Risk Of Fetal Growth Retardation Research Articles

Resolvin D1 level during different trimesters of pregnancy for predicting the risk of fetal growth retardation in elderly pregnancy

Resolvin D1 (RvD1) is potentially associated with fetal growth retardation (FGR) through alleviating maternal inflammation and its linkage with several pregnancy complications. Thus, this study detected RvD1 levels at different trimesters of pregnancy, aiming to investigate its role in predicting FGR risk of elderly pregnant women. This prospective, observational cohort study enrolled 165 elderly pregnant women aged ≥35 years. Serum RvD1 was detected at 10–13 weeks (early pregnancy), 20–23 weeks (middle pregnancy), and 30–33 weeks (late pregnancy) of gestational week by enzyme-linked immunosorbent assay. RvD1 was varied among different trimesters of pregnancy in elderly pregnant women (p < 0.001). FGR occurred in 25 (15.2%) women in this study. RvD1 at early (p = 0.009), middle (p = 0.002), and late (p = 0.003) pregnancy was decreased in women with FGR versus those without. By multivariate analysis, RvD1 at middle pregnancy (odds ratio (OR): 0.477, p < 0.001), pre-pregnancy body mass index (OR: 0.763, p = 0.025), and gestational diabetes mellitus (yes versus no) (OR: 0.071, p = 0.031) were independently correlated with declined FGR risk. While age (OR: 1.382, p = 0.009) was independently associated with elevated risk of FGR. Furthermore, the combination of these independent factors as a predictive model exhibited a good potential for assessing FGR risk (area under the curve: 0.802, 95% confidence interval: 0.711–0.894). In conclusion, RvD1 at different trimesters of pregnancy is negatively linked with the risk of FGR, whose level at middle pregnancy serves as an independent factor for FGR risk in elderly pregnant women.

Nutritional Implications of Bariatric Surgery on Pregnancy Management-A Narrative Review of the Literature.

One in three women of reproductive age is obese. The mainstay treatment for obesity is bariatric surgery, and the following weight reduction results in a decrease in pregnancy adverse effects, including gestational diabetes mellitus, pregnancy-induced hypertension, and macrosomia. However, nutritional and vitamin deficiencies due to changes in the gastrointestinal tract after bariatric surgery are associated with an increase in the risk of fetal growth retardation and small for gestational-age neonates. The purpose of this review was to analyze the available recent literature on the subject of the management of pregnancy after bariatric surgery. We searched for available articles from 2007 to 2023 and chose articles of the greatest scientific and clinical value. Micronutrient, vitamin, and protein supplementation is recommended in the prenatal period and throughout the pregnancy. It is advised that pregnant women with a history of bariatric surgery should be provided with regular specialist dietary care. There is still a lack of recommendations about the optimum gestational weight gain after different types of bariatric surgery and for patients of different metabolic statuses. Women of reproductive age undergoing bariatric procedures should be provided with appropriate counseling about adequate contraception, the recommended time-to-conception interval, and the positive and negative influence of bariatric surgery on perinatal outcomes.

Genetic markers of the risk of fetal growth retardation in pregnant women with preeclampsia

Introduction. Preeclampsia (PE) and fetal growth retardation (FGR), the main mechanism of which is the pathology of the placenta, directly affect the structure of both maternal and perinatal morbidity and mortality, which determines the medical and social significance of the study of PE and FGR, especially genetic predictors of the development of these complications of gestation. Objective. To study the involvement of GWAS polymorphism of significant arterial hypertension candidate genes in the formation of FGR in pregnant women with PE. Materials and methods. The samples for the study included 83 pregnant women with PE in combination with FGR and 369 women with isolated PE who were included in the control group. All women underwent a molecular genetic study of four polymorphisms: rs932764 PLCE1, rs167479 RGL3, rs633185 ARHGAP42, rs7302981 CERS5, and studied their relationship with the development of FGR in pregnant women with PE. The functional effects of polymorphic markers, which showed significant associations with the formation of FGR in pregnant women with PE, were examined using international bioinformatic projects on functional genomics (HaploReg, GTExportal, PolyPhen-2). Results and discussion. The AA genotype of the rs9327643 locus of the PLCE1 gene significantly reduces the risk of FGR formation in pregnant women with PE according to the recessive model (OR = 0.37; p = 0.01; pperm = 0.01). The rs932764 polymorphic variant of the PLCE1 gene is located in the region of regulatory DNA motifs for 2 Hdx and Zic transcription factors, localized in the region of histone protein encoding H3K4me1 enhancers in the brain and associated with the expression of the HDAC1P1 gene in male gonad tissues. Conclusions. The polymorphic locus rs9327643 of the PLCE1 gene is associated with the risk of developing FGR in pregnant women with PE.

