We determined the association between gestational weight gain and severe maternal morbidity.
We used data on 84,241 delivery hospitalizations at Magee-Womens Hospital, Pittsburgh, PA (2003–2012). ...Total gestational weight gain (kilogram) was converted to gestational age–standardized z-scores. We defined severe maternal morbidity as having ≥1 of the 21 Centers for Disease Control diagnosis or procedure codes for severe maternal morbidity identification, intensive care unit admission, or extended postpartum stay. We used multivariable logistic regression to determine the association between weight gain and severe maternal morbidity after confounder adjustment.
High gestational weight gain z-scores were associated with an increased risk of severe maternal morbidity. Compared with z-score 0 SD (equivalent to 16 kg at 40 weeks in a normal-weight woman), risk differences (95% confidence intervals) for z-scores −2 SD (7 kg), −1 SD (11 kg), +1 SD (23 kg), and +2 SD (31 kg) were 1.5 (−0.71, 3.7), 0.056 (−0.81, 0.93), 3.4 (1.7, 5.0), and 8.6 (4.0, 13) per 1000 deliveries. The results did not vary by gestational age at delivery or prepregnancy body mass index.
The increased risk of severe maternal morbidity with high pregnancy weight gain may allow scientists to understand and prevent this serious condition.
BACKGROUND:Observational cohort studies have consistently shown that maternal weight gain in pregnancy is positively associated with fetal size, but it is unknown whether the association is causal. ...This study investigated the effect of pregnancy weight gain on fetal growth using a sibling comparison design to control for unmeasured confounding by genetic and shared environmental factors.
METHODS:Our study population included 44,457 infants (21,680 women) with electronic medical records in the Stockholm–Gotland Obstetrical Database, 2008–2014. We standardized pregnancy weight gain into gestational age-specific z-scores. Fetal size was classified as birthweight (gram), and as small- and large-for-gestational-age birth (birthweight <10th or >90th percentiles, respectively). Our sibling comparison analyses used multivariable linear fixed effects models for birthweight and hybrid logistic fixed effects models for small- and large-for-gestational-age birth (SGA and LGA). We repeated analyses using conventional (unmatched) regression models.
RESULTS:Sibling comparison analyses showed a clinically meaningful association between weight gain and fetal size (e.g., adjusted difference of +89 g birthweight 95% CI = 82, 95 g; adjusted risk ratios aRR for SGA of 0.80 95% CI = 0.75, 0.86 per 1 z-score increase in weight gain for a woman of body mass index BMI = 25). These findings were consistent across the range of BMI. Estimates were only modestly attenuated compared with conventional approach (+97 g 95% CI = 92, 102 g, aRR for SGA of 0.70 95% CI = 0.67, 0.73 per 1 z-score increase in weight gain).
CONCLUSION:The positive association between pregnancy weight gain and fetal size we found using a sibling comparison design suggests that this relation has minimal confounding by familial factors that remain constant between pregnancies.
Recent evidence from the United States and Canada suggests an unexplained increase in small-for-gestational-age (SGA) births (<10th percentile). This study aimed to identify reasons for the recent ...increase in SGA births in Canada.
Using Canada's Vital Statistics - Birth Database, the study population included all singleton live births, 2000 to 2016, inclusive. Temporal changes in birth weight (grams), birth weight for gestational age z-scores, and SGA births were examined. Multivariable logistic regression was used to determine if the ncreased risk of an SGA birth over time was eliminated or attenuated by adjusting for selected individual and sociodemographic factors that have previously been associated with SGA births.
There were 5,941,820 singleton live births in Canada between 2000 and 2016. Mean birth weight for all births decreased from 3,442 grams in 2000, to 3,367 grams in 2016, while SGA birth increased from 7.2% in 2000 to 8.0% in 2016. The multivariable model showed higher odds of SGA birth among births to parents born outside of Canada, unmarried women, older women, nulliparous women and women residing in low income neighborhoods. After adjusting for sociodemographic factors, the crude 12% increase in odds of SGA birth in 2016 compared to 2000 (95% Confidence Interval (CI): 10 to 14%) was attenuated, ut not eliminated (adjusted odds ratio for calendar time 1.08 (95% CI: 1.06, 1.10)).
This study identified a decrease in fetal size in Canada between 2000 and 2016. The rise in SGA births in Canada was explained only partly as a result of concurrent changes in the demography of childbirth.
Corneal fibrosis (or scarring) occurs in response to ocular trauma or infection, and by reducing corneal transparency, it can lead to visual impairment and blindness. Studies highlight important ...roles for transforming growth factor (TGF)-β1 and -β3 as modulators in corneal wound healing and fibrosis, leading to increased extracellular matrix (ECM) components and expression of α-smooth muscle actin (αSMA), a myofibroblast marker. In this study, human corneal fibroblasts (hCF) were cultured as a monolayer culture (2D) or on poly-transwell membranes to generate corneal stromal constructs (3D) that were treated with TGF-β1, TGF-β3, or TGF-β1 + FAK inhibitor (FAKi). Results show that hCF 3D constructs treated with TGF-β1 or TGF-β3 impart distinct effects on genes involved in wound healing and fibrosis-
,
,
and
. Notably, in the 3D construct model, TGF-β1 enhanced αSMA and focal adhesion kinase (FAK) protein expression, whereas TGF-β3 did not. In addition, in both the hCF 2D cell and 3D construct models, we found that TGF-β1 + FAKi attenuated TGF-β1-mediated myofibroblast differentiation, as shown by abrogated αSMA expression. This study concludes that FAK signaling is important for the onset of TGF-β1-mediated myofibroblast differentiation, and FAK inhibition may provide a novel beneficial therapeutic avenue to reduce corneal scarring.
