The ec-NOS gene intron 4 VNTR, E298A and IVF 23+10 G/T polymorphisms were evaluated in the isolated DNA blood samples obtained from the patient group with ED (n=96), from the group received sildenafil (n=67) and from the healthy group (n=167).
We performed a meta-analysis of published studies investigating the association between ED and three eNOS polymorphisms, intron 4 VNTR, G894T and T786C in humans.
Our meta-analysis showed that the two single nucleotide polymorphisms in eNOS gene, G894T and T-786C, are strongly associated with the risk of erectile dysfunction.
To evaluate a potential association between the G894T polymorphism in the eNOS gene and ED complaints in a population-based sample in São Paulo, Brazil.
The eNOS 894T allele carriers are at greater risk for both MtS and ED, suggesting that eNOS G894T gene polymorphism might play an implication as a common genetic susceptibility factor to develop both disorders.
The distributions of alleles (G894T, P < .005; T-786C, P < .015), genotypes (G894T, P < 0.015; T-786C, P < .010), and haplotypes (G894T/T-786C, P < .015) of the NOS3 polymorphisms were significantly different between patients with ED and controls.
The purpose of this study was to determine the relationship between erectile dysfunction (ED), coronary artery disease (CAD), and T(-786)C and intron 4 a/b endothelial nitric oxide synthase (eNOS) polymorphisms in 419 patients with suspected or known CAD referred for coronary angiography.
Five genetic models and a generalized odds ratio (OR(G) ) were used to estimate the association between eNOSG894T and variable number of 27-bp tandem repeats in intron 4 (4 VNTR) and the risk of ED.
Several studies have focused on the impaired role of endothelial nitric oxide synthase (NOS3) gene polymorphism and its association to erectile dysfunction (ED).
We studied 118 patients; 63 patients had ED secondary to radical prostatectomy (PED) and 55 had organic, clinical ED. eNOS genotypes for three eNOS polymorphisms (T(-786)C, rs2070744; a variable number of tandem repeats (VNTR) in intron 4; and rs1799983" genes_norm="4846">Glu298Asp, rs1799983) were determined, and eNOS haplotypes were estimated using PHASE 2.1.
The results showed that diabetes mellitus (odds ratio [OR] = 3.27, P < .01), hypertension (OR = 3.47, P < .01), and having the VEGF 2578A allele (OR = 1.54, P = .01) were the three most independent risk factors for ED.
We determined VEGF genotypes for three polymorphisms in VEGF promoter: -2578C>A (rs699947), -1154G>A (rs1570360) and -634G>C (rs2010963) in 126 patients with erectile dysfunction (ED; 66 patients with PED and 60 patients with CED).
Among men with type 1 diabetes not using antihypertensive medications, higher SBP is associated with increased risk of developing erectile dysfunction.
Despite significant advances regarding ED pharmacological management, there are still insufficient responders to existing pharmacological treatments e.g., approximately 30% of patients are insufficient responders to phosphodiesterase type 5 inhibitors (PDE5-Is).
Efficacy of treatment of ED in the CKD population is comparable to non-CKD patients across multiple modalities, including PDE5 inhibitors, vacuum erectile devices, intracavernosal injections and penile prostheses.
Not only have phosphodiesterase-5 (PDE5) inhibitors improved the treatment of erectile dysfunction (ED), they have indirectly contributed to the treatment of male factor infertility.