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Objective To explore conditions and outcomes of a first delivery at term that might predict later preterm birth. Design Population based, prospective register based study. Setting Medical Birth Registry of Norway, 1999-2015. Participants 302 192 women giving birth (live or stillbirth) to a second singleton child between 1999 and 2015. Main outcome measures Main outcome was the relative risk of preterm delivery ( Results Women with any of the five complications at term showed a substantially increased risk of preterm delivery in the next pregnancy. The absolute risks for preterm delivery in a second pregnancy were 3.1% with none of the five term complications (8202/265 043), 6.1% after term pre-eclampsia (688/11 225), 7.3% after term placental abruption (41/562), 13.1% after term stillbirth (72/551), 10.0% after term neonatal death (22/219), and 6.7% after term small for gestational age (463/6939). The unadjusted relative risk for preterm birth after term pre-eclampsia was 2.0 (95% confidence interval 1.8 to 2.1), after term placental abruption was 2.3 (1.7 to 3.1), after term stillbirth was 4.2 (3.4 to 5.2), after term neonatal death was 3.2 (2.2 to 4.8), and after term small for gestational age was 2.2 (2.0 to 2.4). On average, the risk of preterm birth was increased 2.0-fold (1.9-fold to 2.1-fold) with one term complication in the first pregnancy, and 3.5-fold (2.9-fold to 4.2-fold) with two or more complications. The associations persisted after excluding recurrence of the specific complication in the second pregnancy. These links between term complications and preterm delivery were also seen in the reverse direction: preterm birth in the first pregnancy predicted complications in second pregnancies delivered at term. Conclusions Pre-eclampsia, placental abruption, stillbirth, neonatal death, or small for gestational age experienced in a first term pregnancy are associated with a substantially increased risk of subsequent preterm delivery. Term complications seem to share important underlying causes with preterm delivery that persist from pregnancy to pregnancy, perhaps related to a mother’s predisposition to disorders of placental function.

Importance Clinicians have been urged to delay the use of obstetric interventions (eg, labor induction, cesarean delivery) until 39 weeks or later in the absence of maternal or fetal indications for intervention. Objective To describe recent trends in late preterm and early term birth rates in 6 high-income countries and assess association with use of clinician-initiated obstetric interventions. Design Retrospective analysis of singleton live births from 2006 to the latest available year (ranging from 2010 to 2015) in Canada, Denmark, Finland, Norway, Sweden, and the United States. Exposures Use of clinician-initiated obstetric intervention (either labor induction or prelabor cesarean delivery) during delivery. Main Outcomes and Measures Annual country-specific late preterm (34-36 weeks) and early term (37-38 weeks) birth rates. Results The study population included 2 415 432 Canadian births in 2006-2014 (4.8% late preterm; 25.3% early term); 305 947 Danish births in 2006-2010 (3.6% late preterm; 18.8% early term); 571 937 Finnish births in 2006-2015 (3.3% late preterm; 16.8% early term); 468 954 Norwegian births in 2006-2013 (3.8% late preterm; 17.2% early term); 737 754 Swedish births in 2006-2012 (3.6% late preterm; 18.7% early term); and 25 788 558 US births in 2006-2014 (6.0% late preterm; 26.9% early term). Late preterm birth rates decreased in Norway (3.9% to 3.5%) and the United States (6.8% to 5.7%). Early term birth rates decreased in Norway (17.6% to 16.8%), Sweden (19.4% to 18.5%), and the United States (30.2% to 24.4%). In the United States, early term birth rates decreased from 33.0% in 2006 to 21.1% in 2014 among births with clinician-initiated obstetric intervention, and from 29.7% in 2006 to 27.1% in 2014 among births without clinician-initiated obstetric intervention. Rates of clinician-initiated obstetric intervention increased among late preterm births in Canada (28.0% to 37.9%), Denmark (22.2% to 25.0%), and Finland (25.1% to 38.5%), and among early term births in Denmark (38.4% to 43.8%) and Finland (29.8% to 40.1%). Conclusions and Relevance Between 2006 and 2014, late preterm and early term birth rates decreased in the United States, and an association was observed between early term birth rates and decreasing clinician-initiated obstetric interventions. Late preterm births also decreased in Norway, and early term births decreased in Norway and Sweden. Clinician-initiated obstetric interventions increased in some countries but no association was found with rates of late preterm or early term birth.

