Talk:Abnormal Development - Hypertension: Difference between revisions
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==2018== | |||
===Pharmacogenomics of Hypertension and Preeclampsia: Focus on Gene-Gene Interactions=== | |||
Front Pharmacol. 2018 Feb 28;9:168. doi: 10.3389/fphar.2018.00168. eCollection 2018. | |||
Luizon MR1,2, Pereira DA2, Sandrim VC3. | |||
Abstract | |||
Hypertension is a leading cause of cardiovascular mortality, but only about half of patients on antihypertensive therapy achieve blood pressure control. Preeclampsia is defined as pregnancy-induced hypertension and proteinuria, and is associated with increased maternal and perinatal mortality and morbidity. Similarly, a large number of patients with preeclampsia are non-responsive to antihypertensive therapy. Pharmacogenomics may help to guide the personalized treatment for non-responsive hypertensive patients. There is evidence for the association of genetic variants with variable response to the most commonly used antihypertensive drugs. However, further replication is needed to confirm these associations in different populations. The failure to replicate findings from single-locus association studies has prompted the search for novel statistical methods for data analysis, which are required to detect the complex effects from multiple genes to drug response phenotypes. Notably, gene-gene interaction analyses have been applied to pharmacogenetic studies, including antihypertensive drug response. In this perspective article, we present advances of considering the interactions among genetic polymorphisms of different candidate genes within pathways relevant to antihypertensive drug response, and we highlight recent findings related to gene-gene interactions on pharmacogenetics of hypertension and preeclampsia. Finally, we discuss the future directions that are needed to unravel additional genes and variants involved in the responsiveness to antihypertensive drugs. | |||
KEYWORDS: | |||
antihypertensive therapy; epistasis; gene–gene interactions; hypertension; pathways; pharmacogenomics; preeclampsia | |||
PMID: 29541029 PMCID: PMC5835759 DOI: 10.3389/fphar.2018.00168 | |||
==2017== | ==2017== | ||
Revision as of 22:05, 19 March 2018
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Cite this page: Hill, M.A. (2024, April 19) Embryology Abnormal Development - Hypertension. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Abnormal_Development_-_Hypertension |
2018
Pharmacogenomics of Hypertension and Preeclampsia: Focus on Gene-Gene Interactions
Front Pharmacol. 2018 Feb 28;9:168. doi: 10.3389/fphar.2018.00168. eCollection 2018.
Luizon MR1,2, Pereira DA2, Sandrim VC3.
Abstract
Hypertension is a leading cause of cardiovascular mortality, but only about half of patients on antihypertensive therapy achieve blood pressure control. Preeclampsia is defined as pregnancy-induced hypertension and proteinuria, and is associated with increased maternal and perinatal mortality and morbidity. Similarly, a large number of patients with preeclampsia are non-responsive to antihypertensive therapy. Pharmacogenomics may help to guide the personalized treatment for non-responsive hypertensive patients. There is evidence for the association of genetic variants with variable response to the most commonly used antihypertensive drugs. However, further replication is needed to confirm these associations in different populations. The failure to replicate findings from single-locus association studies has prompted the search for novel statistical methods for data analysis, which are required to detect the complex effects from multiple genes to drug response phenotypes. Notably, gene-gene interaction analyses have been applied to pharmacogenetic studies, including antihypertensive drug response. In this perspective article, we present advances of considering the interactions among genetic polymorphisms of different candidate genes within pathways relevant to antihypertensive drug response, and we highlight recent findings related to gene-gene interactions on pharmacogenetics of hypertension and preeclampsia. Finally, we discuss the future directions that are needed to unravel additional genes and variants involved in the responsiveness to antihypertensive drugs. KEYWORDS: antihypertensive therapy; epistasis; gene–gene interactions; hypertension; pathways; pharmacogenomics; preeclampsia PMID: 29541029 PMCID: PMC5835759 DOI: 10.3389/fphar.2018.00168
2017
Maternal and neonatal outcomes in Korean women with type 2 diabetes
Korean J Intern Med. 2017 Jan 26. doi: 10.3904/kjim.2016.105. [Epub ahead of print]
Jang HJ1, Kim HS2, Kim SH3.
