Leptin receptor gene polymorphisms c.668A>G and c.1968G>C in Sudanese women with preeclampsia: a case-control study.

BACKGROUND: Leptin receptor gene (LEPR) variants may affect the leptin levels and act as a risk factor for preeclampsia. Two LEPR gene missense variants rs1137101 (c.668A>G) and rs1805094 (c.1968G>C) were investigated in Sudanese women with preeclampsia. METHODS: A matched case-control study (122 women in each arm) was conducted in Saad Abualila Maternity Hospital in Khartoum, Sudan from May to December 2018. The cases were women with preeclampsia and the controls were healthy pregnant women. Genotyping for LEPR gene variants c.668A>G and c.1968G>C was performed using polymerase chain reaction-restriction fragment length polymorphism. Logistic regression models (adjusted for age, parity, body mass index and hemoglobin level) were conducted. RESULTS: Genotype frequency of LEPR gene variants c.668A>G and c.1968G>C was in accordance with Hardy-Weinberg equilibrium (P > 0.05) in the controls. Allele G in LEPRc.668A>G variant was significantly more frequent in the cases compared with the controls [43.4% vs. 10.2%; OR = 6.44; 95%CI (3.98-10.40); P < 0.001]. In variant LEPRc.668A>G, genotype AG was the prevalent genotype in the cases compared with the controls, and it was significantly associated with preeclampsia risk [37.7% vs. 15.5%; AOR = 3.48; 95%CI (1.15-10.54); P = 0.027]. Likewise, the GG genotype was the second most common genotype in the cases compared with the controls, and was associated with preeclampsia risk [24.6% vs. 2.5%; AOR = 14.19; 95%CI (1.77-113.76); P = 0.012]. None of the LEPRc.1968G>C variant genotypes were associated with preeclampsia. The CC genotype was not detected in neither the cases nor the controls. The haplotype A-G 70.1% was the prevalent haplotype in this population, and it significantly protected against preeclampsia [OR = 0.14; 95%CI (0.09-0.23); P < 0.001]. However, the haplotype G-G 26.8% was significantly associated with preeclampsia risk [OR = 6.70; 95%CI (4.16-11.05); P < 0.001]. Both variants c.668A>G and c.1968G>C were in strong linkage disequilibrium (D' = 1, r2 = 0.012). CONCLUSIONS: Our data indicate that the rs1137101 (c.668A>G) variant and G-G haplotype may independently associate with the development of preeclampsia.

Factor-V Leiden G1691A and prothrombin G20210A polymorphisms in Sudanese women with preeclampsia, a case -control study.

BACKGROUND: Preeclampsia can lead to adverse maternal and perinatal outcomes. There are few studies on the association of preeclampsia with thrombophilia in Africa including Sudan. METHODS: 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). RESULTS: 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. CONCLUSIONS: 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.

Thyroid function/antibodies in sudanese women with polycystic ovarian disease.

OBJECTIVE: To evaluate thyroid function and hormonal profile in women with polycystic ovary syndrome (PCOS). METHODS: A case-control study was conducted at Saad Abualila Center, Khartoum, Sudan. The cases were women with confirmed PCOS based on Rotterdam criteria. The controls were infertile women with no evidence of PCOS. The socio-demographic characteristics and medical history were gathered using a questionnaire. Thyroid hormones (thyroid-stimulating hormone, free tri-iodothyronine, and free thyroxine), anti-thyroid peroxidase, and anti-thyroglobulin antibodies were measured. RESULTS: While there were no significant differences in the age and haemoglobin levels of the two studied groups (55 women in each arm), body mass index was significantly higher in women with PCOS. There were no significant differences in the levels of thyroid-stimulating hormone, luteinizing hormone, follicle stimulating hormone, luteinizing hormone/follicle stimulating hormone, anti-thyroid peroxidase, anti-thyroglobulin antibodies, cholesterol, triglycerides and low-density lipoprotein cholesterol between the cases and the controls. The mean±standard deviation of free tri-iodothyronine (3.50±0.2 vs. 3.38±0.3 pg/mL, P=0.040) and median (interquartile) high-density lipoprotein cholesterol (37.0 [34.0 to 42.0] vs. 35.80 [29.0 to 41.0] mg/dL, P=0.015) were significantly higher in PCOS patients compared with the control group. In linear regression, PCOS (0.151 pg/mL, P=0.023) and anti-thyroid peroxidase levels (-0.078 pg/mL, P=0.031) were significantly associated with free tri-iodothyronine. CONCLUSION: Free tri-iodothyronine was a significantly higher among PCOS patients compared with the control group.

