Article

Maternal overweight and obesity and the risk of congenital anomalies: a systematic review and meta-analysis.

Institute of Health and Society, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, United Kingdom NE2 4HH.
JAMA The Journal of the American Medical Association (Impact Factor: 29.98). 03/2009; 301(6):636-50. DOI: 10.1001/jama.2009.113
Source: PubMed

ABSTRACT Evidence suggests an association between maternal obesity and some congenital anomalies.
To assess current evidence of the association between maternal overweight, maternal obesity, and congenital anomaly.
MEDLINE, EMBASE, CINAHL, and Scopus (January 1966 through May 2008) were searched for English-language studies using a list of keywords. Reference lists from relevant review articles were also searched.
Observational studies with an estimate of prepregnancy or early pregnancy weight or body mass index (BMI) and data on congenital anomalies were considered. Of 1944 potential articles, 39 were included in the systematic review and 18 in the meta-analysis. Data Extraction and Synthesis Information was extracted on study design, quality, participants, congenital anomaly groups and subtypes, and risk estimates. Pooled odds ratios (ORs) comparing risk among overweight, obese, and recommended-weight mothers (defined by BMI) were determined for congenital anomaly groups and subtypes for which at least 150 cases had been reported in the literature.
Pooled ORs for overweight and obesity were calculated for 16 and 15 anomaly groups or subtypes, respectively. Compared with mothers of recommended BMI, obese mothers were at increased odds of pregnancies affected by neural tube defects (OR, 1.87; 95% confidence interval [CI], 1.62-2.15), spina bifida (OR, 2.24; 95% CI, 1.86-2.69), cardiovascular anomalies (OR, 1.30; 95% CI, 1.12-1.51), septal anomalies (OR, 1.20; 95% CI, 1.09-1.31), cleft palate (OR, 1.23; 95% CI, 1.03-1.47), cleft lip and palate (OR, 1.20; 95% CI, 1.03-1.40), anorectal atresia (OR, 1.48; 95% CI, 1.12-1.97), hydrocephaly (OR, 1.68; 95% CI, 1.19-2.36), and limb reduction anomalies (OR, 1.34; 95% CI, 1.03-1.73). The risk of gastroschisis among obese mothers was significantly reduced (OR, 0.17; 95% CI, 0.10-0.30).
Maternal obesity is associated with an increased risk of a range of structural anomalies, although the absolute increase is likely to be small. Further studies are needed to confirm whether maternal overweight is also implicated.

1 Bookmark
 · 
262 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Infertility affects one in seven couples, and its rate is on the increase. Ovulatory defects and unexplained causes account for >50% of infertile aetiologies. It is postulated that a significant proportion of these cases are either directly or indirectly related to obesity. The prevalence of overweight and obese men and women has topped 50% in some developed countries. Obesity is on the increase worldwide; in turn, the consequences in terms of the associated morbidity and mortality have also been increasing. Obesity is associated with various reproductive sequelae including anovulation, subfertility and infertility, increased risk of miscarriage and poor neonatal and maternal pregnancy outcomes. Thus, the combination of infertility and obesity poses some very real challenges in terms of both the short- and long-term management of these patients. The mechanism with which obesity impacts female reproductive function is summarised in this review. Copyright © 2014 Elsevier Ltd. All rights reserved.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Trichomonas vaginalis is an infectious agent of the vaginal flora which has been associated with cervical cancer. Galectin-1 (Gal 1) is a cell receptor expressed in cervical epithelial cells binding T. vaginalis’ lipophosphoglican (LPG). Interaction between T. vaginalis and the epithelial cell is mediated by poly-LacNac domains (galactoside and acetil-lactosamin) and is related to cell adherence as well. Cell signaling occurs by the time Src (SH2) domains are correlated with this interaction and PI3K phosphorilation brings up phosphatidil inositol lipid membranes (PIP and PIP2). T. vaginalis adheres to cytoplasm membrane and secrets specific enzymes that probably lead to membrane rupture. Moreover this parasite may phagocyte epithelial cells in vaginal discharge. Gal 1 nucleus called N-acetil-lactosamin can mediate growth development through GRB2 protein and may contribute to inflammation suppression owing to apoptosis induction of activated T cells.
    Femina: revista da Federação Brasileira das Sociedades de Ginecologia e Obstetrícia 05/2014; 42(3):129-134.
  • Source

Full-text (3 Sources)

Download
532 Downloads
Available from
May 28, 2014