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The optimal process for detecting and treating gestational diabetes mellitus (GDM) remains controversial, with wide variances in practice within and between countries. A recent pragmatic randomized controlled trial (RCT) undertaken by Hillier et al. [1] in the USA has raised renewed worldwide interest in and discussion of GDM diagnosis.

In Australia's Northern Territory, Indigenous mothers account for 33% of births and have high rates of hyperglycemia in pregnancy. The prevalence of type 2 diabetes (T2D) in pregnancy is up to 10-fold higher in Indigenous than non-Indigenous Australian mothers, and the use of metformin is common. We assessed birth outcomes in relation to metformin use during pregnancy from a clinical register.The study included women with gestational diabetes (GDM), newly diagnosed diabetes in pregnancy (DIP), or pre-existing T2D from 2012 to 2016. Data were analyzed for metformin use in the third trimester. Regression models were adjusted for maternal age, body mass index, parity, and insulin use.Of 1649 pregnancies, 814 (49.4%) were to Indigenous women, of whom 234 (28.7%) had T2D (vs 4.6% non-Indigenous women; P 0.001). Metformin use was high in Indigenous women (84%-90% T2D, 42%-48% GDM/DIP) and increased over time in non-Indigenous women (43%-100% T2D, 14%-35% GDM/DIP). Among Indigenous women with GDM/DIP, there were no significant differences between groups with and without metformin in cesarean section (51% vs 39%; adjusted odds ratio [aOR] 1.25, 95% confidence interval [CI] 0.87-1.81), large for gestational age (24% vs 13%; aOR 1.5, 95% CI 0.9-2.5), or serious neonatal adverse events (9.4% vs 5.9%; aOR 1.32, 95% CI 0.68-2.57). Metformin use was independently associated with earlier gestational age (37.7 vs 38.5 weeks), but the risk did not remain independently higher after exclusion of women managed with medical nutrition therapy alone, and the increase in births37 weeks was not significant on multivariate analysis.We found no clear evidence of any adverse outcomes related to the use of metformin for the treatment of hyperglycemia in pregnancy.摘要: 背景 在澳大利亚北部地区, 原住民母亲的婴儿出生率占33%, 她们妊娠期间出现高血糖的风险很高。原住民母亲在妊娠期间的2型糖尿病(T2D)患病率与非原住民澳大利亚母亲相比较要高10倍, 并且经常使用二甲双胍治疗。我们利用临床登记表数据评估了妊娠期间使用二甲双胍治疗与出生结果之间的关系。 方法 这项研究从2012至2016年纳入了妊娠糖尿病(gestational diabetes, GDM)、妊娠期新诊断糖尿病(newly diagnosed diabetes in pregnancy, DIP)以及既往已经存在T2D的妇女。对妊娠晚期使用二甲双胍的数据进行了分析。根据母亲年龄、体重指数、产次以及胰岛素使用情况校正了回归模型。 结果 在1649名孕妇中有814名(49.4%)为原住民妇女, 其中234名(28.7%)为T2D(非原住民妇女T2D比例为4.6%；P 0.001)。原住民妇女的二甲双胍使用率更高(在T2D中为84%-90%, 在GDM/DIP中为42%-48%), 并且在非原住民妇女中随着时间的推移使用率在上升(在T2D中为43%-100%, 在GDM/DIP中为14%-35%)。在合并GDM/DIP的原住民妇女中, 使用二甲双胍治疗组与不使用二甲双胍治疗组之间的剖宫产率(分别为51%与39%; 校正后的odds ratio [aOR]为1.25, 95%置信区间[CI]为0.87-1.81)、出现大胎龄率(分别为24%与13%；aOR为1.5, 95% CI为0.9-2.5)、新生儿出现严重不良事件率(分别为9.4%与5.9%；aOR为1.32, 95% CI为0.68-2.57)都没有显著性差异。使用二甲双胍治疗与胎龄更小(分别为37.7与38.5周)独立相关, 但是将单独接受药物营养治疗的妇女排除之后, 这种风险没有独立地处于较高的水平, 并且多变量分析显示37周的出生率并没有显著地升高。 结论 我们没有发现任何与妊娠期间高血糖妇女使用二甲双胍治疗出现不良结果相关的明确证据。.