Objective To examine whether changes in postpartum haemorrhage, hypertensive disorders of pregnancy, or other risk factors explain the increase in obstetric acute renal failure in Canada.Design ...Retrospective cohort study.Setting Canada (excluding the province of Quebec).Participants All hospital deliveries from 2003 to 2010 (n=2 193 425).Main outcome measures Obstetric acute renal failure identified by ICD-10 diagnostic codes.Methods Information on all hospital deliveries in Canada (excluding Quebec) between 2003 and 2010 (n=2 193 425) was obtained from the Canadian Institute for Health Information. Temporal trends in obstetric acute renal failure were assessed among women with and without postpartum haemorrhage, hypertensive disorders of pregnancy, or other risk factors. Logistic regression was used to determine if changes in risk factors explained the temporal increase in obstetric acute renal failure.Results Rates of obstetric acute renal failure rose from 1.66 to 2.68 per 10 000 deliveries between 2003-04 and 2009-10 (61% increase, 95% confidence interval 24% to 110%). Adjustment for postpartum haemorrhage, hypertensive disorders, and other factors did not attenuate the increase. The temporal increase in acute renal failure was restricted to deliveries with hypertensive disorders (adjusted increase 95%, 95% confidence interval 38% to 176%), and was especially pronounced among women with gestational hypertension with significant proteinuria (adjusted increase 171%, 71% to 329%). No significant increase occurred among women without hypertensive disorders (adjusted increase 12%, −28 to 72%).Conclusions The increase in obstetric acute renal failure in Canada between 2003 and 2010 was restricted to women with hypertensive disorders and was especially pronounced among women with pre-eclampsia. Further study is required to determine the cause of the increase among women with pre-eclampsia.
High gestational weight gain is associated with excess postpartum weight retention, yet excess postpartum weight retention is not an exclusion criterion for current gestational weight gain charts. We ...aimed to assess the impact of excluding individuals with high interpregnancy weight change (a proxy for excess postpartum weight retention) on gestational weight gain distributions.
We included individuals with an index birth from 2008 to 2014 and a subsequent birth before 2019, in the population-based Stockholm-Gotland Perinatal Cohort. We estimated gestational weight gain (kg) at 25 and 37 weeks, using weight at first prenatal visit (<14 weeks) as the reference. We calculated high interpregnancy weight change (≥10 kg and ≥5 kg) using the difference between weight at the start of an index and subsequent pregnancy. We compared gestational weight gain distributions and percentiles (stratified by early-pregnancy body mass index) before and after excluding participants with high interpregnancy weight change.
Among 55,723 participants, 17% had ≥10 kg and 34% had ≥5 kg interpregnancy weight change. The third, tenth, 50th, 90th and 97th percentiles of gestational weight gain were similar (largely within 1 kg) before versus after excluding participants with high interpregnancy weight change, at both 25 and 37 weeks. For example, among normal weight participants at 37 weeks, the 50th and 97th percentiles were 14 kg and 23 kg including versus 13 kg and 23 kg excluding participants with ≥5 kg interpregnancy weight change.
Excluding individuals with excess postpartum weight retention from normative gestational weight gain charts may not meaningfully impact the charts' percentiles.
Objective
To link the INTERGROWTH‐21st gestational weight gain standard with the risks of excess maternal postpartum weight retention, approximated by women's weight change between successive ...pregnancies.
Methods
A population‐based retrospective cohort study of 58,534 women delivering successive pregnancies in British Columbia, Canada (2000‐2015) was conducted. Pregnancy weight gain (kg) in the index pregnancy was converted into a gestational age‐standardized z‐score using the INTERGROWTH‐21st standard. Excess interpregnancy weight gain was defined as weight increases of 5 kg, 10 kg, or obesity (≥30 kg/m2) at the next pregnancy. Weight gain z‐scores and excess interpregnancy weight change were associated using logistic regression.
Results
For all definitions of excess interpregnancy weight gain, risks remained low and stable below a weight gain z‐score of 0 (50th percentile) but rose sharply with increasing z‐scores above zero. Compared with women gaining −1 to 0 SD (16th to 50th percentiles), women gaining > 0 to +1 SD (51st to 84th percentiles) were 55% to 84% more likely to retain excess weight between pregnancies. Risks were three‐ to sixfold higher in women gaining >+1 SD.
Conclusions
A large range of the INTERGROWTH‐21st percentiles were associated with increased risks of excess interpregnancy weight gain. The standard may normalize high weight gains of women at increased risk of excess weight retention.
