856 resultados para maternal hability
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Aim: This study examines the transition from fertility to obstetrical care of women who conceived through IVF. Materials & methods: 33 women filled out questionnaires before IVF, during pregnancy and after birth on infertility stress, maternal adjustment and depressive symptoms. During pregnancy, they participated in an interview about their emotional experiences regarding the transition. Responses were sorted into three categories: Autonomy, Dependence and Avoidance. Results: Exploratory results show that 51.5% of women had no difficulties making the transition (Autonomy), 21.2% had become dependent (Dependence) and 27.3% had distanced themselves from the specialists (Avoidance). Women who became dependent had more trouble adjusting to motherhood and more depressive symptoms. Conclusion: Difficulty making the transition may be linked to decreased ability to adjust to motherhood and more postpartum depressive symptoms.
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Vitamin K deficiency bleeding within the first 24 h of life is caused in most cases by maternal drug intake (e.g. coumarins, anticonvulsants, tuberculostatics) during pregnancy. Haemorrhage is often life-threatening and usually not prevented by vitamin K prophylaxis at birth. We report a case of severe intracranial bleeding at birth secondary to phenobarbital-induced vitamin K deficiency and traumatic delivery. Burr hole trepanations of the skull were performed and the subdural haematoma was evacuated. Despite the severe prognosis, the infant showed an unexpected good recovery. At the age of 3 years, neurological examinations were normal as was the EEG at the age of 9 months. CT showed close to normal intracranial structures. CONCLUSION: This case report stresses the importance of antenatal vitamin K prophylaxis and the consideration of a primary Caesarean section in maternal vitamin K deficiency states and demonstrates the successful management of massive subdural haemorrhage by a limited surgical approach.
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Introduction: Mirtazapine is a noradrenergic and serotonergic antidepressant mainly acting through blockade of presynaptic alpha-2 receptors. Published data on pregnancy outcome after exposure to mirtazapine are scarce. This study addresses the risk associated with exposure to mirtazapine during pregnancy. Patients (or Materials) and Methods: Multicenter (n = 11), observational prospective cohort study comparing pregnancy outcomes after exposure to mirtazapine with 2 matched control groups: exposure to any selective serotonin reuptake inhibitor (SSRI) as a diseasematched control group, and general controls with no exposure to medication known to be teratogenic or to any antidepressant. Data were collected by members of the European Network of Teratology Information Services (ENTIS) during individual risk counseling between 1995 and 2011. Standardized procedures for data collection were used in each center. Results: A total of 357 pregnant women exposed to mirtazapine at any time during pregnancy were included in the study and compared with 357 pregnancies from each control group. The rate of major birth defects between the mirtazapine and the SSRI group did not differ significantly (4.5% vs 4.2%; unadjusted odds ratio, 1.1; 95% confidence interval, 0.5-2.3, P = 0.9). A trend toward a higher rate of birth defects in the mirtazapine group compared with general controls did not reach statistical significance (4.2% vs 1.9%; OR, 2.4; 95% CI, 0.9-6.3; P = 0.08). The crude rate of spontaneous abortions did not differ significantly between the mirtazapine, the SSRI, and the general control groups (9.5% vs 10.4% vs 8.4%; P = 0.67), neither did the rate of deliveries resulting in live births (79.6% vs 84.3% in both control groups; P = 0.15). However, a higher rate of elective pregnancy-termination was observed in the mirtazapine group compared with SSRI and general controls (7.8% vs 3.4% vs 5.6%; P = 0.03). Premature birth (< 37 weeks) (10.6% vs 10.1% vs 7.5%; P = 0.38), gestational age at birth (median, 39 weeks; interquartile range (IQR), 38-40 in all groups; P = 0.29), and birth weight (median, 3320 g; IQR, 2979-3636 vs 3230 g; IQR, 2910-3629 vs 3338 g; IQR, 2967-3650; P = 0.34) did not differ significantly between the groups. Conclusion: This study did not observe a statistically significant difference in the rate of major birth defects between mirtazapine, SSRI-exposed, and nonexposed pregnancies. A slightly higher rate of birth defects was, however, observed in the mirtazapine and SSRI groups compared with the low rate of birth defects in our general controls. Overall, the pregnancy outcome after mirtazapine exposure in this study is very similar to that of the SSRI-exposed control group.
