Incidence and risk factors for hyperglycemia in pregnancy among nulliparous women: A Brazilian multicenter cohort study.
- 作者列表："Nicolosi BF","Souza RT","Mayrink J","Feitosa FE","Rocha Filho EA","Leite DF","Vettorazzi J","Sousa MH","Costa ML","Baker PN","Kenny LC","Cecatti JG","Calderon IM","Preterm SAMBA Study Group.
OBJECTIVE:To assess the incidence and risk factors for hyperglycemia in pregnancy in a cohort of Brazilian nulliparous pregnant women. MATERIALS AND METHODS:This is a secondary analysis of a multicenter cohort study that enrolled 1,008 nulliparous pregnant women at 19-21 weeks. Exclusion criteria included chronic exposure to corticosteroids and previous diabetes. Bivariate and multivariate analyses by Poisson regression were used to identify associated factors. RESULTS:The incidence of hyperglycemia in pregnancy was 14.9% (150/1,008), and 94.7% of these cases were gestational diabetes mellitus (142/150). Significant associated factors included a family history of diabetes mellitus, maternal overweight or obesity at enrollment, and previous maternal conditions (polycystic ovarian syndrome, thyroid dysfunctions and hypertensive disorders). A BMI ≥ 26.3Kg/m2 (RRadj 1.87 [1.66-2.10]) and a family history of diabetes mellitus (RRadj 1.71 [1.37-2.15]) at enrollment were independent risk factors for HIP. CONCLUSIONS:A family history of diabetes mellitus and overweight or obesity (until 19-21 weeks of gestation) may be used as selective markers for HIP in Brazilian nulliparous women. Given the scarcity of results in nulliparous women, our findings may contribute to determine the optimal diagnostic approach in populations of similar socioeconomic characteristics.
目的: 评估巴西未产妇队列中妊娠期高血糖的发生率和危险因素。 材料和方法: 这是一项多中心队列研究的二次分析，该研究在19-21周时纳入了1,008名未产妇。排除标准包括长期暴露于皮质类固醇和既往糖尿病。使用泊松回归的双变量和多变量分析来确定相关因素。 结果: 妊娠期高血糖的发生率为14.9% (150/1，008)，其中94.7% 为妊娠期糖尿病 (142/150)。显著相关因素包括糖尿病家族史，入组时母亲超重或肥胖，以及既往母亲疾病 (多囊卵巢综合征，甲状腺功能障碍和高血压疾病)。入组时BMI ≥ 26.3千克/m2 (RRadj 1.87 [1.66-2.10]) 和糖尿病家族史 (RRadj 1.71 [1.37-2.15]) 是髋部的独立危险因素。 结论: 糖尿病家族史和超重或肥胖 (直到妊娠19-21周) 可作为巴西未产妇髋部的选择性标志物。鉴于未生育女性的结果不足，我们的研究结果可能有助于确定具有相似社会经济特征的人群的最佳诊断方法。
METHODS::Objective: To determine the association of maternal glycemia with childhood obesity and metabolic dysfunction.Study design: Secondary analysis of follow-up data 5-10 years after a mild gestational diabetes mellitus (GDM) treatment trial. The relationship between maternal oral glucose tolerance testing (OGTT) at 24-31-week gestation and body mass index (BMI), fasting glucose, insulin, and anthropometric measurements (sum of skinfolds, subscapular/triceps ratio, and waist circumference) in the offspring of untreated mild GDM and non-GDM (abnormal 50-g screen/normal OGTT) women was assessed. Multivariable regression modeling controlling for maternal and neonatal characteristics was employed.Results: A cohort of 236 untreated mild GDM and 480 non-GDM offspring were analyzed. In the combined cohort, significant correlations existed between fasting, 1, 2, and 3 h maternal glucose and subscapular/triceps ratio (all p < .04) and in all OGTT values other than the 2-hour value for homeostatic model assessment-estimated insulin resistance (HOMA-IR) (all p < .04) and sum of skinfold measurements (all p < .03). No correlation was found between OGTT values and childhood BMI Z-score. Multivariable regression modeling showed that OGTT values were associated with only sum of skinfolds and subscapular/triceps ratio and not with childhood BMI Z-score. Hispanic ethnicity and prepregnancy maternal BMI were most consistently related to childhood BMI Z-score and HOMA-IR, and Hispanic ethnicity with fasting glucose.Conclusions: Among women with untreated mild GDM and those without GDM, maternal glycemia is associated with childhood anthropometric measures of obesity but not childhood BMI, fasting glucose, or insulin resistance. Hispanic ethnicity, maternal BMI, and gestational weight gain were consistently related to childhood BMI.