Preterm delivery before 37 completed weeks' gestation is the commonest reason for infant death in the United States, and continues to become more frequent in the United States and elsewhere. Previous delivery of a preterm infant is a strong risk factor for a recurrence. The investigators used data from the Medical Birth Registry of Norway in the years 1967-2004 to identify 191,282 mothers and 127,830 fathers who later had at least 1 singleton infant. The risk of preterm delivery of firstborn infants was calculated by stratifying parents according to whether or not they themselves had been born before term. The study was limited to parents who had been singleton births and their singleton offspring. Preterm births were those occurring between 22 and 36 weeks' gestation, while "early" preterm births took place from 22 to 34 weeks' gestation. Of all parents analyzed, 3.9% had themselves been preterm births. The rate of preterm delivery among all firstborn offspring was 5.5%, and the risk was higher if the parents themselves been delivered preterm. The risk of preterm birth was 8.5% of births of mothers born preterm, compared with 5.5% if the mother had been born at term (relative risk [RR], 1.54; 95% confidence interval [CI], 1.42-1.67). The comparable figures for fathers were 6.0% and 5.3%, respectively (RR, 1.12; 95% CI, 1.01-1.25). The contrast between mothers and fathers was more marked when analyzing "early" preterm births. Using less than 35 weeks as the outcome in the second generation, the risk of early preterm delivery depended strongly on the degree of the mother's own preterm birth. Mothers born before 28 weeks' gestation had a 3-fold increase in the risk of delivering early. No such trend was noted for preterm fathers. These findings suggest that paternal genes have little or no effect on the risk of preterm delivery. It would appear that fetal genes inherited from either patient do not make a major contribution. The increased risk of preterm delivery in mothers who themselves had been born preterm is consistent with inheritable maternal phenotypes that increase the risk of preterm delivery.

A postterm pregnancy is defined as a pregnancy lasting for >294 days (42 or more completed weeks). Infants born postterm have increased perinatal morbidity and mortality. The etiology of prolonged pregnancy is poorly understood. A number of studies have found that several birth outcomes, including b

Hyperemesis gravidarum (hyperemesis) is the most common cause of admission to hospital in early pregnancy and is associated with a number of adverse pregnancy outcomes. A previous population-based cohort study conducted in Norway reported that women who had hyperemesis in their first pregnancy were at high risk of recurrence (15.2%) compared with those who had not (0.7%). The risk of hyperemesis was reduced by a change in paternity (from 16% with the same father to 10.9% with a different father). These data suggest a genetic contribution to the risk of hyperemesis that may involve both maternal and fetal genes. This population-based cohort study examined the risk of hyperemesis according to whether the women and men under study were born after pregnancies complicated by hyperemesis. The study also estimated the risk of hyperemesis in a population of women who had been born after pregnancies not complicated by hyperemesis but whose mothers had hyperemesis in a previous or later pregnancy. Records from the medical birth registry of Norway on 2.3 million births reported for the period 1967-2006 were used to obtain linked generational data on 544,087 units of mother and childbearing daughter and 399,777 units of mother and child producing son. The relative risk of hyperemesis was assessed by logistic regression in the following 3 categories: (1) women born after a pregnancy complicated by hyperemesis; (2) female partners of sons born after a pregnancy complicated by hyperemesis; and (3) woman born after a pregnancy not complicated by hyperemesis but whose mother had hyperemesis in a previous or subsequent pregnancy. The risk of hyperemesis in the daughters of women who had hyperemesis was 3.00% compared with 1.05% of those whose mothers did not have hyperemesis (unadjusted odds ratio [OR], 2.90; 95% confidence interval [CI], 2.35-3.57). There was no significant difference in the risk among the female partners of sons who were born after pregnancies either complicated or uncomplicated by hyperemesis (unadjusted OR, 1.04; 95% CI, 0.7-1.6). The risk of hyperemesis was increased among daughters born after a pregnancy not complicated by hyperemesis, whose mothers had hyperemesis in a previous (unadjusted OR, 3.15; 95% CI, 1.55-6.41) or subsequent (unadjusted OR, 3.70; 95% CI, 1.51-9.08) pregnancy. Neither adjustment for potential confounders (maternal age at childbirth, period of birth, and parity) nor restriction to firstborns in both generations affected the results. These findings indicate that the maternal genotype has a stronger influence than the fetal genotype on the risk of hyperemesis. However, it is possible that common environmental factors shared by mothers and daughters may contribute to risk.