Role of intergenic interactions among folate cycle genes in the development of fetal growth retardation

Objective: Metabolic disturbances in the folate cycle in mothers can lead to fetal growth retardation (FGR). This study was to analyze the role of intergenic interactions among maternal folate cycle genes in the development of FGR. Methods: This case-control study recruited 365 women in the third trimester of pregnancy, including 122 FGR patients and 243 controls. The women were genotyped for 5 polymorphisms of the 4 folate cycle genes: MTR (rs1805087), MTRR (rs1801394), serine hydroxymethyl transferase (SHMT1; rs1979277), and TYMS (rs699517 and rs2790). The SNP × SNP interactions in the two-, three-, and four-locus models were analyzed using the multifactor dimensionality reduction method and a modification of it (the model-based multifactor dimensionality reduction method). Results: Four loci of maternal folate cycle genes (rs1805087 MTR, rs2790 TYMS, rs1801394 MTRR, and rs1979277 SHMT1) were associated with FGR in 3 significant models of single nucleotide polymorphism (SNP) × SNP interactions (two-, three-, and four-locus models) (P &lt;0.05). The highest contribution to FGR was made by polymorphic loci rs1979277 SHMT1 (1.70% of entropy), rs1805087 MTR (0.96%), and interactions between rs1979277 SHMT1 × rs1805087 MTR (-1.11%) and rs1801394 MTRR × rs1979277 SHMT1 (−0.64%). The four-locus maternal genotype combination AG rs1801394 MTRR × AA rs1805087 MTR × CT rs1979277 SHMT1 × AG rs2790 TYMS was associated with an increased risk of FGR (β = 2.69, P = 0.012). FGR-associated SNPs were correlated with the expression of 16 genes (MTR, MTRR, SHMT1, ALKBH5, CTD-2303H24.2, ENOSF1, FAM106A, FOXO3B, LGALS9C, LLGL1, MIEF2, NOS2P2, RP11-806L2.6, SMCR8, TOP3A, and USP32P2) in various tissues and organs related to FGR pathophysiology. Conclusion: SNP × SNP interactions of maternal folate cycle genes (MTR, MTRR, SHMT1, and TYMS) are associated with the development of FGR.

Renal graft and pregnancy (Literature review)

The article is devoted to a review of the literature, which highlights the issues of maternal and perinatal complications and management of pregnant women who are renal transplant recipients.The risks of the development of hypertensive complications, preeclampsia, infectious complications, gestational diabetes and the risk of the fetus during pregnancy in these women are discussed in details. Pregnancy does not cause graft rejection, but pregestational hypertension, increased plasma creatinine and significant pregestational proteinuria are the risk factors for this complication. Pregnant women with a kidney transplant have a significantly higher risk of fetal growth retardation and premature birth.The article provides recommendations for the optimal period for pregnancy after transplantation which are recommended by various professional medical societies, although there is still no agreement on this issue: the American Society of Transplantation claims that the ideal period is 12-24 months after transplantation, while European best practice guidelines recommends to plan pregnancy no earlier than 2 years after surgery.The observation of pregnant women who are renal transplant recipients should be performed by an obstetrician-gynecologist with experience in high-risk pregnancy together with a transplantologist and perinatologist or neonatologist. All pregnant women who are kidney transplant recipients should be monitored for blood pressure, and aggressive antihypertensive therapy should be prescribed if it increases. It is also necessary to monitor the function of the graft, on suspicion of rejection it is possible to perform ultrasound-controlled kidney biopsy.The principles of immunosuppressive therapy during pregnancy, which includes prednisolone, methylprednisolone, tacrolimus, cyclosporine and azathioprine, and the description the side effects for the mother, the impact on the fetus and breastfeeding of each of the drugs are presented in the article. In the absence of obstetric complications, the optimal method of delivery is spontaneous delivery through the natural birth canal in the term of 38-40 weeks of pregnancy. Breastfeeding is recommended despite immunosuppressive therapy. Breast-feeding should be avoided when such medications as mycophenolate mofetil, sirolimus, everolimus and belatacept are used.Despite the high risk of pregnancy and childbirth, kidney transplant recipients have a good chance of pregnancy outcomes and giving birth to a living child while maintaining their own health. Therefore, motherhood should be encouraged among such women, supported and provided with highly qualified medical care.

