| Autor: |
Sharma N; Department of Obstetrics and Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore., Watkins OC; Department of Obstetrics and Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore., Chu AHY; Singapore Institute for Clinical Sciences, Agency for Science, Technology and Research, Singapore, Singapore., Cutfield W; Liggins Institute, University of Auckland, Auckland, New Zealand., Godfrey KM; MRC Lifecourse Epidemiology Centre and NIHR Southampton Biomedical Research Centre, University of Southampton and University Hospital Southampton NHS Foundation Trust, Southampton, UK., Yong HEJ; Singapore Institute for Clinical Sciences, Agency for Science, Technology and Research, Singapore, Singapore., Chan SY; Department of Obstetrics and Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.; Singapore Institute for Clinical Sciences, Agency for Science, Technology and Research, Singapore, Singapore. |
| Abstrakt: |
The incidence of preterm birth (PTB), delivery before 37 completed weeks of gestation, is rising in most countries. Several recent small clinical trials of myo -inositol supplementation in pregnancy, which were primarily aimed at preventing gestational diabetes, have suggested an effect on reducing the incidence of PTB as a secondary outcome, highlighting the potential role of myo -inositol as a preventive agent. However, the underlying molecular mechanisms by which myo -inositol might be able to do so remain unknown; these may occur through directly influencing the onset and progress of labour, or by suppressing stimuli that trigger or promote labour. This paper presents hypotheses outlining the potential role of uteroplacental myo -inositol in human parturition and explains possible underlying molecular mechanisms by which myo -inositol might modulate the uteroplacental environment and inhibit preterm labour onset. We suggest that a physiological decline in uteroplacental inositol levels to a critical threshold with advancing gestation, in concert with an increasingly pro-inflammatory uteroplacental environment, permits spontaneous membrane rupture and labour onset. A higher uteroplacental inositol level, potentially promoted by maternal myo -inositol supplementation, might affect lipid metabolism, eicosanoid production and secretion of pro-inflammatory chemocytokines that overall dampen the pro-labour uteroplacental environment responsible for labour onset and progress, thus reducing the risk of PTB. Understanding how and when inositol may act to reduce PTB risk would facilitate the design of future clinical trials of maternal myo -inositol supplementation and definitively address the efficacy of myo -inositol prophylaxis against PTB. |
