Disease relevance of Obstetric Labor, Premature

• Treatment with metronidazole did not reduce the occurrence of preterm labor, intraamniotic or postpartum infections, neonatal sepsis, or admission of the infant to the neonatal intensive care unit [1].
• Myocardial infarction during nifedipine therapy for preterm labor [2].
• Angina pectoris associated with use of terbutaline for premature labor [3].
• Ritodrine- and terbutaline-induced hypokalemia in preterm labor: mechanisms and consequences [4].
• This experimental model of E. coli Dr(+)-induced preterm delivery in mice may help in understanding the molecular mechanisms involved in UTI-induced preterm labor involving bacterial adhesins [5].

Psychiatry related information on Obstetric Labor, Premature

• Thus, selective COX-2 inhibitors may demonstrate new important therapeutic benefits as anticancer agents, as well as in preventing premature labor and perhaps even retarding the progression of Alzheimer's disease [6].
• Beta-receptor agonist (terbutalin or isoxsuprin) administration to pregnant women either because of premature labor (therapy group; T; n = 8) or as prophylactic treatment (prophylaxis group; p; n = 8) resulted in a marked drop in serum potassium (p less than 0.001) during the first two hours of infusion in all patients [7].
• Several studies have implicated CRF in the etiology of anxiety, depression, substance abuse, stress-related gastrointestinal disorders and preterm labor, and intensive research into the design of safe and effective CRF antagonists is currently being pursued in several laboratories [8].

High impact information on Obstetric Labor, Premature

• Neonatal complications after the administration of indomethacin for preterm labor [9].
• Treatment of preterm labor with the beta-adrenergic agonist ritodrine [10].
• Fetal fibronectin and preterm labor [11].
• Indomethacin in the treatment of premature labor. Effects on the fetal ductus arteriosus [12].
• Efficacy of 17alpha-hydroxyprogesterone caproate in the prevention of premature labor [13].

Chemical compound and disease context of Obstetric Labor, Premature

• Terbutaline, as currently used to prevent premature labor, is a potent inotropic and chronotropic agent [14].
• It may result from intrauterine infection, which mediates premature labor by stimulating the production of inflammatory lipid mediators such as prostaglandin F2alpha (PGF2alpha) [15].
• The patient was initially treated with chloroquine; however, she developed bilateral pulmonary infiltrates and premature labor, and her condition appeared to clinically deteriorate [16].
• Inflammatory cytokines such as interleukin-1 (IL-1) have been implicated as paracrine mediators of decidual prostaglandin (PG) production during preterm labor [17].
• To study the effect of increased circulating level of corticosteroids on the serum concentration of progestins, 74 women with premature labor with or without premature rupture of membranes were treated with either placebo or 4 im injections of dexamethasone phosphate (5 mg each) at 12-h intervals [18].

Biological context of Obstetric Labor, Premature

• Although improved regulation of maternal IDDM during pregnancy has resulted in a major fall in the stillbirth rate, the rates for other problems, such as spontaneous preterm labor, fetuses small for gestational age, congenital malformation, and the incidence of large placentas, remain raised [19].
• METHODS: Sixty white women with preterm labor between 24 and 34 weeks' gestation were treated for 48 hours with intravenous hexoprenaline [20].
• Elevated CRH concentrations and bioavailability of free cortisol may both be implicated in the pathogenesis of preterm labor in some women [21].
• The significant increase in CRH peptide and mRNA content in both spontaneous term and androstenedione-induced preterm labor indicates a role for CRH in the process of parturition [22].
• The effects of ritodrine and terbutaline on potassium homeostasis, renal function, and cardiac rhythm were assessed in women treated with these drugs for preterm labor [4].

Anatomical context of Obstetric Labor, Premature

• This study was conducted as part of an investigation to evaluate the hypothesis that bacterial toxins (LPS or lipoteichoic acid), acting on macrophage-like uterine decidua to cause increased formation of cytokines, may be involved in the pathogenesis of infection-associated preterm labor [23].
• Expression and localization of prostaglandin E synthase isoforms in human fetal membranes in term and preterm labor [24].
• Furthermore, preterm labor is associated with the elevated expression of the two PGHS isoenzymes in the chorion laeve [25].
• OBJECTIVE: The objective of this study was to evaluate urocortin levels in maternal and fetal [umbilical cord artery (UCA) and vein (UCV)] plasma at term and preterm labor [26].
• Because IL-1 and IL-8 are found in the myometrium at term and have been implicated in the etiology in premature labor we focus on this cytokines [27].

Gene context of Obstetric Labor, Premature

• Therefore, COX-1-selective inhibitors may provide effective treatment to delay preterm labor with fewer adverse effects on fetal or neonatal health than nonselective or COX-2-selective inhibitors [28].
• In contrast, the inhibition of COX-1 during pregnancy lacked these prenatal and postnatal adverse effects on the DA and effectively delayed the initiation of full-term labor and LPS-induced preterm labor [28].
• IL-1beta plays a key role in infection-induced preterm labor and increases prostaglandin H synthase 2 (PGHS-2) and IL-8 expression [29].
• As such, it has been suggested that IL-10 could have therapeutic potential, including the treatment of preterm labor [30].
• Our data support the concept that a complex cytokine network between maternal and fetal gestational tissues exists, and that activation of inflammatory cytokine production in these tissues, including IL-8, likely contributes to the pathophysiology of infection-induced preterm labor [31].

Analytical, diagnostic and therapeutic context of Obstetric Labor, Premature

• To study these effects we used serial fetal echocardiography in 13 pregnant women in premature labor who received indomethacin according to three different dose schedules, ranging from 100 to 175 mg per day, for a maximum of 72 hours [12].
• Among women in preterm labor with culture-negative AF, those who failed to respond to subsequent tocolytic treatment had higher AF IL-6 concentrations than those who responded to therapy (median = 50 ng/ml vs. median = 1.2 ng/ml, respectively, P less than 0.05) [32].
• In situ hybridization suggested that the enhanced PGHS-1 and -2 mRNA expression occurred predominantly in the mesenchymal cells of the fetal membranes at preterm labor [25].
• A 19-yr-old woman developed adult respiratory distress syndrome (ARDS) in the postnatal period after treatment with dexamethasone and ritodrine for premature labor [33].
• Ovariectomy on Day 17 induced preterm labor 96 h after surgery and a significant increase in myometrial OTR mRNA levels 48 and 96 h after surgery [34].

References