Nada Mohammed Aljuaid1,2, Ebtesam Ibrahim Muharram3, Nouf Nasser Loqtum2, Reem Mohammed Al-Amoudi4, Hadiah Bassam AlMahdi2,5, Mohammed Assem Salama2,5, Babajan Banaganapalli5,6, Noor Ahmad Shaik5,6, Ramu Elango5,6, Nabeel Salem Bondagji5,7. 1. Department of Biological Sciences, Faculty of Science, University of Jeddah, Jeddah, Saudi Arabia. 2. Department of Biological Sciences, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia. 3. Department of Biochemistry, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia. 4. Department of Obstetrics and Gynecology, Maternity and Children's Hospital, Jeddah, Saudi Arabia. 5. Princess Al-Jawhara Al-Brahim Center of Excellence in Research of Hereditary Disorders, King Abdulaziz University, Jeddah, Saudi Arabia. 6. Department of Genetic Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia. 7. Department of Obstetrics and Gynecology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Abstract
OBJECTIVE: The objective of this study was to investigate the association of rs1051740, rs2234922 (in microsomal epoxide hydrolase 1; EPHX1), rs268 (in lipoprotein lipase; LPL) and rs6025 (in Factor V Leiden; F5) genetic variants with the risk of preeclampsia development in Saudi women. MATERIALS AND METHODS: This case-control study recruited 233 Saudi women (94 preeclampsia cases and 139 healthy controls) who visited the Gynecology and Obstetrics Departments of two hospitals in Jeddah, Saudi Arabia, for routine postpregnancy clinical follow-ups. All the women underwent thorough clinical and biochemical investigations conducted according to the standard clinical guidelines. Genotyping of the study participants was done using real-time polymerase chain reaction-based TaqMan allelic discrimination assay. The strength of the association between genetic variants and disease development was assessed using chi-square, odds ratio, 95% confidence interval and multifactor dimensionality reduction tests. RESULT: The minor alleles "G" in rs268 (LPL) and "A" in rs6025 (F5) were absent in Saudi women. The frequencies of rs1051740 and rs2234922 of EPHX1, both in the homozygous and allelic forms, were not significantly different between preeclampsia patients and healthy controls (for all tests, P > 0.05). The multifactor dimensionality reduction analysis also indicated that the interaction between the four studied single-nucleotide polymorphisms (SNPs) had no significant association with preeclampsia risk. CONCLUSION: This study found that none of the studied genetic variants (neither the single SNP nor the SNP-SNP interactions) explain the development of preeclampsia in the Saudi population. These findings not only underscore the disease heterogeneity but also highlight the need to develop population-specific diagnostic genetic biomarkers for preeclampsia. Copyright:
OBJECTIVE: The objective of this study was to investigate the association of rs1051740, rs2234922 (in microsomal epoxide hydrolase 1; EPHX1), rs268 (in lipoprotein lipase; LPL) and rs6025 (in Factor V Leiden; F5) genetic variants with the risk of preeclampsia development in Saudi women. MATERIALS AND METHODS: This case-control study recruited 233 Saudi women (94 preeclampsia cases and 139 healthy controls) who visited the Gynecology and Obstetrics Departments of two hospitals in Jeddah, Saudi Arabia, for routine postpregnancy clinical follow-ups. All the women underwent thorough clinical and biochemical investigations conducted according to the standard clinical guidelines. Genotyping of the study participants was done using real-time polymerase chain reaction-based TaqMan allelic discrimination assay. The strength of the association between genetic variants and disease development was assessed using chi-square, odds ratio, 95% confidence interval and multifactor dimensionality reduction tests. RESULT: The minor alleles "G" in rs268 (LPL) and "A" in rs6025 (F5) were absent in Saudi women. The frequencies of rs1051740 and rs2234922 of EPHX1, both in the homozygous and allelic forms, were not significantly different between preeclampsia patients and healthy controls (for all tests, P > 0.05). The multifactor dimensionality reduction analysis also indicated that the interaction between the four studied single-nucleotide polymorphisms (SNPs) had no significant association with preeclampsia risk. CONCLUSION: This study found that none of the studied genetic variants (neither the single SNP nor the SNP-SNP interactions) explain the development of preeclampsia in the Saudi population. These findings not only underscore the disease heterogeneity but also highlight the need to develop population-specific diagnostic genetic biomarkers for preeclampsia. Copyright:
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