Genetic association study of the GNB3 C825T, the ACE I/D and the eNOS G894T polymorphisms and the risk to develop erectile dysfunction in a German ED population

Abstract

Erectile dysfunction (ED) is often associated with cardiovascular disorders such as hypertension, coronary heart disease, hypercholesterolaemia and diabetes mellitus. The genotypes in the GNB3 C825T, the ACE I/D and the eNOS G894T polymorphisms have been identified as genetic risk factors for cardiovascular disorders. The association between the genotypes in these polymorphisms and the risk to develop ED was analysed. In 455 German ED patients and 111 age-matched healthy controls genotyping in the candidate polymorphisms was performed after DNA extraction from whole blood. Association studies between the genotype distribution in the control group in comparison with the ED-group and age of onset of the disease as well as erectile response to intracorporal prostaglandin injection in dependence of candidate polymorphism genotype were performed using the SPSS-Software(R). Genotype distribution of the GNB3 C825T, the ACE I/D and the eNOS G894T polymorphisms was similar in the ED population and the healthy control group. The age of onset of the disease as well as the erectile response to intracorporal prostaglandin injection was independent of the genotypes in the three candidate polymorphisms. In contrast to the previous studies in this analysis, the risk to develop ED is not influenced by the genotypes in the GNB3 C825T, the ACE I/D and the eNOS G894T polymorphisms.

The insertion/deletion (I/D) polymorphism in the angiotensin‐converting enzyme gene and erectile dysfunction risk: a meta‐analysis

“…More recently, However, Andersen and colleagues did not detect a significant association between the ACE gene polymorphism and ED risk in Brazilian population (Andersen et al, 2010). This is in agreement with two other studies demonstrating no association between the gene I/ D polymorphism and ED in a Mexican (Rosas-Vargas et al, 2004) and German population (Eisenhardt et al, 2010).…”

“…Rosas-Vargas et al (2004) 22 (42) 26 (49) 5 (9) 18 (29) 31 (50) 13 (21) 70 (66) 36 (34) 67 (54) 57 (46) 0.002 0.958 Mazo et al (2008) 10 (6) 48 (26) 124 (68) 15 (10) 78 (52) 56 (38) 68 (19) 296 (81) 108 (36) 190 (64) 2.626 0.105 Andersen et al (2010) 11 (16) 33 (46) 27 (38) 50 (15) 159 (48) 125 (37) 55 (39) 87 (61) 259 (39) 409 (61) 0.002 0.961 Eisenhardt et al (2010) 86 (19) 238 (52) 131 (29) 17 (16) 62 (57) 29 (27) 410 (45) 500 (55) 96 (44) 120 (56) 2.852 0.091 Latino and European. Thus, the polymorphism may not increase ED risk in different population.…”

“…Of these, one article Eisenhardt & Siffert, 2003) was excluded because it contained overlapping data from the same investigators. Thus, a total of six case-control studies were finally included in our meta-analysis (Park et al, 1999;Kim et al, 2001;Rosas-Vargas et al, 2004;Mazo et al, 2008;Andersen et al, 2010;Eisenhardt et al, 2010). Characteristics of the six case-control studies included are summarized in Table 1.…”

“…Studies were carried out in various ethnicities: two involved Asian (Park et al, 1999;Kim et al, 2001), two involved Latino (Rosas-Vargas et al, 2004;Andersen et al, 2010) and two involved European (Mazo et al, 2008;Eisenhardt et al, 2010). Assessment of ED was from a variety of sources, including colour doppler ultrasonography (Park et al, 1999;Kim et al, 2001;Eisenhardt et al, 2010), vasoactive drug-induced erection test (Rosas-Vargas et al, 2004), International index of Erectile Function-5 (IIEF-5) (Mazo et al, 2008) and an eight-item questionnaire (Andersen et al, 2010). The determination of the genetic polymorphisms used in all the studies are polymerase chain reaction (PCR).…”

Genetics of Erectile Dysfunction

“…21 In a study of German patients with ED compared with controls there was no difference in the ACE I/D genotype. 13 However, that study included patients with ED attributable to various causes, including vascular, neurogenic, psychogenic, hormonal and mixed etiologies, as well as 11% of men for whom no specific ED etiology could be identified. A lack of association was also noted between ACE genotypes in the Korean population.…”