Polymorphism of the maternal EGF gene is associated with the fetal growth retardation: a prospective comparative study

Aim. To study the involvement of polymorphism of growth factor genes and their receptors in the formation of fetal growth retardation (FGR).&#x0D; Materials and methods. In this prospective comparative study, genetic analysis of five polymorphic loci of growth factor genes and their receptors (rs4444903 EGF, rs833061 VEGFA, rs2981582 FGFR2, rs6214 IGF1, rs1800469 TGF1) was performed in 196 pregnant women with FGR and 324 pregnant women in the control group. For genotyping single-nucleotide polymorphism, the polymerase chain reaction method was used. The biomedical mechanisms underlying the identified associations were evaluated using modern bioinformatic resources: GTExportal (effect on gene transcription) and HaploReg (regulatory potential).&#x0D; Results. The allelic variant G rs4444903 of the EGF gene determines an increased risk of FGR in the following genetic models: allelic (OR 1.28, 95% CI 1.001.65; рperm=0.033), additive (OR 1.33, 95% CI 1.021.75; рperm=0.039) and dominant (OR 1.62, 95% CI 1.062.47; рperm=0.031). The polymorphism rs4444903 of the EGF gene has a significant epigenetic potential (in the field of promoters, enhancers, "open chromatin", transcription regulatory proteins), determines the expression of the EGF and GAR1 genes and alternative splicing of the GAR1 gene in organs and tissues (placenta, fetal and adult brain, etc.), which are significant for the pathophysiology of FGR.&#x0D; Conclusion. The associations rs4444903 of the EGF gene with the FGR are shown.

PECULIARITIES OF PREGNANCY COURSE, CHILDBIRTH, AND MORPHOFUNCTIONAL STATE OF PLACENTA IN WOMEN WITH INTRAUTERINE FETAL GROWTH RETARDATION

Fetal growth retardation is a severe obstetric pathology that is accompanied by significant reproductive losses and the cost of treating newborns. The aim of the study is to investigate the clinical difference between the course of pregnancy, childbirth, and morphofunctional state of the placenta in women who gave birth to children with low birth weight before gestational age and normal anthropometric parameters. Materials and methods. The study included 37 women; the individuals of the main group gave birth to a child with low birth weight before gestational age (n = 25), the comparison group consisted of women who had uneventful pregnancy and children born with normal anthropometric parameters (n = 12) . Results and discussion. Pregnancy and childbirth in the main group were registered mostly within the age range of 30 and 39, burdened with bad habits, accompanied by somatic and obstetric pathology. The predominant mode of preterm delivery in most of the main group was cesarean section caused by fetal distress in contrast to women in the comparison group. Analysis of the morphofunctional state of the placenta from the women in the main groups revealed both general structural-adaptive and structural-morphological changes that indicated compensatory hyperplasia of placental tissue in women with foetal intrauterine growth retardation that is characteristic of the compensated stage of chronic placental insufficiency. Conclusion. The multicomponent impact of various factors may contribute to an increased risk of fetal growth retardation and its progression, so timely correction of risk factors will help to improve the management of pregnancy and perinatal outcomes.

Assessment of Applying Clinical Audit for Pregnant Woman with Iron Deficiency Anemia.

