Overview. Preterm labour: mechanisms and management

被引:21
作者
Andrés López Bernal
机构
[1] Clinical Science at South Bristol (Obstetrics and Gynaecology),University of Bristol
[2] St Michael's Hospital and Dorothy Hodgkin Building,undefined
关键词
Corpus Luteum; Preterm Labour; Ritodrine; Myometrial Cell; Uterine Contractility;
D O I
10.1186/1471-2393-7-S1-S2
中图分类号
学科分类号
摘要
Preterm birth remains a major cause of perinatal mortality and long term handicap in surviving infants. This is one of the most important clinical problems in Europe and across the world. While some preterm births are iatrogenic, associated with severe complications of pregnancy (e.g. hypertensive disorders, antepartum haemorrhage, infection), or the result of multiple pregnancies following assisted reproduction, a high proportion of preterm births occur following spontaneous preterm labour of unknown cause. Early intervention in this group of women would have a significant impact on neonatal mortality and morbidity figures. However, the endocrine changes preceding parturition in women remain elusive and this makes it difficult to predict spontaneous labour at term, let alone preterm labour. Moreover our understanding of myometrial physiology remains rudimentary, limiting our options to devise improved pharmacological strategies to control uterine contractility when this is indicated. There is a need for concerted European and international research efforts to improve our knowledge of the mechanism of labour in women, to identify diagnostic markers to predict preterm labour and to develop uterine selective drugs to inhibit uterine contractions in a safe and efficient manner. This aim will be achieved by multidisciplinary research efforts from academics and industry, using traditional laboratory and clinical research methods, as well as novel technologies.
引用
收藏
相关论文
共 298 条
[41]  
Katsuyama M(2005)2,2'-Dichlorobiphenyl decreases amplitude and synchronization of uterine contractions through MAPK1-mediated phosphorylation of GJA1 (connexin43) and inhibition of myometrial gap junctions Biol Reprod 73 974-undefined
[42]  
Hasumoto K(2006)Ablation of connexin43 in uterine smooth muscle cells of the mouse causes delayed parturition J Cell Sci 119 1715-undefined
[43]  
Murata T(1994)Human myometrial chorionic gonadotropin/luteinizing hormone receptors in preterm and term deliveries J Clin Endocrinol Metab 79 907-undefined
[44]  
Hirata M(2001)Human chorionic gonadotrophin inhibition of pregnant human myometrial contractility Bjog 108 704-undefined
[45]  
Ushikubi F(1994)Direct regulation of human myometrial contractions by human chorionic gonadotropin J Clin Endocrinol Metab 79 1582-undefined
[46]  
Negishi M(1994)Novel regulation of pregnant human myometrial smooth muscle cell gap junctions by human chorionic gonadotropin Endocrinology 135 2772-undefined
[47]  
Ichikawa A(2005)Regulation of phosphodiesterase 5 expression and activity in human pregnant and non-pregnant myometrial cells by human chorionic gonadotropin J Soc Gynecol Investig 12 570-undefined
[48]  
Narumiya S(2005)Regulation of expression of the chorionic gonadotropin/luteinizing hormone receptor gene in the human myometrium: involvement of specificity protein-1 (Sp1), Sp3, Sp4, Sp-like proteins, and histone deacetylases J Clin Endocrinol Metab 90 3479-undefined
[49]  
Csapo AI(2002)Silencing of transcription of the human luteinizing hormone receptor gene by histone deacetylase-mSin3A complex J Biol Chem 277 33431-undefined
[50]  
Pulkkinen M(1993)Identification and expression of G-proteins in human myometrium: up-regulation of G alpha s in pregnancy Endocrinology 132 2484-undefined