Nadir A. Ahmed
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Nadir A. Ahmed has a total of 5 co-authors. Here are the top co-authors by number of shared publications:
- Hamdan Zaki Hamdan
Department of Pathology, College of Medicine, Qassim University, Buraidah 51452, Saudi Arabia
2 shared publications - Ishag Adam
Department of Obstetrics and Gynecology, College of Medicine, Qassim University, Buraydah 52389, Saudi Arabia
2 shared publications Ammar H. Kamis
Hamdan Bin Mohammed College of Dental Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai, United Arab Emirates
1 shared publication- Hiba A. Awooda
Department of Biochemistry and Molecular Biology, Faculty of Medicine, Al-Neelain University, PO BOX 12702, Khartoum, Sudan
1 shared publication - Salah Eldin Elzaki
Department of Epidemiology, Tropical Medicine Research Institute, National Centre for Research, Khartoum, Sudan
1 shared publication
Latest Publications
- Open Access
- 5 January 2019
- Published by Springer Nature in BMC Medical Genetics
- Vol. 20 (1) , 1-5
Factor-V Leiden G1691A and prothrombin G20210A polymorphisms in Sudanese women with preeclampsia, a case -control study
Preeclampsia can lead to adverse maternal and perinatal outcomes. There are few studies on the association of preeclampsia with thrombophilia in Africa including Sudan. A case –controls study was conducted at Saad Abualila Hospital in Khartoum, Sudan during the period of February through November 2017. The cases were women with preeclampsia and healthy pregnant women were the controls (180 women in each arm of the study). Genotyping for Factor-V Leiden 1691G/A and Prothrombin gene variation 20210G/A was done by polymerase chain reaction–restriction fragment length polymorphism (PCR–RFLP). There was no significant difference in the age, parity, body mass index (BMI) and the other characteristics between the cases and the controls. Genotypes distribution of Factor V Leiden 1691G/A and prothrombin gene 20210G/A in controls was in accordance with the Hardy–Weinberg equilibrium (P > 0.05). The factor V Leiden-variation was present in 9.6% of the cases compared with 0.6% of the controls, P < 0.001 (OR = 18.60, 95% CI = 2.38–136.1). Only 4 patients with severe preeclampsia had homozygous variation A/A and it was not detected in the controls. Prothrombin G20210A variations not detected neither in the cases nor in the controls group. High prevalence of Factor V Leiden 1691G/A variation in preeclamptic patients compared to controls suggest an involvement of this variation in predisposing to preeclampsia in this setting.
- 5 January 2019
- Published by Springer Nature in BMC Medical Genetics
- Vol. 20 (1) , 1-5
Open AccessFactor-V Leiden G1691A and prothrombin G20210A polymorphisms in Sudanese women with preeclampsia, a case -control study
Preeclampsia can lead to adverse maternal and perinatal outcomes. There are few studies on the association of preeclampsia with thrombophilia in Africa including Sudan. A case –controls study was conducted at Saad Abualila Hospital in Khartoum, Sudan during the period of February through November 2017. The cases were women with preeclampsia and healthy pregnant women were the controls (180 women in each arm of the study). Genotyping for Factor-V Leiden 1691G/A and Prothrombin gene variation 20210G/A was done by polymerase chain reaction–restriction fragment length polymorphism (PCR–RFLP). There was no significant difference in the age, parity, body mass index (BMI) and the other characteristics between the cases and the controls. Genotypes distribution of Factor V Leiden 1691G/A and prothrombin gene 20210G/A in controls was in accordance with the Hardy–Weinberg equilibrium (P > 0.05). The factor V Leiden-variation was present in 9.6% of the cases compared with 0.6% of the controls, P < 0.001 (OR = 18.60, 95% CI = 2.38–136.1). Only 4 patients with severe preeclampsia had homozygous variation A/A and it was not detected in the controls. Prothrombin G20210A variations not detected neither in the cases nor in the controls group. High prevalence of Factor V Leiden 1691G/A variation in preeclamptic patients compared to controls suggest an involvement of this variation in predisposing to preeclampsia in this setting.