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This study examines trends and geographical differences in total and live birth prevalence of trisomies 21, 18 and 13 with regard to increasing maternal age and prenatal diagnosis in Europe. Twenty-one population-based EUROCAT registries covering 6.1 million births between 1990 and 2009 participated. Trisomy cases included live births, fetal deaths from 20 weeks gestational age and terminations of pregnancy for fetal anomaly. We present correction to 20 weeks gestational age (ie, correcting early terminations for the probability of fetal survival to 20 weeks) to allow for artefactual screening-related differences in total prevalence. Poisson regression was used. The proportion of births in the population to mothers aged 35+ years in the participating registries increased from 13% in 1990 to 19% in 2009. Total prevalence per 10 000 births was 22.0 (95% CI 21.7-22.4) for trisomy 21, 5.0 (95% CI 4.8-5.1) for trisomy 18 and 2.0 (95% CI 1.9-2.2) for trisomy 13; live birth prevalence was 11.2 (95% CI 10.9-11.5) for trisomy 21, 1.04 (95% CI 0.96-1.12) for trisomy 18 and 0.48 (95% CI 0.43-0.54) for trisomy 13. There was an increase in total and total corrected prevalence of all three trisomies over time, mainly explained by increasing maternal age. Live birth prevalence remained stable over time. For trisomy 21, there was a three-fold variation in live birth prevalence between countries. The rise in maternal age has led to an increase in the number of trisomy-affected pregnancies in Europe. Live birth prevalence has remained stable overall. Differences in prenatal screening and termination between countries lead to wide variation in live birth prevalence.
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In 2008, the Confidential Enquiry into Maternal and Child Health (CEMACH), now known as the Centre for Maternal and Child Enquiries (CMACE), commenced a 3-year UK-wide Obesity in Pregnancy project. The project was initiated in response to a number of factors. At the time, these included: i) growing evidence that obesity is associated with increased morbidity and mortality for both mother and baby, ii) evidence from the CEMACH 'Saving Mothers' Lives' report showed that women with obesity were over-represented among those who died of direct deaths compared to those who died of indirect deaths, 1 iii) unknown national and regional prevalence rates of maternal obesity, and iv) the need for a national clinical guideline for the care of women with obesity in pregnancy.
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Question: Are maternal effects (i.e. maternal transfer of immune components to their offspring via the placenta or the egg) specifically directed to the offspring on which ectoparasites predictably aggregate? Organisms: The barn owl (Tyto alba) because late-hatched offspring are the main target of the ectoparasitic fly Carnus hemapterus. Hypothesis: Pre-hatching maternal effects enhance parasite resistance of late- compared with early-hatched nestlings. Search method: To disentangle the effect of natal from rearing ranks on parasite intensity, we exchanged hatchlings between nests to allocate early- and late-hatched hatchlings randomly in the within-brood age hierarchy. Result: After controlling for rearing ranks, cross-fostered late-hatched nestlings were less parasitized but lighter than cross-fostered early-hatched nestlings. Conclusion: Pre-hatching maternal effects increase parasite resistance of late-hatched offspring at a growth cost.
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The findings in this report are based on stillbirths and neonatal deaths with a date of birth between 1 January 2008 and 31 December 2008 notified to AWPS/CMACE and reported to the Office for National Statistics (ONS). For maternity provider rates, denominators are based on live births reported to AWPS/CMACE by hospitals. For country rates, denominators are based on live births reported to ONS and NISRA-GRO.Perinatal mortality rates for 2008 are assigned to a geographical area. Country specific findings are derived using maternal postcode of residence. Findings for maternity providers within Northern Ireland are derived using the place of death, and any deaths at home are allocated to the maternity provider that provided the care at the time of death.
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The findings in this report are based on stillbirths and neonatal deaths with a date of birth between 1 January 2009 and 31 December 2009 notified to CMACE and reported to the Office for National Statistics (ONS). For Trust rates, denominators are based on live births reported to CMACE by hospitals. For Strategic Health Authority (SHA) and country rates, denominators are based on live births reported to ONS and Northern Ireland Statistics and Research Agency (NISRA).Perinatal mortality rates for 2009 are assigned to a geographical area and are derived using maternal postcode of residence. Findings for Trusts are derived using the place of death, and any deaths at home are allocated to the Trusts that provided the care at the time of death.
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This guidance provides information for professionals on Maternal and Pre-school Nutrition for infants and children.
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Introduction Statin use in women of childbearing age is increasingly common. However, published data on pregnancy outcome after exposure to statins are scarce and conflicting. This contribution addresses the safety of statin use during pregnancy.Materials and Methods In a multi-centre (n = 11), prospective study we compared the outcomes of 249 women exposed during the 1st trimester of pregnancy to simvastatin (n = 124), atorvastatin (n = 67), pravastatin (n = 32), rosuvastatin (n = 18), fl uvastatin (n = 7) or cerivastatin (n = 1) with a control group exposed to agents known to be non-teratogenic (n = 249). Data were collected by members of the European Network of Teratology Information Services during individual risk counselling.Results The difference in the rate of major birth defects between the statinexposed and the control group was statistically insignificant (4.0% versus 2.7% OR 1.5; 95% CI 0.5-4.5, p = 0.44). The crude rate of spontaneous abortions (12.8% versus 7.1%, OR 1.9, 95% CI 1.0-3.6, p = 0.04) was higher in the exposed group. However, after adjustment to maternal age and gestational age at initial contact, the difference became insignificant. The rate of elective pregnancy-termination (8.8% versus 4.4%, p = 0.05) was higher and the rate of live births was lower in the exposed group (77.9% versus 88.4%, p = 0.002). Prematurity was more frequent in exposed pregnancies (16.1% versus 8.5%; OR 2.1, 95% CI 1.1- 3.8, p = 0.02). Nonetheless, gestational age at birth (median 39 weeks, IQR 37-40 versus 39 weeks, IQR 38-40, p = 0.27) and birth weight (median 3280 g, IQR 2835-3590 versus 3250 g, IQR 2880- 3600, p = 0.95) did not differ between exposed and non-exposed pregnancies.Conclusion This study did not detect a teratogenic effect of statins. Its statistical power however is not sufficient to reverse the recommendation of treatment discontinuation during pregnancy.
