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      Comparison of Machine Learning Methods and Conventional Logistic Regressions for Predicting Gestational Diabetes Using Routine Clinical Data: A Retrospective Cohort Study

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          Abstract

          Background

          Gestational diabetes mellitus (GDM) contributes to adverse pregnancy and birth outcomes. In recent decades, extensive research has been devoted to the early prediction of GDM by various methods. Machine learning methods are flexible prediction algorithms with potential advantages over conventional regression.

          Objective

          The purpose of this study was to use machine learning methods to predict GDM and compare their performance with that of logistic regressions.

          Methods

          We performed a retrospective, observational study including women who attended their routine first hospital visits during early pregnancy and had Down's syndrome screening at 16-20 gestational weeks in a tertiary maternity hospital in China from 2013.1.1 to 2017.12.31. A total of 22,242 singleton pregnancies were included, and 3182 (14.31%) women developed GDM. Candidate predictors included maternal demographic characteristics and medical history (maternal factors) and laboratory values at early pregnancy. The models were derived from the first 70% of the data and then validated with the next 30%. Variables were trained in different machine learning models and traditional logistic regression models. Eight common machine learning methods (GDBT, AdaBoost, LGB, Logistic, Vote, XGB, Decision Tree, and Random Forest) and two common regressions (stepwise logistic regression and logistic regression with RCS) were implemented to predict the occurrence of GDM. Models were compared on discrimination and calibration metrics.

          Results

          In the validation dataset, the machine learning and logistic regression models performed moderately (AUC 0.59-0.74). Overall, the GBDT model performed best (AUC 0.74, 95% CI 0.71-0.76) among the machine learning methods, with negligible differences between them. Fasting blood glucose, HbA1c, triglycerides, and BMI strongly contributed to GDM. A cutoff point for the predictive value at 0.3 in the GBDT model had a negative predictive value of 74.1% (95% CI 69.5%-78.2%) and a sensitivity of 90% (95% CI 88.0%-91.7%), and the cutoff point at 0.7 had a positive predictive value of 93.2% (95% CI 88.2%-96.1%) and a specificity of 99% (95% CI 98.2%-99.4%).

          Conclusion

          In this study, we found that several machine learning methods did not outperform logistic regression in predicting GDM. We developed a model with cutoff points for risk stratification of GDM.

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          Most cited references25

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          The Pathophysiology of Gestational Diabetes Mellitus

          Gestational diabetes mellitus (GDM) is a serious pregnancy complication, in which women without previously diagnosed diabetes develop chronic hyperglycemia during gestation. In most cases, this hyperglycemia is the result of impaired glucose tolerance due to pancreatic β-cell dysfunction on a background of chronic insulin resistance. Risk factors for GDM include overweight and obesity, advanced maternal age, and a family history or any form of diabetes. Consequences of GDM include increased risk of maternal cardiovascular disease and type 2 diabetes and macrosomia and birth complications in the infant. There is also a longer-term risk of obesity, type 2 diabetes, and cardiovascular disease in the child. GDM affects approximately 16.5% of pregnancies worldwide, and this number is set to increase with the escalating obesity epidemic. While several management strategies exist—including insulin and lifestyle interventions—there is not yet a cure or an efficacious prevention strategy. One reason for this is that the molecular mechanisms underlying GDM are poorly defined. This review discusses what is known about the pathophysiology of GDM, and where there are gaps in the literature that warrant further exploration.
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            International Association of Diabetes and Pregnancy Study Groups Recommendations on the Diagnosis and Classification of Hyperglycemia in Pregnancy: Response to Weinert

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              Growth and function of the normal human placenta.

              The placenta is the highly specialised organ of pregnancy that supports the normal growth and development of the fetus. Growth and function of the placenta are precisely regulated and coordinated to ensure the exchange of nutrients and waste products between the maternal and fetal circulatory systems operates at maximal efficiency. The main functional units of the placenta are the chorionic villi within which fetal blood is separated by only three or four cell layers (placental membrane) from maternal blood in the surrounding intervillous space. After implantation, trophoblast cells proliferate and differentiate along two pathways described as villous and extravillous. Non-migratory, villous cytotrophoblast cells fuse to form the multinucleated syncytiotrophoblast, which forms the outer epithelial layer of the chorionic villi. It is at the terminal branches of the chorionic villi that the majority of fetal/maternal exchange occurs. Extravillous trophoblast cells migrate into the decidua and remodel uterine arteries. This facilitates blood flow to the placenta via dilated, compliant vessels, unresponsive to maternal vasomotor control. The placenta acts to provide oxygen and nutrients to the fetus, whilst removing carbon dioxide and other waste products. It metabolises a number of substances and can release metabolic products into maternal and/or fetal circulations. The placenta can help to protect the fetus against certain xenobiotic molecules, infections and maternal diseases. In addition, it releases hormones into both the maternal and fetal circulations to affect pregnancy, metabolism, fetal growth, parturition and other functions. Many placental functional changes occur that accommodate the increasing metabolic demands of the developing fetus throughout gestation.
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                Author and article information

                Contributors
                Journal
                J Diabetes Res
                J Diabetes Res
                JDR
                Journal of Diabetes Research
                Hindawi
                2314-6745
                2314-6753
                2020
                12 June 2020
                : 2020
                : 4168340
                Affiliations
                1Obstetrics and Gynecology Hospital, Fudan University, Shanghai, China
                2The Shanghai Key Laboratory of Female Reproductive Endocrine-Related Diseases, Shanghai, China
                3The Shanghai Key Laboratory of Birth Defects, Shanghai, China
                4Institute of Biochemical Science, Fudan University, Shanghai, China
                Author notes

                Academic Editor: Ferdinando Carlo Sasso

                Author information
                https://orcid.org/0000-0002-7136-3680
                https://orcid.org/0000-0002-6765-459X
                https://orcid.org/0000-0002-4268-870X
                https://orcid.org/0000-0003-4378-2391
                https://orcid.org/0000-0002-2051-4581
                https://orcid.org/0000-0002-6949-055X
                Article
                10.1155/2020/4168340
                7306091
                32626780
                e3671ae5-c50e-412a-8ee1-32c5f70ab694
                Copyright © 2020 Yunzhen Ye et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 26 March 2020
                : 6 May 2020
                : 14 May 2020
                Funding
                Funded by: Science and Technology Commission of Shanghai Municipality
                Award ID: 18411963400
                Funded by: National Natural Science Foundation for Young Scholars of China
                Award ID: 81701470
                Funded by: National Natural Science Foundation of China
                Award ID: 8197061089
                Award ID: 81871183
                Funded by: Shanghai Medical Center of Key Programs for Female Reproductive Diseases
                Award ID: 2017ZZ01016
                Funded by: Shanghai Key Program of Clinical Science and Technology Innovation
                Award ID: 17411950501
                Award ID: 18511105602
                Award ID: 17411950500
                Categories
                Research Article

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