Oxidative/nitrosative stress in rats subjected to focal cerebral ischemia/reperfusion.

BACKGROUND: Ischemic stroke usually initiates inflammation and oxidative/nitrosative stress leading to neuronal death. AIM: To investigate the existence of oxidative/nitrosativestress in rats subjected to focal cerebral ischemia/reperfusion and its effects on the consequent neurological deficits. MATERIAL AND METHOD: Experimental procedures were performed on 30 adult males Wister rats. In the test group, transient focal cerebral ischemia was induced in 15 rats by occlusion of the left common carotid artery (CCA) for 30 minutes followed by reperfusion for 24 hours. Another 15 rats underwent the surgery at the same neck region without occlusion of CCA and served as a control group. Neurobehavioral tests were evaluated, the levels of malondialdehyde (MDA), total antioxidant capacity (TAC) and nitric oxide (NO) metabolites were measured in the serum and brain tissue to detect the effect of surgery on in each group. RESULT: The serum and brain tissue levels of MDA and NO in the test group were significantly higher compared to the control group (P < 0.001). In contrast, serum and brain tissue levels of TAC of rats subjected to ischemia reperfusion was significantly lower compared to the sham operated rats (P < 0.001). Neurological deficit of the test group correlated positively with serum TAC (CC = 0.937, P = 0.000) and brain tissue TAC (CC = 0.949, P = 0.000) and negatively with serum MDA (CC = -0.949, P = 0.000), brain tissue MDA (CC = -0.963, P = 0.000), serum NO (CC = -0.942, P = 0.000) and brain tissue NO (CC = -0.952, P = 0.000). CONCLUSION: The study provided further evidence for the presence of oxidative/nitrosative stress in rats subjected to cerebral ischemia/reperfusion and demonstrates a relationship between oxidative/nitrosative biomarkers and the consequent neurological deficits.

Role of N-Nitro-L-Arginine-Methylester as anti-oxidant in transient cerebral ischemia and reperfusion in rats.

BACKGROUND: Previous reports assessing the neuroprotective role of nonselective Nitric Oxide synthase (NOS) inhibitor N-nitro-L-arginine-methylester (L-NAME) following cerebral ischemia/reperfusion are contradictory. The aim of this work was to examine the potential benefits of L-NAME on rats subjected to transient focal cerebral ischemia/reperfusion. METHODS: The study involved 30 adult male Wistar rats divided into three groups 10 rats in each: First group was sham-operated and served as a control, a ischemia/reperfusion (I/R) group of rats infused with 0.9% normal saline intraperitoneally 15 minutes prior to 30 minutes of left common carotid artery (CCA) occlusion and a test group infused with L-NAME intraperitoneally 15 minutes prior to ischemia. Neurobehavioral assessments were evaluated and quantitative assessment of malondialdehyde (MDA), Nitric oxide (NO) metabolites and total antioxidant capacity (TAC) in both serum and the affected cerebral hemisphere were achieved. RESULTS: Rats' neurological deficit and TAC were significantly decreased while NO and MDA were significantly increased in the I/R compared with the control group (P < 0.001). Alternatively in the L-NAME group, neurological deficit and TAC were significantly improved while NO and MDA were significantly decreased compared to I/R group (P < 0.001). CONCLUSIONS: L-NAME pretreatment for rats undergoing cerebral ischemia/reperfusion significantly improves neurological deficit while reducing oxidative stress biomarkers in the affected cerebral hemisphere.