Background: clinical audit is a complementary part of the standards it includes a checklist and action plan. The checklist can be used to test or audit standards. The action plan is a conclusive part of the audit. Iron deficiency anemia during pregnancy is one of the most significant health problems in the world. Impact of iron deficiency anemia on the pregnant women its outcomes that it has many serious consequences on increase the risk of fetal growth retardation, premature delivery. Aim of the study: To assess clinical audit which used for the pregnant woman with iron deficiency anemia. Research design: descriptive design was carried out in this study. Setting: All Maternal and Child Health centers in Qena City and Minia City which were four centers in Minia and six centers in Qena. Sample: convenient sample of 500 records of pregnant women. Tool of data collection: Tool 1: questionnaire sheet includes the socio-demographic include personal and obstetrical history. Tool 2: Standard of care for the pregnant with iron deficiency anemia adopted from (WHO) source. Results: we found that 76% in Qena city versus 82%in Minia city had mild anemia, while 24% in Qena city versus17.6% had moderate anemia. Absence of woman with severe and very severe anemia .distribution of Mild and Moderate anemia was higher in urban. More than 75% of standard points were applicable in the two governorates. Conclusion: The present study concluded that the nurses of Maternal and Child Health centers didn’t apply all points of WHO audit. Recommendations: Every healthcare facility should develop and implement an Annual Clinical Audit Forward Plan as part of its annual planning and delivery cycle for clinical audit activities and the facility's safety and quality governance framework. Health care providers need further training to apply clinical audit completely .Health care records needed updated to conclude all point of WHO clinical audit related to absence of some of care services to pregnant woman.

The evaluating of pregnancy-associated plasma protein-A with the likelihood of small for gestational age.

ObjectiveRecently, strong evidences were obtained on the association between low pregnancy-associated plasma protein-A (PAPP-A) levels in the first trimester and poor outcomes of pregnancy.MethodsThis cross-sectional study was conducted on all pregnant women who were referred to the Obstetrics and Gynecology Clinic at Imam Hossein Hospital in Tehran, Iran in 2014. Women were asked to attend clinical examinations and screening at 11–14 weeks of gestation.ResultsBased on the definition, 14.5% of neonates found to be small for gestational age (SGA). There was a strong association between PAPP-A levels and birth weight. The mean PAPP-A level in the mothers of neonates who were SGA was significantly lower than those without this poor outcome. Based on the receiver operating characteristic curve analysis, serum PAPP-A level was a main determinant in the prediction of SGA neonates.ConclusionThe serum PAPP-A level at 11–13 weeks of gestation can effectively predict the increased risk for fetal growth retardation. In patients in this study, the best cutoff value for PAPP-A was 0.75 MOM, which signifies that lower levels of this marker can predict fetal growth restriction with high sensitivity and specificity.

Associations between in utero exposure to polybrominated diphenyl ethers, pathophysiological state of fetal growth and placental DNA methylation changes