Previous studies indicate that women born after a pregnancy complicated by preeclampsia are at increased risk in their own pregnancies. This increase in risk could reflect the inheritance of genes that enhance maternal susceptibility to preeclampsia or transmission to the fetus of fetal genes that can trigger preeclampsia. If fetal genes do play a role, it is logical that an increased risk of preeclampsia could also be transmitted through the father. These possibilities were examined in a population-based cohort study based on data in a medical birth registry in Norway from 1967 to 2003. Linked generational data were available on 438,597 mother-offspring units and 286,945 father-offspring units. Compared with women born after nonpreeclamptic pregnancies, women born after a preeclamptic pregnancy had an increased risk of having the disorder in both their first pregnancy (odds ratio [OR], 2.2; 95% confidence interval [CI], 2.0-2.4) and their second (relative risk [RR], 1.5; 95% CI, 1.1-2.1). For men born after a preeclamptic pregnancy, the risk of preeclampsia in their partner's first pregnancy was also increased (RR, 1.5; 95% CI, 1.3-1.7). Sisters of affected women, whose own births were not complicated by preeclampsia, were nevertheless at increased risk compared with women with no family history of the disorder (RR, 2.0; 95% CI, 1.7-2.3). No increased risk was found for brothers of affected women whose own births were not complicated by preeclampsia. Data on the clinical severity of the preeclampsia were available from 1999 on. Women having a child between 1999 and 2003 who had early-onset or clinically severe preeclampsia were much more likely to have been born after a preeclamptic pregnancy (RR, 3.0; 95% CI, 2.4-3.7). A similar but more modest effect was noted in men who fathered a pregnancy complicated by severe or early preeclampsia (RR, 1.9; 95% CI, 1.4-2.5). These findings support the view that both maternal genes and fetal genes from either parent may contribute to preeclampsia. The maternal association is stronger than the fetal (or paternal) association.

Some believe that key characteristics of preeclampsia, gestational hypertension and proteinuria, represent pathogenetically distinct conditions. When fetal growth is restricted, preeclampsia could result from abnormal implantation. An infant with appropriate or high birth weight could signify a range of conditions from mild preeclampsia with modest placental involvement to a hypertensive disorder without placental disease. The investigators obtained information on gestational length and preeclampsia from 1,679,205 singleton infants born in the years 1967 to 1978 and entered it in a population-based registry. Preeclampsia was diagnosed in 44,220 pregnancies, 2.6% of the total. Criteria included a rise in blood pressure to at least 140/90 mm Hg after 20 weeks gestation, with a diastolic pressure at least 15 mm Hg higher than before week 20 or a systolic pressure at least 30 mm Hg higher. Proteinuria of at least 0.3 g/24 hours also had to be present. If the infant weighed less than 2 standard deviations (SDs) below the mean, the relative risk (RR) of preeclampsia was 5.9. If birth weight was 3 or more SDs above the mean, the RR was 2.4. When delivery was at term (37-42 weeks), the RR of preeclampsia was 4.5 when birth weight was less than 2 SDs below the mean and 2.6 with a birth weight 3 or more SDs above the mean. For preterm preeclampsia, the risk increased with declining birth weight. Gestational diabetes was approximately 3 times more prevalent in preterm than in term preeclampsia. These findings support the view that preeclampsia includes pathogenetically separate conditions rather than 1 basic process with varying degrees of severity. Placental dysfunction probably underlies preeclampsia associated with low birth weight, preterm delivery, and gestational diabetes. In contrast, placental function is normal when preeclampsia develops at term and the infant appears to be unaffected.