The purpose of this study was to examine the association of parental pre-pregnancy weight and body mass index (BMI) on offspring weight and BMI change from childhood to adulthood.

The International Journal of Gynecology and Obstetrics regrets that, in the above article, an error appeared in the 5.3.4 Measurement of uterine artery pulsatility index section on page 17, 5th paragraph, second last sentence: The first-trimester abnormal UTPI is defined as less than the 90th percentile, achieving a detection rate of 48%, at 8% false-positive rate, for the identification of early-onset PE. should have been: The first-trimester abnormal UTPI is defined as greater than the 90th percentile, achieving a detection rate of 48%, at 8% false-positive rate, for the identification of early-onset PE. Affiliation of the author, Mary D'Alton has been corrected to the following: Obstetrician and Gynecologist in-Chief, Columbia University Irving Medical Center, NewYork-Presbyterian The online version is corrected with the above changes after first online publication. We apologize for the inconvenience caused.

Several factors including placental hormones (PH) released from the human placenta have been associated with the development of insulin resistance and gestational diabetes mellitus (GDM). However, circulating levels of PH does not correlate well with maternal insulin sensitivity across gestation, suggesting that other, previously unrecognized, mechanisms may be involved. The levels of circulating exosomes are higher in GDM compared to normal. GDM derived exosomes produce greater release of pro-inflammatory cytokines from endothelial cells compared to exosomes from normal, suggesting that their contents may differ compared to normal pregnancies. Using a quantitative, information-independent acquisition (Sequential Windowed Acquisition of All Theoretical Mass Spectra [SWATH]) approach, differentially abundant circulating exosome proteins are identified in women with normal glucose tolerance (NGT) and GDM at the time of GDM diagnosis. A total of 78 statistically significant proteins in the relative expression of exosomal proteins in GDM are compared with NGT. Bioinformatic analysis shows that the exosomal proteins in GDM target pathways are mainly associated with energy production, inflammation, and metabolism. Finally, an independent cohort of patients is used to validate some of the proteins identified by SWATH. The data obtained may be of utility in elucidating the underlying physiological mechanisms associated with insulin resistance in GDM.

Diabet. Med. 29, e199e204 (2012) Abstract Aims To assess associations between maternal serum vitamin D concentration and glucose metabolism in a cohort of pregnant women living in an Australian subtropical environment. Methods Cross-sectional assessment of 25-hydroxy vitamin D concentrations in 399 Hyperglycemia and Adverse Pregnancy Outcome ancillary study participants, treated at an obstetric teaching hospital in Brisbane, Australia. All patients underwent a blinded 75-g oral glucose tolerance test at 2432 (target 28) weeks gestation. Results The mean (+/- standard deviation) fasting plasma glucose was 4.5 +/- 0.4 mmol/l. Mean (+/- standard deviation) serum 25-hydroxy vitamin D was 132.5 +/- 44.0 nmol/l. A difference of one standard deviation in maternal 25-hydroxy vitamin D was inversely related to fasting glucose (fasting glucose lower by 0.047 mmol/l, P = 0.012) when assessed with multiple linear regression after adjusting for confounders. Maternal 25-hydroxy vitamin D correlated with beta-cell function as estimated by the log-transformed homeostasis model assessment beta-cell function equation (r = 0.131, P = 0.009), but not with the homeostasis model assessment of insulin resistance. Conclusions An association between mid-gestational 25-hydroxy vitamin D and fasting glucose was confirmed in a largely normoglycaemic and vitamin D-replete pregnant population. The correlation between 25-hydroxy vitamin D and beta-cell function suggests that vitamin D may influence glucose metabolism through this mechanism. Intervention studies are required to determine causality and the role of vitamin D replacement in deficient individuals.