BackgroundPolybrominated diphenyl ethers (PBDEs) are environmental chemicals with harmful effects on pregnancy, but their effects on adverse developmental outcomes are not fully understood. The placental DNA methylation is strongly influenced by prenatal environmental factors and has been linked to fetal growth. ObjectiveTo evaluate the association between in utero PBDEs exposure, placental DNA methylation changes (growth regulatory genes), and pathophysiology of fetal growth (birth outcomes, fetal growth retardation) in a population-based pregnancy cohort study. MethodsThis was a nested case-control study within the prospective Wenzhou Birth Cohort including 130 fetal growth retardation (FGR) cases and 130 healthy controls and their mothers recruited from June 2016 to June 2017. FGR was diagnosed based on the comprehensive evaluation of ultrasound results at 24, 28, and 32 weeks of gestation. Neonatal birth measurements were obtained from medical records. Gestational exposure to 19 PBDEs, including 13 lower BDE congeners (BDE-17–190) and 6 higher brominated BDE congeners (BDE-196–209), were determined by gas chromatography tandem mass spectrometry in the umbilical cord blood. Placental DNA methylation changes of one repetitive element (LINE1) and two candidate genes (HSD11B2, IGF2) were characterized by quantitative polymerase chain reaction-pyrosequencing. Multiple linear regression and logistic regression models were used to examine the associations among PBDEs exposure, fetal growth indicators, and DMR (differential methylation region) methylation fractions. Sobel tests were conducted to assess DNA methylation as a mediator in multivariate models. ResultsAfter excluding women who withdrew from the study or were lost to follow-up or failed to provide placenta or umbilical cord blood, 249 mother-newborn pairs (124 FGR cases, 125 controls) were included in the final analysis. Elevated BDE-206 (OR: 1.569, 95% CIs: 1.053–2.338), BDE-17–190 (OR: 2.860, 95% CIs: 1.233–6.634), BDE-196–209 (OR: 1.688, 95% CIs: 1.024–2.783) and ∑19PBDEs (OR: 2.387, 95% CIs: 1.220–4.668) concentrations were associated with increased risk of FGR in newborns. FGR birth was also associated with increased DNA methylation of HSD11B2 (OR: 1.145, 95% CIs: 1.032–1.270) and decreased DNA methylation of IGF2 (OR: 0.892, 95% CIs: 0.845–0.941). In addition, BDE-17–190 showed significant associations with DNA methylation of HSD11B2 and IGF2 (β: 1.127, 95% CIs: 0.069–2.186; β: −3.452, 95% CIs: −5.512–1.392), indicating placental DNA methylation changes of HSD11B2 and IGF2 were related to both lower BDE congeners exposure and fetal growth. Further mediation analyses showed that IGF2 methylation mediated about 40% of the effects of BDE-17–190 in umbilical cord blood on neonatal FGR. ConclusionWe report an inverse association between in utero exposures to PBDEs and fetal growth and provide evidence supporting epigenetic gene plasticity in these associations. Changes in placental DNA methylation might be part of the underlying biological pathway between prenatal PBDEs exposure and adverse fetal growth.

Heparin prophylaxis of gestational complications in women with Factor V Leiden mutation (GA genotype)

The aim of the study was to determine the efficacy of heparin prophylaxis in preventing pregnancy complications in patients with the manifested laboratory phenotype – resistance to activated protein C (APC-resistance with NR ≤ 0.49) Factor V Leiden mutation (GA genotype). Materials and methods. A single-center, randomized, controlled trial of 141 pregnant women – carriers of the FVL(1691)GA mutation with APC-resistance ≤ 0.49 was determined at a gestation age of 7-8 weeks. Of these, 70 patients were included in the main group (mean age 30.2 ± 4.7 years); after the confirmation of the APC-resistance at 7-8 weeks of gestation, these women received a 14 day low-molecular-weight heparin (LMWH) course at elevated prophylactic doses. The comparison group (71 pregnant women of 30.3 ± 3.9 years old) received no LMWH. Results. The heparin prophylaxis (started from 7-8 weeks of gestation) at elevated doses in carriers of the FVL(1691)GA mutation with pronounced APC-resistance reduced the absolute risk (ARR) of pre-eclampsia by 29.5% (ARR: 29.5; p = 0.0003; NTT: 3.4; 95% Cl: 2.356.12), the risk of fetal growth retardation by 23.8% (ARR: 23.8; p = 0.0016; NTT: 4.2; 95% Cl: 2.8-8.7) and the risk of induced premature birth by 12.6% (ARR: 12.6; p = 0.0242; NTT: 5.8; 95% Cl: 3.7-14.1). Conclusion. The administration of LMWH at prophylactic doses for 14 days is indicated in patients with a manifested subclinical (laboratory) phenotype (APC-resistance with NR ≤ 0.49) of the FVL(1691)GA mutation starting from the gestation period of 7-8 weeks. If necessary (with a value of NR ≤ 0.49), it is advisable to repeat the courses of heparin prophylaxis at 18-19 and 27-28 weeks of pregnancy.

Genetic markers for inherited thrombophilia are associated with fetal growth retardation in the population of Central Russia.

