To assess whether women with a history of preterm birth, independent on the presence of prelabour rupture of the membranes (PROM) and growth deviation of the newborn, are more likely to develop ...preeclampsia with preterm or preterm birth in a subsequent pregnancy.
We conducted a population-based cohort study, based on Medical Birth Registry of Norway between 1967 and 2012, including 742,980 women with singleton pregnancies who were followed up from their 1st to 2nd pregnancy. In the analyses we included 712,511 women after excluding 30,469 women with preeclampsia in the first pregnancy.
After preterm birth without preeclampsia in the first pregnancy, the risk of preterm preeclampsia in the second pregnancy was 4-7 fold higher than after term birth (odds ratios 3.5; 95% confidence interval (CI) 3.0-4.0 to 6.5; 95% CI 5.1-8.2). The risk of term preeclampsia in the pregnancy following a preterm birth was 2-3 times higher than after term birth (odds ratios 1.6; 95% CI 1.5-1.8 to 2.6; 95% CI 2.0-3.4). After spontaneous non-PROM preterm birth and preterm PROM, the risk of preterm preeclampsia was 3.3-3.6 fold higher than after spontaneous term birth. Corresponding risks of term preeclampsia was 1.6-1.8 fold higher. No significant time trends were found in the effect of spontaneous preterm birth in the first pregnancy on preterm or term preeclampsia in the second pregnancy.
The results suggest that preterm birth, regardless of the presence of PROM, and preeclampsia share pathophysiologic mechanisms. These mechanisms may cause preterm birth in one pregnancy and preeclampsia in a subsequent pregnancy in the same woman. The association was particularly evident with preterm preeclampsia.
Low Birth Weight Increases Risk for End-Stage Renal Disease BJORN EGIL VIKSE; IRGENS, Lorentz M; LEIVESTAD, Torbjørn ...
Journal of the American Society of Nephrology,
2008, 2008-Jan, 2008-01-00, 20080101, Letnik:
19, Številka:
1
Journal Article
Recenzirano
Odprti dostop
Case-control studies have shown an association between low birth weight and risk for renal failure. The Medical Birth Registry of Norway, which comprises data on all births in Norway since 1967, and ...the Norwegian Renal Registry, which comprises data on all patients who have developed ESRD in Norway since 1980, were used to examine whether birth-related variables were associated with risk for ESRD. Of the 2,183,317 children born between 1967 and 2004, 526 were found in the ESRD registry. Compared with birth weight in the 10th to 90th percentiles, births <10th percentile had a relative risk (RR) for ESRD of 1.7 (95% confidence interval 1.4 to 2.2; P < 0.001). Births with a weight for gestational age <10th percentile had an RR of 1.5 (95% confidence interval 1.2 to 1.9; P = 0.002). These associations were virtually identical after adjustment for birth-related confounders such as congenital malformations, multiple delivery, maternal age at birth, and maternal preeclampsia. Low birth weight was more strongly associated with development of ESRD during the first 14 years of life than after age 15. Low birth weight and low birth weight for gestational age were similarly associated with multiple causes of ESRD. In conclusion, in this cohort study with a maximum follow-up of 38 years, low birth weight and intrauterine growth restriction were associated with increased risk for ESRD.
In pregnancies after a previous cesarean section (CS), a planned repeat CS delivery has been associated with excess risk of adverse outcome. However, also the alternative, a trial of labor after CS ...(TOLAC), has been associated with excess risks. A TOLAC failure, involving a non-planned CS, carries the highest risk of adverse outcome and a vaginal delivery the lowest. Thus, the decision regarding delivery mode is pivotal in clinical handling of these pregnancies. However, even with a high TOLAC rate, as seen in Norway, repeat CSs are regularly performed for no apparent medical reason. The objective of the present study was to assess to which extent demographic, socioeconomic, and health system factors are determinants of TOLAC and TOLAC failure in low risk pregnancies, and whether any effects observed changed with time.
The study group comprised 24 645 second deliveries (1989-2014) after a first delivery CS. Thus, none of the women had prior vaginal deliveries or more than one CS. Included pregnancies were low risk, cephalic, single, and had gestational age ≥ 37 weeks. Data were obtained from the Medical Birth Registry of Norway (MBRN). The exposure variables were (second delivery) maternal age, length of maternal education, maternal country of origin, size of the delivery unit, health region (South-East, West, Mid, North), and maternal county of residence. The outcomes were TOLAC and TOLAC failure, as rates (%), relative risk (RR) and relative risk adjusted (ARR). Changes in determinant effects over time were assessed by comparing rates in two periods, 1989-2002 vs 2003-2014, and including these periods in an interaction model.
The TOLAC rate was 74.9%, with a TOLAC failure rate of 16.2%, resulting in a vaginal birth rate of 62.8%. Low TOLAC rates were observed at high maternal age and in women from East Asia or Latin America. High TOLAC failure rates were observed at high maternal age, in women with less than 11 years of education, and in women of non-western origin. The effects of health system factors, i.e. delivery unit size and administrative region were considerable, on both TOLAC and TOLAC failure. The effects of several determinants changed significantly (P < 0.05) from 1989-2002 to 2003-2014: The association between non-TOLAC and maternal age > 39 years became weaker, the association between short education and TOLAC failure became stronger, and the association between TOLAC failure and small size of delivery unit became stronger.