Abstract
BACKGROUND/AIMS: The purpose of this study was to compare maternal and neonatal outcomes in Korean women with type 2 diabetes and nondiabetic controls.
METHODS: We performed a retrospective survey of 200 pregnancies in women with type 2 diabetes (n = 100) and nondiabetic controls (n = 100) who delivered from 2003 to 2010 at Cheil General Hospital & Women's Healthcare Center, Korea. We compared maternal characteristics as well as maternal and neonatal outcomes between groups matched by age, pre-pregnancy weight, body mass index, parity, and gestational age at delivery.
RESULTS: The number of infants that were small for gestational age and the rate of major congenital malformations were not significantly different. However, women with type 2 diabetes showed a slightly higher risk for primary caesarean section (35.0% vs. 18.0%, p = 0.006) as well as pre-eclampsia (10.0% vs. 2.0%, p = 0.017), infections during pregnancy (26.0% vs. 2.0%, p < 0.001), neonatal weight (3,370 ± 552.0 vs. 3,196 ± 543.3, p = 0.025), large for gestational age (22.0% vs. 9.0%, p = 0.011), and macrosomia (15.0% vs. 5.0%, p = 0.018) compared to nondiabetic controls.
CONCLUSIONS: Maternal and neonatal outcomes for women with type 2 diabetes were worse than those for nondiabetic controls. Diabetic women have a higher risk for primary caesarean section, pre-eclampsia, infections during pregnancy, large neonatal birth weight, large for gestational age, and macrosomia.
KEYWORDS: Diabetes mellitus, type 2; Pregnancy outcome
PMID 28122420 DOI: 10.3904/kjim.2016.105
The INSR rs2059806 single nucleotide polymorphism, a genetic risk factor for vascular and metabolic disease, associates with pre-eclampsia
Reprod Biomed Online. 2017 Jan 11. pii: S1472-6483(17)30001-9. doi: 10.1016/j.rbmo.2017.01.001. [Epub ahead of print]
Andraweera PH1, Gatford KL2, Dekker GA3, Leemaqz S2, Jayasekara RW4, Dissanayake VH4, McCowan L5, Roberts CT2.
Abstract
Pre-eclampsia is a risk factor for later life vascular and metabolic diseases. This study postulates that this reflects a common genetic cause, and investigates whether the INSR rs2059806 single nucleotide polymorphism (SNP) (a risk factor for essential hypertension, type 2 diabetes and metabolic syndrome) is also associated with pre-eclampsia. The association of INSR rs2059806 with pre-eclampsia was tested in two cohorts - a Caucasian case control group (123 pre-eclamptic mother-father-baby trios and 1185 mother-father-baby trios from uncomplicated pregnancies) and an independent cohort of Sinhalese women (175 women with pre-eclampsia and 171 women with uncomplicated pregnancies). In the Caucasian cohort, the prevalence of the INSR rs2059806 AA genotype was greater among pre-eclamptic women compared with the uncomplicated pregnancies (12.7% versus 4.7%, OR[95%CI] = 3.1[1.6-5.8], P = 0.0003). In the Sinhalese cohort, maternal INSR rs2059806 AA genotype was greater among pre-eclamptic women who delivered small for gestational age infants compared with the uncomplicated pregnancies (10.8% versus 4.2%, OR[95%CI] = 2.8[1.0-7.4], P = 0.03). Thus, it was found that the INSR rs2059806 SNP is also associated with pre-eclampsia phenotypes in two independent cohorts suggesting that genetic susceptibility may be implicated in the link between pre-eclampsia and subsequent vascular and metabolic diseases.
Copyright © 2017 Reproductive Healthcare Ltd. Published by Elsevier Ltd. All rights reserved.
KEYWORDS: INSR; Pre-eclampsia; SNP; Single nucleotide polymorphism; rs2059806 PMID 28117222 DOI: 10.1016/j.rbmo.2017.01.001