The aim of this study was to examine the role of hereditary thrombophilia in the development of fetal growth retardation (FGR) in the population of Central Russia. The case-control study sample included 497 women in the third trimester of pregnancy recruited during 2009-2013. The participants were enrolled into two groups: patients with FGR (n = 250) and controls without FGR (n = 247). The participants were genotyped for four genetic markers of hereditary thrombophilia: factor V Leiden (G > A FV, rs6025), prothrombin (G > A FII, rs1799963), factor VII (G > A FVII, rs6046), and fibrinogen (G > A FI, rs1800790). The genetic factors for an increased risk of FGR were allele G of rs6046 (odds ratio [OR]=2.34) and genotype GG of rs6046 (OR =2.64), whereas genotype GA of rs6046 had the protective value (OR=0.42). A combination of alleles G of rs1799963, A of rs6046, and G of rs1800790 (OR=0.31) reduces the risk of FGR. Polymorphism rs6046 of the FVII gene is associated with the development of FGR.

The association between adverse pregnancy outcomes and maternal factor V Leiden genotype: a meta-analysis.

The conclusions of studies to date which evaluate a possible association between factor V Leiden and adverse pregnancy outcome have been conflicting. This study was undertaken to further investigate this association. Our objective was to evaluate the association between adverse pregnancy outcomes and maternal factor V Leiden genotype by meta-analysis. Inclusion criteria were: (a) cohort or case control design; (b) outcomes clearly defined as one of the following: first or second/ third trimester miscarriage or intrauterine death, preeclampsia, fetal growth retardation, or placental abruption; (c) both the case and control mothers tested for the factor V Leiden mutation; (d) sufficient data for calculation of an odds ratio. Both fixed and random effect models were used to pool results and heterogeneity and publication bias were checked. For first trimester fetal loss, the pooled odds ratio was heterogeneous (p=0.06) and no dose-response curve could be found. For second/third trimester fetal loss, there was a consistent and graded increase in risk: the odds ratio was 2.4 (95% CI 1.1-5.2) for isolated (non-recurrent) third trimester fetal loss, rising to 10.7 (95% CI 4.0-28.5) for those with 2 or more second/third trimester fetal losses. Factor V Leiden is associated with a 2.9 fold (95% CI 2.0-4.3) increased risk of severe preeclampsia, and a 4.8 fold (95% CI 2.4-9.4) increased risk of fetal growth retardation. These results support factor V Leiden testing for women with recurrent fetal loss in the second/third trimester. Women with only 1 event may also warrant testing if the fetal loss occurred in the third trimester. Conversely, in those women known to have the factor V Leiden mutation, monitoring for adverse pregnancy outcomes is warranted; whether this means increased vigilance or anti-coagulant prophylaxis is still contentious.

Serial measurements of serum human placental lactogen (hPL) and serial ultrasound examinations in the evaluation of fetal growth.

Serial serum hPL measurements and serial ultrasound fetometry were compared in the evaluation of fetal growth by relating these two parameters to size at birth and to clinical factors known to influence size at birth. The data were from a prospective study of 1000 consecutive pregnant women considered to be at risk for fetal growth retardation with retrospective analysis. Serum hPL was measured by radioimmunoassay and fetal weight estimated by ultrasound every 3 weeks during the last trimester. hPL values were expressed as multiples of the median (MoM) and linear regression analysis of the hPL MoM values was carried out for each pregnancy to find the slope of the line (hPL-slope); at least 3 serum hPL values were required. The estimated fetal weight and weight-for-age at birth was expressed in Z-scores. The individual intrauterine growth velocity was calculated by regression analysis and expressed as change in Z-score for 12 weeks. At least two ultrasound measurements over an interval of at least 42 days were used to estimate the fetal growth velocity. In 588 women the file was complete. The main outcome measures were the individual mean hPL, hPL-slope, fetal growth velocity, birth weight deviation, smoking in pregnancy and diagnosis of preeclampsia. A significant correlation was found between the hPL-slope and the intrauterine fetal growth velocity (r=0.34), and between hPL-slope and birth weight deviation (r=0.32). Mean hPL was correlated to birth weight deviation (r=0.27), but only very weakly to intrauterine growth velocity (r=0.08). hPL-slope and intrauterine growth velocity independently predicted birth weight deviation. Heavy smoking which was stopped before the third trimester was not associated with low intrauterine growth velocity, but with a low hPL-slope. Preeclampsia was associated with a trend towards low and decreasing hPL and with an increasing intrauterine growth velocity and birth weight deviation. In conclusion the rate of change of serial hPL measurements correlated well to intrauterine fetal growth velocity in the third trimester as estimated by ultrasound and to the deviation in birth weight, but hPL seems to have a separate physiological significance, since it did not pick up when smoking was stopped and growth velocity was normalised and it did not at all detect the increased growth associated with preeclampsia.

