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Da «Medisinsk melding om fødsel» ble etablert 1. januar 1967, var dette en melderutine som representerte noe nytt ikke bare i et norsk, men også i et internasjonalt perspektiv. Bakgrunnen var thalidomid-katastrofen som hadde rystet verden noen år tidligere. Men man hadde fra begynnelsen også et ønske om å skaffe et kunnskapsbasert grunnlag for fremtidens obstetrikk, neonatalogi og habilitering. Initiativet ble tatt av Helsedirektoratet. I den opprinnelige planen skulle fødselsmeldingene bearbeides og analyseres i Statistisk sentralbyrå (SSB), men det ble tidlig klart at dette ville sprenge de rammene SSB vanligvis arbeidet innenfor. SSB hadde heller ikke den medisinske kompetansen som var en forutsetning for en fullverdig utnyttelse av de innsamlede data. På denne tiden arbeidet dr.med. Tor Bjerkedal som medisinsk statistisk konsulent/forsker I i SSB. Da han i 1969 tiltrådte sitt professorat ved Institutt for hygiene og sosialmedisin (IHS), Universitetet i Bergen (UiB), brakte han MFRs første årganger av fødselsmeldinger med seg. I en avtale med helsedirektør Karl Evang ble Bjerkedal gitt i oppdrag å opprette og drive et register basert på meldingene. I informasjonsteknologiens barndom representerte denne oppgaven en pionerinnsats. Meldeskjemaets data ble punchet på et 80 karakterers hullkort som ble prosessert i UiBs store sentrale regnemaskin. Arbeidet ble utført av en liten, men entusiastisk gruppe medarbeidere, i det alt vesentlige finansiert ved hjelp av lokale UiB-ressurser. I tillegg gikk Norges almenvitenskapelige forskningsråd de første årene inn med midler, dels fordi ITaspektene ble sett på som innovative, dels fordi man forsto at de innsamlede data ville få stor forskningsmessig verdi. MFR ble raskt operativt med et system for overvåking av medfødte misdannelser og andre uønskede svangerskapsutfall. For å sikre oppfølgning av barn med behov for spesielle medisinske hjelpetiltak ble det startet prøveprosjekter med elektronisk registrering av data fra helsestasjonenes 1-års og 4- årsundersøkelser samtidig som data fra vaksinasjonsprogrammet ble registrert, videreført i det nåværende SYSVAK. Etablering av alle driftsrutinene knyttet til MFR krevet omfattende innsats. Derfor ble den forskningsmessige utnyttelsen av de innsamlede data til å begynne med relativt beskjeden. Men etter hvert vokste det frem en omfattende vitenskapelig produksjon samtidig som antall ansatte økte; de første årene var 6-8 personer tilknyttet MFR mens i 2002 da MFR ble integrert som en avdeling i Folkehelseinstituttet var ca. 60 personer ansatt, herunder stipendiater. Virksomheten ved MFR kom til å bli avgjørende for at registerbasert epidemiologi ble et prioritert innsatsområde for Det medisinske fakultet ved UiB og for den videre etablering av helseregistre ved Folkehelseinstituttet i Bergen.

The Medical Birth Registry of Norway (MBRN) has registered all births in Norway since 1967 and diabetes is registered as a maternal diagnosis. We present original data assessing the validity of the diabetes diagnosis. Among women with known pre-gestational type 1 diabetes, 97% of births during 1976-1998 (old registration form) were identified as pre-gestational diabetes in the MBRN. For births 1999-2004 (new registration form), 94% were identified as pre-gestational diabetes in the MBRN. Of cases coded as pre-gestational diabetes by the MBRN, 80% were confirmed by the medical record for births during 1998, while more than half of the births incorrectly coded as pre-gestational diabetes really were gestational diabetes. Among births coded as gestational diabetes, 89% were confirmed in the medical record. In conclusion, the sensitivity of the pregestational diabetes diagnosis in the Medical Birth Registry of Norway was very good, particularly in the earlier period, but the information in the MBRN on births before 1999 was not sufficient to classify pregestational diabetes as type 1 – or type 2 diabetes. The type of diabetes can be specified for births from 1999 onwards, but the predictive values are unknown. The predictive value for pre-gestational diabetes in 1998 was less than optimal but acceptable for a routine registry not specialised for diabetes

INTRODUCTION: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. MATERIALS AND METHODS: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. RESULTS: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. CONCLUSION: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.

BACKGROUND: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. METHODS AND FINDINGS: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. CONCLUSIONS: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.

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.

BACKGROUND: 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. METHODOLOGY/PRINCIPAL FINDINGS: 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. CONCLUSIONS: 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.