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HRG C633T polymorphism and risk of gestational hypertensive disorders: a pilot study
BACKGROUND: Preeclampsia and gestational hypertensive disorders are thought to occur due to endothelial cell dysfunction and abnormal placentation, triggered by angiogenesis-related factors yet undetermined. The aim of this study was to investigate whether a genetic polymorphism (SNP) of Histidine-r...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5853153/ https://www.ncbi.nlm.nih.gov/pubmed/29540166 http://dx.doi.org/10.1186/s12881-018-0550-8 |
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author | Elenis, Evangelia Skalkidou, Alkistis Skoog-Svanberg, Agneta Sydsjö, Gunilla Stavreus-Evers, Anneli Åkerud, Helena |
author_facet | Elenis, Evangelia Skalkidou, Alkistis Skoog-Svanberg, Agneta Sydsjö, Gunilla Stavreus-Evers, Anneli Åkerud, Helena |
author_sort | Elenis, Evangelia |
collection | PubMed |
description | BACKGROUND: Preeclampsia and gestational hypertensive disorders are thought to occur due to endothelial cell dysfunction and abnormal placentation, triggered by angiogenesis-related factors yet undetermined. The aim of this study was to investigate whether a genetic polymorphism (SNP) of Histidine-rich glycoprotein (HRG), HRG C633T SNP, is associated with gestational hypertensive disorders. METHODS: It was performed a nested case-control study from the BASIC Cohort of Uppsala University Hospital comprising 92 women diagnosed with gestational hypertensive disorders without other comorbidities and 200 women with full term uncomplicated pregnancies, all genotyped regarding HRG C633T SNP. RESULTS: The genetic analysis of the study sample showed that C/C genotype was more prevalent among controls. The presence of the T-allele showed a tendency towards an increased risk of gestational hypertensive disorders. After clustering the study participants based on their genotype, it was observed that the odds for gestational hypertensive disorders among heterozygous C/T or homozygous T/T carriers were higher compared to homozygous C/C carriers [OR 1.72, 95% CI (1.04–2.84)]. The association remained significant even after adjustment for maternal age, BMI and parity. CONCLUSIONS: The HRG C633T genotype seems to be associated with gestational hypertensive disorders, and as part of a greater algorithm, might contribute in the future to the prediction of the individual susceptibility to the condition. |
format | Online Article Text |
id | pubmed-5853153 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-58531532018-03-22 HRG C633T polymorphism and risk of gestational hypertensive disorders: a pilot study Elenis, Evangelia Skalkidou, Alkistis Skoog-Svanberg, Agneta Sydsjö, Gunilla Stavreus-Evers, Anneli Åkerud, Helena BMC Med Genet Research Article BACKGROUND: Preeclampsia and gestational hypertensive disorders are thought to occur due to endothelial cell dysfunction and abnormal placentation, triggered by angiogenesis-related factors yet undetermined. The aim of this study was to investigate whether a genetic polymorphism (SNP) of Histidine-rich glycoprotein (HRG), HRG C633T SNP, is associated with gestational hypertensive disorders. METHODS: It was performed a nested case-control study from the BASIC Cohort of Uppsala University Hospital comprising 92 women diagnosed with gestational hypertensive disorders without other comorbidities and 200 women with full term uncomplicated pregnancies, all genotyped regarding HRG C633T SNP. RESULTS: The genetic analysis of the study sample showed that C/C genotype was more prevalent among controls. The presence of the T-allele showed a tendency towards an increased risk of gestational hypertensive disorders. After clustering the study participants based on their genotype, it was observed that the odds for gestational hypertensive disorders among heterozygous C/T or homozygous T/T carriers were higher compared to homozygous C/C carriers [OR 1.72, 95% CI (1.04–2.84)]. The association remained significant even after adjustment for maternal age, BMI and parity. CONCLUSIONS: The HRG C633T genotype seems to be associated with gestational hypertensive disorders, and as part of a greater algorithm, might contribute in the future to the prediction of the individual susceptibility to the condition. BioMed Central 2018-03-14 /pmc/articles/PMC5853153/ /pubmed/29540166 http://dx.doi.org/10.1186/s12881-018-0550-8 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Elenis, Evangelia Skalkidou, Alkistis Skoog-Svanberg, Agneta Sydsjö, Gunilla Stavreus-Evers, Anneli Åkerud, Helena HRG C633T polymorphism and risk of gestational hypertensive disorders: a pilot study |
title | HRG C633T polymorphism and risk of gestational hypertensive disorders: a pilot study |
title_full | HRG C633T polymorphism and risk of gestational hypertensive disorders: a pilot study |
title_fullStr | HRG C633T polymorphism and risk of gestational hypertensive disorders: a pilot study |
title_full_unstemmed | HRG C633T polymorphism and risk of gestational hypertensive disorders: a pilot study |
title_short | HRG C633T polymorphism and risk of gestational hypertensive disorders: a pilot study |
title_sort | hrg c633t polymorphism and risk of gestational hypertensive disorders: a pilot study |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5853153/ https://www.ncbi.nlm.nih.gov/pubmed/29540166 http://dx.doi.org/10.1186/s12881-018-0550-8 |
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