The effect of work activity in pregnancy on the risk of fetal growth retardation.

The relationship between physical activity at work and risk of fetal growth restriction is controversial. For the most part, previous studies investigated the effect of work activity on birthweight alone. We evaluated the impact of type of occupation and physical effort at work on the risk of ultrasonographically confirmed fetal growth retardation among nulliparous women. We compared the characteristics of work and the intensity of occupational fatigue (work posture, weekly working hours, physical effort at work) in 349 patients with ultrasonographically confirmed fetal growth retardation and 698 control pregnancies with appropriate fetal growth. Physical demands at work were evaluated by interview at birth. Logistic regression analysis was used to evaluate the association of employment status, type of occupation, and intensity of occupational fatigue with the risk of fetal growth retardation, correcting for potential confounders (maternal age, pre-pregnancy body mass index, mean weight gain in pregnancy, education, partner's social status, smoking in pregnancy, alcohol use, illicit drug use, time of stopping work, and hypertension). After adjusting for confounding, the risk of fetal growth retardation was similar between unemployed and formally employed women at the beginning of pregnancy (OR = 1.26; 95% confidence interval = 0.86 - 1.83). However, manual workers were at slightly higher risk of IUGR than not formally employed women (OR = 1.81; 95% CI = 1.15 - 2.85). Among formally employed women, standing or walking at work, and working > or = 30 hours a week were not significantly associated with IUGR. Finally, the risk of IUGR was significantly higher (OR = 2.46; 95% CI = 1.36 - 4.21) among women reporting moderate-to-heavy as compared to light physical effort at work. Formal employment at the beginning of pregnancy is not associated with an increased risk of IUGR. However, moderate-to-heavy physical effort at work seems to increase the risk of sonographically confirmed fetal growth retardation.

Effect Measures for Behavioral Factors Adversely Affecting Fetal Growth

The purpose of this study was to estimate the proportion of ultrasonically diagnosed fetal growth retardation that may be attributable to potentially remediable factors (for example, cigarette smoking, alcohol use, and drug addition). We computed multivariate odds ratios for fetal growth retardation associated with cigarette smoking and alcohol and illicit drug consumption in 350 singleton pregnancies complicated by fetal growth retardation and 700 controls. The odds ratio of fetal growth retardation among women who smoked throughout pregnancy was 2.61 (95% confidence interval, 1.38 to 4.93) compared to women who claimed to have stopped smoking by the 18th week of gestation. The summary attributable risk of fetal growth retardation associated with behavioral variables measured during the first trimester and thereafter ranged from 18 to 21%. By implication, the maximum proportion of fetal growth retardation that could theoretically be prevented by eliminating these risk factors accounts for about 1% of all births. However, allowance for the limited modifiability of preventable factors and the consistent overlap between them would probably reduce such estimate to less than 1%. We conclude that only interventions to reduce the prevalence of strong risk factors (for example, preeclampsia, sociodemographic variables) may have a substantial effect on the incidence of impaired fetal growth and subsequent infant morbidity.

Safety of drug therapy for inflammatory bowel disease in pregnant and nursing women

: Drug therapy is justified in pregnant patients with active inflammatory bowel disease. Selection of medical treatment depends on disease severity and the potential for fetal toxicity. Preferably, pregnancy should be planned to coincide with periods of disease quiescence, so that drug requirements can be minimized. Sulphasalazine and prednisolone are clearly safe in pregnancy and lactation. Preliminary studies suggest that lowto-moderate-dose mesalazine is well tolerated in pregnant and nursing mothers. Immunosuppressive therapy during pregnancy in transplant and nontransplant recipients may be associated with an increased risk of fetal growth retardation and prematurity. The risk of congenital malformations from azathioprine and cyclosporin is not markedly increased, although exposure to methotrexate during the first trimester may cause fetal loss and characteristic anomalies. Short-term therapy with metronidazole in the first trimester is not associated with an increased risk of teratogenicity, although the safety of this drug in pregnancy as primary therapy for Crohn's disease using higher doses for prolonged periods has not been confirmed.