Low maternal age, high education, and western country of origin were associated with high TOLAC rates, and low TOLAC failure rates. Maternity unit characteristics (size and region) contributed with effects on the same level as individual determinants studied. Temporal changes were observed in determinant effects.
The first European Perinatal Health Report showed wide variability between European countries in fetal (2.6-9.1‰) and neonatal (1.6-5.7‰) mortality rates in 2004. We investigated gestational age ...patterns of fetal and neonatal mortality to improve our understanding of the differences between countries with low and high mortality.
Data on 29 countries/regions participating in the Euro-Peristat project were analyzed. Most European countries had no limits for the registration of live births, but substantial variations in limits for registration of stillbirths before 28 weeks of gestation existed. Country rankings changed markedly after excluding deaths most likely to be affected by registration differences (22-23 weeks for neonatal mortality and 22-27 weeks for fetal mortality). Countries with high fetal mortality ≥28 weeks had on average higher proportions of fetal deaths at and near term (≥37 weeks), while proportions of fetal deaths at earlier gestational ages (28-31 and 32-36 weeks) were higher in low fetal mortality countries. Countries with high neonatal mortality rates ≥24 weeks, all new member states of the European Union, had high gestational age-specific neonatal mortality rates for all gestational-age subgroups; they also had high fetal mortality, as well as high early and late neonatal mortality. In contrast, other countries with similar levels of neonatal mortality had varying levels of fetal mortality, and among these countries early and late neonatal mortality were negatively correlated.
For valid European comparisons, all countries should register births and deaths from at least 22 weeks of gestation and should be able to distinguish late terminations of pregnancy from stillbirths. After excluding deaths most likely to be influenced by existing registration differences, important variations in both levels and patterns of fetal and neonatal mortality rates were found. These disparities raise questions for future research about the effectiveness of medical policies and care in European countries.
Introduction
Hypertensive disorders of pregnancy (HDP) tend to recur from one pregnancy to the next. The aims of the study were to assess the recurrence risk according to type of HDP defined by ...gestational age at birth and to examine whether recurrence is associated with the following additional risk factors for HDP: maternal age, smoking, inter‐delivery interval, diabetes, body mass index, and fetal growth restriction, and to assess temporal trends in these associations.
Material and methods
All women with two singleton births in the Medical Birth Registry of Norway 1967–2012 (n = 742 980) were included in this population‐based cohort study. Logistic regression was used to calculate odds ratios for the risk of recurrent HDP according to type of HDP.
Results
The highest odds ratio of recurrence was observed for the same type of HDP based on gestational age at delivery. After gestational hypertension and term preeclampsia, the risk for the same type to recur increased 10‐fold, whereas after late and early preterm preeclampsia, the risk increased 27‐ and 97‐fold, respectively. The recurrence of early preterm preeclampsia was less influenced by additional risk factors compared with term HDP. Recurrence of early preterm HDP was significantly lower from 1993 onwards.
Conclusions
Recurrent HDP tended to be of the same type as the previous HDP. Risk of recurrence associated with additional risk factors was observed particularly after term. The odds ratio of recurrence of early preterm HDP was significantly lower from 1993 onwards.
Clinical trials of therapeutic angiogenesis by vascular endothelial growth factor (VEGF) gene delivery failed to show efficacy. Major challenges include the need to precisely control in vivo ...distribution of growth factor dose and duration of expression. Recombinant VEGF protein delivery could overcome these issues, but rapid in vivo clearance prevents the stabilization of induced angiogenesis. Here, we developed an optimized fibrin platform for controlled delivery of recombinant VEGF, to robustly induce normal, stable, and functional angiogenesis. Murine VEGF164 was fused to a sequence derived from α2-plasmin inhibitor (α2-Pl1–8) that is a substrate for the coagulation factor fXIIIa, to allow its covalent cross-linking into fibrin hydrogels and release only by enzymatic cleavage. An α2-Pl1–8–fused variant of the fibrinolysis inhibitor aprotinin was used to control the hydrogel degradation rate, which determines both the duration and effective dose of factor release. An optimized aprotinin-α2-Pl1–8 concentration ensured ideal degradation over 4 wk. Under these conditions, fibrin-α2-Pl1–8-VEGF164 allowed exquisitely dose-dependent angiogenesis: concentratios ≥25 μg/mL caused widespread aberrant vascular structures, but a 500-fold concentration range (0.01–5.0 μg/mL) induced exclusively normal, mature, nonleaky, and perfused capillaries, which were stable after 3 mo. Optimized delivery of fibrin-α2-Pl1–8-VEGF164 was therapeutically effective both in ischemic hind limb and wound-healing models, significantly improving angiogenesis, tissue perfusion, and healing rate. In conclusion, this optimized platform ensured (i) controlled and highly tunable delivery of VEGF protein in ischemic tissue and (ii) stable and functional angiogenesis without introducing genetic material and with a limited and controllable duration of treatment. These findings suggest a strategy to improve safety and efficacy of therapeutic angiogenesis.
