Inflammatory cytokines seem to play a key role in mechanisms initiating labor. Since cytokine levels are higher in preterm than in term labor, it has been hypothesized that labor-inducing effects of cytokines are inhibited by an upregulated production of cytokine antagonists, such as soluble cytokine receptors, at early stages of gestation. In this study, TNF, IL-1, IL-6, IL-8 and soluble TNF receptors (sTNFRs) were measured in amniotic fluid samples from a) 39 women in premature labor, b) 25 women who where not in labor but delivered prematurely, and c) 33 women in term labor. Fifty-four of the placentas from premature deliveries were evaluated for presence of histological chorioamnionitis. Chorioamnionitis was associated with increased levels of TNF, IL-1 and IL-6, whereas elevated IL-1, IL-6 and IL-8 concentrations were found in premature parturition with no signs of infection. Concentrations of sTNFR were lower in preterm than in term deliveries. The present study confirms the participation of inflammatory cytokines in parturition. Multivariate analysis suggests a dominant, role of IL-1 in the presence of chorioamnionitis, whereas IL-6 seems to be more important during idiopathic premature labor. TNFR data do not support the hypothesis that production of cytokine antagonists is upregulated prematurely to prevent partirution.

No abstract

The aim of the present study was to assess indications for induction and describe the characteristics and delivery outcome in medical compared to non-medical/elective inductions. During a three-month period, 1663 term inductions were registered in 24 delivery units in Norway. Inclusion criteria were singleton pregnancies with cephalic presentation at gestational age 37+0 and beyond. Indications, pre-induction Bishop scores, mode of delivery and adverse maternal and fetal outcomes were registered, and compared between the medically indicated and elective induction groups. Ten percent of the inductions were elective, and the four most common indications were maternal request (35%), a previous negative delivery experience or difficult obstetric history (19%), maternal fatigue/tiredness (17%) and anxiety (15%). Nearly half of these inductions were performed at 39+0–40+6 weeks. There were fewer nulliparous women in the elective compared to the medically indicated induction group, 16% vs. 52% (p<0.05). The cesarean section rate in the elective induction group was 14% and 17% in the medically indicated group (14% vs. 17%, OR = 0.8, 95% CI 0.5–1.3). We found that one in ten inductions in Norway is performed without a strict medical indication and 86% of these inductions resulted in vaginal delivery.

<strong><span style="font-family: TimesNewRomanPS-BoldMT;"><span style="font-family: TimesNewRomanPS-BoldMT;"><p align="left"> </p></span></span><span style="font-size: x-small; font-family: TimesNewRomanPS-BoldMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-BoldMT;">SAMMENDRAG</span></span></strong><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><p align="left">Infeksjon i det intrauterine miljø kan være en viktig årsak til premature rier. Intrauterine infeksjoner</p><p align="left">underdiagnostiseres med dagens metoder. Ny kunnskap om molekylære mekanismer gir nye diagnostiske</p><p align="left">muligheter og kan åpne for alternative behandlingsformer.</p><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><p align="left">Arntzen KJ, Kjøllesdal AM, Vatten L, Austgulen R.</p></span></span></span><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><p align="left"> </p></span></span><p align="left"><strong><span style="font-size: x-small; font-family: TimesNewRomanPS-BoldMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-BoldMT;">Infection and premature birth.</span></span></strong><em><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;"><em><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;"><p align="left">Nor J Epidemiol</p></span></span></em></span><em><span style="font-size: x-small; font-family: TimesNewRomanPS-ItalicMT;"><p align="left"> </p></span></em></span><strong><span style="font-size: x-small; font-family: TimesNewRomanPS-BoldMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-BoldMT;">ENGLISH SUMMARY</span></span></strong><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><p align="left">Prematurity is the cause of a substantial proportion of perinatal morbidity and mortality. It has become</p><p align="left">clear that intrauterine infection is an important underlying cause of premature labour. Unfortunately, our</p><p align="left">ability to diagnose these infections at an early stage is not well developed, and the effectiveness of available</p><p align="left">therapeutic agents is low. Premature labour caused by infection involves the activation of a network</p><p align="left">of inflammatory cytokines and the production of intrauterine prostaglandins. In this paper, we have</p><p align="left">attempted to describe recent developments in this area that are relevant to prematurity, and we also discuss</p><p>whether this knowledge may provide possibilities for therapeutic intervention.</p></span></span></em><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;">1997; </span></span><strong><span style="font-size: x-small; font-family: TimesNewRomanPS-BoldMT;"><span style="font-size: x-small; font-family: TimesNewRomanPS-BoldMT;">7 </span></span></strong><span style="font-size: x-small; font-family: TimesNewRomanPSMT;"><span style="font-size: x-small; font-family: TimesNewRomanPSMT;">(1): 79-84.</span></span></p>