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Pregnancy reduces maternal risk of breast cancer in the long term, but the biological determinants of the protection are unknown. Animal experiments suggest that estrogens and progesterone could be involved, but direct human evidence is scant. A case-control study (536 cases and 1,049 controls) was nested within the Finnish Maternity Cohort. Eligible were primiparous women who delivered at term a singleton offspring before age 40. For each case, two individually matched controls by age (±6 months) and date of sampling (±3 months) were selected. Estradiol, estrone and progesterone in first-trimester serum were measured by high-performance liquid chromatography tandem mass spectrometry and sex-hormone binding globulin (SHBG) by immunoassay. Odds ratios (OR) and 95% confidence intervals (CI) were estimated through conditional logistic regression. In the whole study population there was no association of breast cancer with any of the studied hormones. In analyses stratified by age at diagnosis, however, estradiol concentrations were positively associated with risk of breast cancer before age 40 (upper quartile OR, 1.81; CI, 1.08-3.06), but inversely associated with risk in women who were diagnosed ≥age 40 (upper quartile OR, 0.64; CI, 0.40-1.04), p(interaction) 0.004. Risk estimates for estrone mirrored those for estradiol but were less pronounced. Progesterone was not associated with risk of subsequent breast cancer. Our results provide initial evidence that concentrations of estrogens during the early parts of a primiparous pregnancy are associated with maternal risk of breast cancer and suggest that the effect may differ for tumors diagnosed before and after age 40.
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OBJECTIVE: To evaluate the effect of vouchers for maternity care in public health-care facilities on the utilization of maternal health-care services in Cambodia. METHODS: The study involved data from the 2010 Cambodian Demographic and Health Survey, which covered births between 2005 and 2010. The effect of voucher schemes, first implemented in 2007, on the utilization of maternal health-care services was quantified using a difference-in-differences method that compared changes in utilization in districts with voucher schemes with changes in districts without them. FINDINGS: Overall, voucher schemes were associated with an increase of 10.1 percentage points (pp) in the probability of delivery in a public health-care facility; among women from the poorest 40% of households, the increase was 15.6 pp. Vouchers were responsible for about one fifth of the increase observed in institutional deliveries in districts with schemes. Universal voucher schemes had a larger effect on the probability of delivery in a public facility than schemes targeting the poorest women. Both types of schemes increased the probability of receiving postnatal care, but the increase was significant only for non-poor women. Universal, but not targeted, voucher schemes significantly increased the probability of receiving antenatal care. CONCLUSION: Voucher schemes increased deliveries in health centres and, to a lesser extent, improved antenatal and postnatal care. However, schemes that targeted poorer women did not appear to be efficient since these women were more likely than less poor women to be encouraged to give birth in a public health-care facility, even with universal voucher schemes.
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Polyphenism is the phenomenon in which alternative phenotypes are produced by a single genotype in response to environmental cues. An extreme case is found in social insects, in which reproductive queens and sterile workers that greatly differ in morphology and behavior can arise from a single genotype. Experimental evidence for maternal effects on caste determination, the differential larval development toward the queen or worker caste, was recently documented in Pogonomyrmex seed harvester ants, in which only colonies with a hibernated queen produce new queens. However, the proximate mechanisms behind these intergenerational effects have remained elusive. We used a combination of artificial hibernation, hormonal treatments, gene expression analyses, hormone measurements, and vitellogenin quantification to investigate how the combined effect of environmental cues and hormonal signaling affects the process of caste determination in Pogonomyrmex rugosus. The results show that the interplay between insulin signaling, juvenile hormone, and vitellogenin regulates maternal effects on the production of alternative phenotypes and set vitellogenin as a likely key player in the intergenerational transmission of information. This study reveals how hibernation triggers the production of new queens in Pogonomyrmex ant colonies. More generally, it provides important information on maternal effects by showing how environmental cues experienced by one generation can translate into phenotypic variation in the next generation.