Neurodevelopmental outcome at 1 year in offspring of women with gestational diabetes mellitus.

OBJECTIVE: To study the metabolic derangements in the second half of pregnancy caused by gestational diabetes mellitus(GDM), on the short term neurodevelopment of infants. DESIGN: A prospective cohort study of 555 mother-child pairs were recruited, which included 177 GDM patients and 378 pregnant women with normal glucose tolerance as controls. Clinical and demographic characteristics were obtained at enrollment, birth and follow-up. Neurodevelopment was examined with the Bayley Scales of Infant Development V.1 mental development index (MDI) and psychomotor development index (PDI). Fatty acids (FA) were analyzed by gas chromatography mass spectrometry (GC-MS). RESULTS: Statistically significant differences were found between the two groups in fasting plasma glucose (FPG) and triglyceride (TG). The scores of MDI and PDI of control group were higher than those of GDM group. The regression analysis showed that maternal age and saturated fatty acid (SFA) were independently associated with lower scores on the MDI whereas gestational age and docosahexaenoic acid (DHA) were associated with higher scores; in addition, lower scores on the PDI were associated with FPG and neonatal weigh associated with higher scores. CONCLUSION: SFA, DHA and FPG as indicators of lipid metabolism were associated with neurodevelopmental outcome at 1 year in offspring of women with gestational diabetes mellitus. Control the level of blood glucose and lipid during pregnancy and the appropriate supplementation of DHA during pregnancy in the second half of pregnancy may be beneficial to the neurodevelopment of infants.

Maternal pre-pregnancy obesity and the risk of macrosomia: a meta-analysis.

PURPOSE: The aim of our meta-analysis was to explore whether pre-pregnancy obesity is regarded as an important risk factor for predicting macrosomia or not. METHODS: Three databases were systematically reviewed and reference lists of relevant articles were checked. Meta-analysis of published cohort studies comparing whether pre-pregnancy obesity was associated with macrosomia and adjusting for potential confounding factors. Calculations of pooled estimates were conducted in random-effect model. Heterogeneity was tested by using Chi-square test and I 2 statistics. Publication bias was estimated from Egger's test (linear regression method) and Begg's test (rank correlation method). RESULTS: Sixteen cohort studies met the inclusion criteria. The meta-analysis showed that pre-pregnancy obesity was associated with macrosomia as an important risk factor. The adjusted odds ratio was 1.93, 95% CI (1.65, 2.27) in random-effect model, stratified analyses showed no differences regarding different quality grade, definition of macrosomia, location of study and number of confounding factors adjusted for. There was no indication of a publication bias either from the result of Egger's test or Begg's test. CONCLUSION: Our findings indicated that pre-pregnancy obesity should be considered as an important risk factor for macrosomia. The effect of pre-pregnancy obesity on macrosomia need to be carefully assessed and monitored.

CTLA-4 polymorphisms and systemic lupus erythematosus (SLE): a meta-analysis.

The aim of this study was to summarize results on the association of cytotoxic T-lymphocyte antigen-4 (CTLA-4) promoter exon-1 +49 and 1722T/C polymorphism with systemic lupus erythematosus (SLE) susceptibility by using the meta-analysis. We searched all the publications about the association between CTLA-4) promoter exon-1 +49 and 1722T/C polymorphism and SLE from PubMed, Elsevier Science Direct, Chinese Biomedical Literature Database (CBM), Chinese National Knowledge Infrastructure (CNKI), and Wanfang (Chinese). Previous CTLA-4 association studies with SLE, however, have produced inconsistent results. We have performed a meta-analysis to better assess the purported associations. A total of 17 independent studies (to June 2012) testing association between one or more CTLA-4 polymorphisms and SLE were used in this analysis. We have compared allele and genotype frequencies at two polymorphic sites found in exon-1 (at +49) and the promoter region (at -1722). The data demonstrate that the exon-1 +49 polymorphism is associated with SLE susceptibility in Asian population. The overall risk, measured by odds ratio (OR), stratification by ethnicity indicates the exon-1 +49 GG+GA genotype is associated with SLE, at least in Asians (OR = 0.85, 95 % CI = 0.73-0.99, P = 0.04 for GG+GA vs. AA; OR = 0.85, 95 % CI = 0.72-1.00, P = 0.05 for AG vs. AA). Similar trends are found in allele-specific risk estimates and disease association. Overall, there was significant association between the 1722T/C polymorphism and overall SLE risks (OR = 0.78, 95 % CI = 0.63-0.97, P = 0.04 for GG+GA vs. AA, OR = 0.87, 95 % CI = 0.76-0.99, P = 0.04 for G vs. A) in Asian population.In summary, this meta-analysis demonstrates that the CTLA-4 promoter +49A/G and promoter -1722C/T polymorphism may confer susceptibility to SLE, especially in Asian-derived population.

Maternal prepregnancy overweight and obesity and the risk of preeclampsia: A meta-analysis of cohort studies.

OBJECTIVE: The aim of our meta-analysis was to explore whether overweight and obesity was associated with preeclampsia or not. DESIGN: Three databases were systematically reviewed and reference lists of relevant articles were checked. Meta-analysis of published cohort studies comparing whether overweight and obesity was associated with preeclampsia and adjusting for potential confounding factors. Calculations of pooled estimates were conducted in random-effects models. Heterogeneity was tested by using Chi-square test with Cochrane and heterogeneity was explored with meta-regression. Publication bias was estimated from Egger's test (linear regression method) and Begg's test (rank correlation method). RESULTS: Nineteen studies met the inclusion criteria. The meta-analysis showed that overweight and obesity was associated with an increased risk of preeclampsia. The aOR calculated for 13 studies (compared overweight to normal weight) was 1.71, 95% CI (1.52, 1.91) for random-effects models and 19 studies (compared obesity to normal weight) was 2.48, 95% CI (2.05, 2.90) for random-effects models, stratified analyses showed no differences regarding quality grade, location of study and period of anthropometric measurement. There was no indication of a publication bias either from the result of Egger's test or Begg's test. CONCLUSIONS: Our results suggested that prepregnancy maternal overweight and obesity are significantly associated with an increased risk of preeclampsia.

The Association between Advanced Maternal Age and Macrosomia: A Meta-Analysis.

PURPOSE: The aim of our meta-analysis was to explore whether advanced maternal age (AMA) is regarded as an important risk factor for predicting macrosomia or not. METHODS: Three databases were systematically reviewed and reference lists of relevant articles were checked. Meta-analysis of published cohort studies was done comparing whether AMA was associated with macrosomia and adjusting for potential confounding factors. Calculations of pooled estimates were conducted in random-effects models. Heterogeneity was tested by using chi-square test and I2 statistics. Publication bias was estimated from Egger's test (linear regression method) and Begg's test (rank correlation method). RESULTS: Twelve cohort studies met the inclusion criteria. The meta-analysis showed that AMA was associated with macrosomia as an important risk factor. The adjusted odds ratio calculated for 12 studies (compared aged 35-39 years to aged <30 years) was 1.42, 95% confidence interval (CI) (1.25-1.60) for random-effect model and 6 studies (compared aged ≥40 years to aged <30 years) was 1.40, 95% CI (1.02-1.78) for random-effect model. There was no indication of a publication bias either from the result of Egger's test or Begg's test. CONCLUSION: Regardless of the underlying mechanism, our finding indicated that AMA should be considered as an important risk factor for macrosomia. To adequately evaluate the clinical evolution of AMA, the effect of AMA on macrosomia need to be carefully assessed and monitored.