the third trimester as a natural rescue response promoting maternal vasodilation to lower blood pressure (169). In the context of gestational diabetes mellitus (GDM), increased Lgals13 serum levels during the early second trimester and lower expression in trophoblast cells of the term placenta have been reported (170, 171). Dysregulation of Lgals13 was suggested to contribute to an imbalance in inflammatory processes in the placenta during pregnancy and therefore possibly lead to GDM.…”