The purpose of this research was to assess the ability of ductus venosus (DV) Doppler velocimetry to predict adverse perinatal outcome in pregnancies complicated by pre-existing diabetes mellitus.This was a prospective study conducted at a tertiary referral obstetric facility in Brisbane, Australia. The study group included women with pregestational diabetes mellitus who delivered in the hospital between 1 January 1995 and 31 December 2006. The DV Doppler index was defined as abnormal if the DV peak velocity index for veins (PVIV) was equal to or greater than the 95(th) percentile for gestation. Adverse perinatal outcome included one or more of the following criteria: small-for-gestational-age infant; Cesarean section for non-reassuring fetal status; fetal acidemia at delivery; a 1-min Apgar score ofor= 3; a 5-min Apgar score of7; hypoxic ischemic encephalopathy; and stillbirth or neonatal death. The maternal characteristics and perinatal outcomes of pregnancies with normal or abnormal DV Doppler indices were compared.Eighty-two pregestational diabetic pregnancies were studied and an abnormal DV-PVIV was identified in 25 (30.5%). Adverse perinatal outcome was identified in eight of 25 (32.0%) pregnancies with an abnormal DV-PVIV compared to seven of 57 (12.3%) pregnancies with a normal DV-PVIV (P0.05). The sensitivity of the DV-PVIV in predicting adverse perinatal outcomes in pregestational diabetic pregnancies was 53.3%, the specificity was 74.6%, the positive predictive value was 32.0% and the negative predictive value was 87.7%.It may be useful to include DV-PVIV in the antenatal screening of pregnancies complicated by pregestational diabetes.

Objectives To assess the detection rate of congenital fetal malformations and specific problems related to routine ultrasound screening in women with pre-existing diabetes. Methods A retrospective study was carried out to assess the performance of routine ultrasound screening in women with pre-existing diabetes (Types 1 and 2) within a tertiary institution. The incidence, type and risk factors for congenital fetal malformations were determined. The detection rate of fetal anomalies for diabetic women was compared with that for the low-risk population. Factors affecting these detection rates were evaluated. Results During the study period, 12 169 low-risk pregnant women and 130 women with pre-existing diabetes had routine ultrasound screening performed within the institution. A total of 10 major anomalies (7.7%) and three minor anomalies (2.3%) were present in the fetuses of the diabetic women. Central nervous system and cardiovascular system anomalies accounted for 60% of the major anomalies. Peri-conceptional hemoglobin A 1 c of more than 9% was associated with a high prevalence of major anomalies (14311000). Women who had fetuses with major anomalies bad a significantly higher incidence of obesity (78% vs. 37%; P < 0.05). Ultrasound examination of these diabetic pregnancies showed high incidences of suboptimal image quality (37%), incomplete examinations, and repeat examinations (17%). Compared to the 'low-risk' non-diabetic population from the same institution, the relative risk for a major congenital anomaly among the diabetic women was 5.9-fold higher (95% confidence interval, 2.9-11.9). The detection rate for major fetal anomalies was significantly lower for diabetic women (30% vs. 73%; P < 0.01), and the mean body mass index for the diabetic group was significantly higher (29 vs. 23 kg/m(2); P < 0.001). Conclusion The incidence of congenital anomalies is higher in diabetic pregnancies. Unfortunately, the detection rate for fetal anomalies by antenatal ultrasound scan was significantly, worse than that for the low-risk population. This is likely to be related to the maternal body habitus and unsatisfactory examinations. Methods to overcome these difficulties are discussed.

Our objectives were to evaluate the psychosocial impact of a novel education programme, comprising an abbreviated curriculum based on the ‘core elements’ of insulin self-management education, with a view to identifying education options for those unable to attend a five-day Dose Adjustment for Normal Eating (DAFNE) programme. The novel programme was developed by DAFNE course facilitators and trialled using participants naive to flexible multiple daily injection (MDI) education. Post-course treatment satisfaction, wellbeing and diabetes distress were compared to baseline. Twenty-one adults attended the programme and 16 participants returned three months post-course. Significant improvements were seen in W-BQ12 total score, PAID score and DTSQ, equivalent to those observed following participation in the five-day programme. It was concluded that short course flexible MDI education is well tolerated by adults with type 1 diabetes, with improvements in treatment satisfaction and psychosocial outcome that are consistent with the five-day DAFNE programme. Further investigation of the longer-term impact on psychosocial and glycaemic outcomes of this novel curriculum is warranted. Copyright © 2017 John Wiley & Sons.