The relationship between maternal and neonatal anthropometric measurements in term newborns

To determine whether measures of maternal lean mass, fat reserves, or a combination of both best predict the various measures of newborn size at birth. The population consisted of 1205 multiparous, predominantly black women at high risk for fetal growth retardation, who delivered at term at the University of Alabama at Birmingham. Maternal body mass index (BMI) was calculated using the reported pre-pregnancy weight. Maternal anthropometric measurements taken at mid-pregnancy included skinfold thicknesses, lean body mass, and mid-arm, calf, and wrist circumferences. Weight and 11 other neonatal measurements were made within 24 hours of birth and related to various maternal anthropometric measurements. Reported maternal pre-pregnancy weight was the best predictor of all neonatal size measures except for the neonatal skinfold thicknesses, which were better predicted by the pre-pregnancy BMI. For example, the range between the tenth and 90th percentiles of maternal pre-pregnancy weight (46.3-86.4 kg) was associated with 295 g birth weight compared to only 188 g birth weight for a measure of lean body mass. Most maternal anthropometric measurements were significantly associated with most neonatal measurements. However, for nearly every neonatal measurement considered, the maternal pre-pregnancy weight was the best predictor.

Fetus-Placenta-Newborn: Accuracy of the middle-cerebral-to-umbilical-artery resistance index ratio in the prediction of neonatal outcome in patients at high risk for fetal and neonatal complications

The purpose of this study was to determine the accuracy of the middle-cerebral-to-umbilical-artery resistance index ratio in the prediction of fetal outcome in pregnancies at high risk for fetal and neonatal morbidity and mortality. A prospective controlled nonrandomized study was conducted in the high-risk pregnancy unit of a teaching hospital. The control group was formed by 20 healthy women with uncomplicated singleton pregnancies and healthy children delivered at term. The study group consisted of 115 women referred to the high-risk pregnancy unit because of a variety of pregnancy complications. Longitudinal evaluation of the control group and cross-sectional evaluation of the study group were carried out at different gestational ages by means of duplex Doppler ultrasonography. The main outcome measures were fetal growth retardation, preterm birth, and neonatal morbidity. The middle-cerebral-to-umbilical-artery ratio remains relatively constant (mean +/- SD 1.33 +/- 0.19) between 27 and 37 weeks. A cutoff value of 1.0 (sensitivity 57.9%, specificity 75.6%, false-positive rate 24.4%) was selected from the receiver-operator characteristic curve analysis. This cutoff value successfully identified a population at significant risk of fetal growth retardation (relative risk 3.07, 95% confidence interval 1.73 to 5.45, exact two-tailed p = 0.0009) and severe neonatal morbidity (Mann-Whitney U = 463.5, two-tailed p = 0.03). The middle-cerebral-to-umbilical-artery ratio was not useful in the prediction of preterm birth. A middle-cerebral-to-umbilical-artery ratio of < or = 1.0 identifies a subgroup of patients at high risk for fetal growth retardation and severe neonatal morbidity.

Factors potentiating the smoking-related risk of fetal growth retardation.

To estimate the risk of fetal growth retardation resulting from the interaction between maternal smoking during pregnancy and other recognized risk factors. Case-control study of prospectively recorded data. Department of Obstetrics and Gynaecology, University of Pavia, Italy. Three hundred and forty-seven singleton pregnancies with diagnosis of fetal growth retardation and 694 control pregnancies with appropriately grown fetuses. The overall odds ratio for fetal growth retardation associated with maternal smoking was 2.87 (95% confidence interval, 2.17-3.80). In logistic models the factors which independently increased the smoking-related risk of fetal growth retardation were a male fetus, nulliparity, maternal age 20 years or less, a history of first trimester haemorrhage and low (less than 50 kg) pre-pregnancy weight. The combined effect of smoking and caffeine consumption on the risk of fetal growth retardation was found to be additive rather than multiplicative. Several factors can affect the risk of fetal growth retardation associated with maternal smoking. The prenatal identification of these factors could help detect subgroups of women at high risk of fetal growth retardation.