To investigate risk factors for obstetric anal sphincter injuries in a large population-based data set, and to assess to what extent changes in these risk factors could account for trends in ...obstetric anal sphincter injuries.
This is a population-based cohort study on data from the Medical Birth Registry of Norway between 1967 and 2004, including all vaginal singleton deliveries of vertex-presenting fetuses weighing 500 g or more. Women with their first birth before 1967 and births with previous obstetric anal sphincter injuries were excluded, leaving 1,673,442 births for study. The outcome variable was third- and fourth-degree obstetric anal sphincter injuries. The associations of obstetric anal sphincter injuries with possible risk factors were estimated by odds ratios (ORs) obtained by logistic regression.
The occurrence of obstetric anal sphincter injuries increased from 0.5% in 1967 to 4.1% in 2004. After adjusting for demographic and other risk factors, as well as possible confounders, the increase of obstetric anal sphincter injuries persisted, although reduced (unadjusted OR 7.1; 95% confidence interval CI 6.8-7.4; adjusted OR 5.6; 95% CI 5.3-5.9). Obstetric anal sphincter injuries were significantly associated with maternal age 30 years or older, vaginal birth order of one, previous cesarean delivery, instrumental delivery, episiotomy, type 1 diabetes, gestational diabetes, induction of labor by prostaglandin, size of maternity unit, birth weight 3,500 g or more, head circumference 35 cm or more, and African or Asian country of birth.
Risk of obstetric anal sphincter injuries considerably increased in Norway in 1967 to 2004. Changes in the risk factors studied could only partially explain this increase.
II.
Background and objective
Tooth loss (TL), one of the most visible results of the evolution of periodontitis, causes physiological and psychological impacts on a patient's life. This prospective study ...aimed to evaluate the incidence, underlying reasons and influence of risk predictors for the occurrence of TL in a program of periodontal maintenance therapy (PMT) over 5 years.
Methods
The sample comprised 212 individuals diagnosed with chronic moderate–severe periodontitis, who had finished active periodontal treatment, were incorporated in a PMT program. Individuals were divided in to two groups: 96 regular compliers (RC) and 116 irregular compliers (IC). Full‐mouth periodontal examination was performed. Social, demographic, behavioral and biological variables of interest were collected at all PMT visits. The effect of risk predictors and confounders for TL, as well as the underlying reasons of TL, were assessed by univariate and multivariate analysis.
Results
TL was significantly lower among RC (0.12 teeth lost/year) in comparison to IC (0.36 teeth lost/year; p < 0.01). Individuals that were > 55 years old, males and smokers lost significantly more teeth in both groups (with IC > RC). The number of teeth lost due to periodontal reasons was significantly higher than TL for other reasons in both groups (p < 0.01). The final linear and logistic model for TL included: male gender, smoking, probing depth 4–6 mm in up to 10% of sites and irregular compliance.
Conclusion
IC individuals undergoing PMT presented higher rates of TL when compared to RC individuals. Findings demonstrated the influence of irregular compliance and the importance of monitoring other risk predictors for TL such as smoking, male gender and severity of probing depth during PMT.
Perinatal mortality according to birth weight has an inverse J-pattern. Our aim was to estimate the influence of familial factors on this pattern, applying a cohort sibling design. We focused on ...excess mortality among macrosomic infants (>2 SD above the mean) and hypothesized that the birth weight-mortality association could be explained by confounding shared family factors. We also estimated how the participant's deviation from mean sibling birth weight influenced the association.
We included 1 925 929 singletons, born term or post-term to mothers with more than one delivery 1967-2011 registered in the Medical Birth Registry of Norway. We examined z-score birth weight and perinatal mortality in random-effects and sibling fixed-effects logistic regression models including measured confounders (e.g. maternal diabetes) as well as unmeasured shared family confounders (through fixed effects models). Birth weight-specific mortality showed an inverse J-pattern, being lowest (2.0 per 1000) at reference weight (z-score +1 to +2) and increasing for higher weights. Mortality in the highest weight category was 15-fold higher than reference. This pattern changed little in multivariable models. Deviance from mean sibling birth weight modified the mortality pattern across the birth weight spectrum: small and medium-sized infants had increased mortality when being smaller than their siblings, and large-sized infants had an increased risk when outweighing their siblings. Maternal diabetes and birth weight acted in a synergistic fashion with mortality among macrosomic infants in diabetic pregnancies in excess of what would be expected for additive effects.
The inverse J-pattern between birth weight and mortality is not explained by measured confounders or unmeasured shared family factors. Infants are at particularly high mortality risk when their birth weight deviates substantially from their siblings. Sensitivity analysis suggests that characteristics related to maternal diabetes could be important in explaining the increased mortality among macrosomic infants.
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