Abstract:
Objective:To profile maternal plasma metabolome in spontaneous preterm birth. Method:In this retrospective case-control study, we have examined plasma of patient with preterm birth (between 22 and 36 weeks of pregnancy (n = 57)), with threatened preterm labor (between 23 and 36 weeks of pregnancy (n = 49)), and with term delivery (n = 25). Plasma samples were analysed using liquid chromatography quadrupole time-of-flight mass spectrometry (LC-Q-TOF-MS) in positive and negative polarity modes. Results:We found 168 differentially expressed metabolites that were significantly distinct between study groups. We determined 51 metabolites using publicly available databases that could be subdivided into one of the five groups: amino acids, fatty acids, lipids, hormones, and bile acids. PLS-DA models, verified by SVM classification accuracy, differentiated preterm birth and term delivery groups. Conclusions:Maternal plasma metabolites are different between term and preterm parturitions. Part of them may be related with preterm labor, while others may be affected by gestational age or the beginning of labor. Metabolite profile can classify preterm or term delivery groups raising the potential of metabolome as a biomarker to identify high-risk pregnancies. Metabolomic studies are also a tool to detect individual compounds that may be further tested in targeted researches.
journal_name
Mediators Inflammjournal_title
Mediators of inflammationauthors
Lizewska B,Teul J,Kuc P,Lemancewicz A,Charkiewicz K,Goscik J,Kacerovsky M,Menon R,Miltyk W,Laudanski Pdoi
10.1155/2018/9362820subject
Has Abstractpub_date
2018-02-15 00:00:00pages
9362820eissn
0962-9351issn
1466-1861journal_volume
2018pub_type
杂志文章abstract:OBJECTIVE:Individuals with inflammation have a myriad of pregnancy aberrations including increasing their preterm birth risk. Toll-like receptors (TLRs) and receptor for advanced glycation end products (RAGE) and their ligands were all found to play a key role in inflammation. In the present study, we reviewed TLR and ...
journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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