Risk Factors for High and Low Placental Weight McNamara, Helen; Hutcheon, Jennifer A.; Platt, Robert W. ...
Paediatric and perinatal epidemiology,
March 2014, Letnik:
28, Številka:
2
Journal Article
Recenzirano
Background
Placental weight is an independent predictor of adverse perinatal outcome. However, risk factors for high and low placental weight are poorly understood. The objective of this study was to ...identify maternal, placental, and umbilical cord determinants of placental weight, before and after accounting for birthweight.
Methods
This cohort study of 87 600 singleton births at the Royal Victoria Hospital in Montreal, Canada assessed the relationship between maternal, placental, and umbilical cord characteristics and placental weight (standardised for sex and gestational age). We separately examined risk factors for high (z‐score >+1) and low (z‐score <−1) placental weight. Multivariable logistic regression was used to study associations after adjusting for confounders and further adjusting for birthweight.
Results
Chronic hypertension was associated with low placental weight {relative risk (RR) 2.1 95% confidence interval (CI) 1.8, 2.4 and 1.8 95% CI 1.5, 2.1 before and after accounting for birthweight}, while pre‐eclampsia was associated with low placenta weight before, but not after adjustment for birthweight. Anaemia and gestational diabetes were linked with high placental weight (RRs 1.2–1.4, respectively) before and after adjustment for birthweight, while smoking was linked with high placental weight only after adjustment for birthweight (RR 1.4 95% CI 1.3, 1.5). Placental and cord determinants of high placental weight included chorioamnionitis, chorangioma/chorangiosis, circumvallate placenta, marginal cord insertion, and other cord abnormalities.
Conclusions
The broad range of risk factors for high placental weight suggests multiple aetiologic pathways. Future work should seek to understand the pathways by which the placenta adapts to unfavourable intrauterine conditions, which may provide insights into potential therapies.
Introduction
Multistakeholder engagement is crucial for conducting health services research. Delphi‐based methodologies combining iterative rounds of questions with feedback on and discussion of ...group results are a well‐documented approach to multistakeholder engagement. This study develops hypotheses about the impact of panel composition and topic on the propensity and meaningfulness of response changes in multistakeholder modified‐Delphi panels.
Methods
We conducted three online modified‐Delphi (OMD) multistakeholder panels using the same protocol. We assigned 60 maternal and child health professionals to a homogeneous (professionals only) panel, 60 pregnant or postpartum women (patients) to a homogeneous panel, and 30 professionals and 30 patients to a mixed panel. In Round 1, participants rated the seriousness of 11 maternal and child health outcomes using a 0–100 scale and explained their ratings. In Round 2, participants saw their own and their panel's Round 1 results and discussed them using asynchronous, anonymous discussion boards moderated by the study investigators. In Round 3, participants revised their original ratings. Our outcome measures included binary indicators of response changes to ratings of the low, medium and high severity maternal and child health outcomes and their meaningfulness, measured by a change of 10 or more points.
Results
Participants changed 818 of 1491 (55%) of responses; the majority of response changes were meaningful. Patterns of response changes were different for patients and professionals and for different levels of outcome seriousness. Using study results and the literature, we developed three hypotheses. First, OMD participants, regardless of their stakeholder group, are more likely to change their responses on preference‐sensitive topics where there is a range of viable alternatives or perspectives. Second, patients are more likely to change their responses and to do so meaningfully in mixed panels, whereas professionals are more likely to do so in homogeneous panels. Third, the association between panel composition and response change varies according to the topic (e.g., the level of outcome seriousness).
Conclusions
Results of our work not only helped generate empirically derived hypotheses to be tested in future research but also offer practical recommendations for designing multistakeholder OMD panels.
Patient or Public Contribution
Pregnant or postpartum women were involved in this study.
Objectives To examine variations in the registration of extremely low birthweight and early gestation births and to assess their effect on perinatal and infant mortality rankings of industrialised ...countries.Design Retrospective population based study.Setting Australia, Canada, European countries, and the United States for 2004; Australia, Canada, and New Zealand for 2007.Population National data on live births and on fetal, neonatal, and infant deaths.Main outcome measures Reported proportions of live births with birth weight/gestational age of less than 500 g, less than 1000 g, less than 24 weeks, and less than 28 weeks; crude rates of fetal, neonatal, and infant mortality; mortality rates calculated after exclusion of births under 500 g, under 1000 g, less than 24 weeks, and less than 28 weeks.Results The proportion of live births under 500 g varied widely from less than 1 per 10 000 live births in Belgium and Ireland to 10.8 per 10 000 live births in Canada and 16.9 in the United States. Neonatal deaths under 500 g, as a proportion of all neonatal deaths, also ranged from less than 1% in countries such as Luxembourg and Malta to 29.6% in Canada and 31.1% in the United States. Rankings of countries based on crude fetal, neonatal, and infant mortality rates differed substantially from rankings based on rates calculated after exclusion of births with a birth weight of less than 1000 g or a gestational age of less than 28 weeks.Conclusions International differences in reported rates of extremely low birthweight and very early gestation births probably reflect variations in registration of births and compromise the validity of international rankings of perinatal and infant mortality.
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