METHODS::Objective: Women with gestational diabetes (GDM) have a 7-12-fold increased risk for developing type 2 diabetes later in life. Postpartum weight retention is highly predictive for future obesity, and further increases risk for type 2 diabetes. We sought to identify predictors of losing at least 75% of gestational weight gain by very early postpartum in women with recent GDM.Methods: We recruited women with GDM during pregnancy or just after delivery. Prepregnancy weight was self-reported at recruitment; gestational weight gain, mode of delivery, and insulin use were extracted from medical records. At a mean of 7.2 (±2.1) weeks postpartum we measured weight and height and administered questionnaires, including demographics, breastfeeding, Edinburgh Postnatal Depression Scale, sleep, Harvard Food Frequency, and the International Physical Activity Questionnaire. We modeled the odds of 75% loss of gestational weight gain at the study visit using multivariable logistic regression models and selected the model with the lowest Akaike information criterion (AIC) as our final model. Analyses were conducted using JMP 10-13 Pro (SAS Institute Inc.)Results: Seventy-five women with recent GDM were included in the study. The mean age of study participants was 33 (SD ±5) years old, of whom 57% were white, 30% were African American, and 20% of the women identified as Hispanic. The mean prepregnancy BMI was 31.4 kg/m2 (SD ±5.6) and the mean pregnancy weight gain was 12.5 kg (SD ±7.8). Fifty-two percent of participants lost at least 75% of their pregnancy weight gain by the early postpartum study visit. Thirty-seven women (49%) exceeded Institute of Medicine (IOM) guidelines for gestational weight gain. In a multivariate model adjusting for weeks postpartum at the time of the study visit, less gestational weight gain (OR 0.56; 95% CI 0.39-0.73), increased age (OR 1.48; 95% CI 1.13-2.20), and lack of insulin use during pregnancy (OR 0.08 for use of insulin; 95% CI 0.00-0.73) were associated with at least 75% postpartum weight loss. Prepregnancy BMI and sleep were not retained in the model. Race/ethnicity, education, breastfeeding, nulliparity, cesarean section, depressive symptoms, dietary composition, glycemic index, and physical activity did not meet criteria for inclusion in the model.Conclusions: A substantial proportion of women with recent GDM lost at least 75% of their gestational weight gain by early postpartum. Older women, those who did not use insulin during pregnancy and those who gained less weight during pregnancy were significantly more likely to have lost 75% of gestational weight by very early postpartum.
METHODS::Background: Low-glycemic index (GI) diet might be beneficial for gestational diabetes. However, the results remained controversial. We conducted a systematic review and meta-analysis to explore the influence of low-GI diet on gestational diabetes.Methods: PubMed, EMbase, Web of Science, EBSCO, and Cochrane library databases were systematically searched. Randomized controlled trials (RCTs) assessing the effect of low-GI diet on gestational diabetes were included. Two investigators independently searched articles, extracted data, and assessed the quality of included studies. This meta-analysis was performed using the random-effect model.Results: Six RCTs involving 532 patients were included in the meta-analysis. Overall, compared with a control intervention in gestational diabetes, low-GI diet was found to significantly reduce 2 h postprandial glucose (Std. MD = -0.46; 95% CI = -0.82 to -0.10; p = .01), but demonstrated no substantial influence on fasting plasma glucose (Std. MD = -0.24; 95% CI = -0.72 to 0.24; p = .33), HbA1c (Std. MD = 0.01; 95% CI = -0.29 to 0.31; p = .94), birth weight (Std. MD = -0.17; 95% CI = -0.41 to 0.06; p = .15), macrosomia (Std. MD = 0.45; 95% CI = 0.16 to 1.30; p = .14) and insulin requirement (Std. MD = 0.91; 95% CI = 0.68 to 1.22; p = .55).Conclusions: Compared with control intervention in gestational diabetes, low-GI diet was found to significantly decrease 2 h postprandial glucose, but showed no notable impact on fasting plasma glucose, HbA1c, birth weight, macrosomia, and insulin requirement.