الفهرس 
Introduction and aim of workOnly 14 pages are availabe for public view
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Abstract
There is increasing evidence that race/ethnicity could be independently associated with erectile dysfunction (ED). Moreover some genes, variants at specific gene loci (polymorphisms), or gene products are proposed to be linked to ED. In addition, there are some published data on the susceptibility to sexual disorders between family members. For example, there is a genetic component involved in the etiology of ED among middle-aged 890 monozygotic (MZ) and 619 dizygotic (DZ) twin pairs of men using Vietnam Era Twin Registry. Familial predisposition to premature ejaculation (PE) was first described by Schapiro in 1943. After that, Waldinger et al. showed that 10 of 14 first-degree relatives of men with lifelong PE also suffered PE, with an intravaginal ejaculation latency time of less than 1 minute. In addition to affection of twins, some investigations have suggested either familial clustering or autosomal-dominant transmission of peyronie’s disease (PD). Twins with sickle cell hemoglobinopathy showed similarities in the prevalence and susceptibility to priapism. Furthermore, there is a significant genetic component to variation in female orgasmic function. There are number of studies in the published literature that provide proof of concept that genetic variation contributes to the variable response or adverse effects that are observed upon administration of drugs used in sexual disorders. Genetic variation in the drug efficacy could be due to genetic variants of drug targets, drug transporters, cellular signaling pathways or drug-metabolizing enzymes. Gene therapy has entered the phase of clinical trials in the last few years. Lastly genomic biomarkers for sexual dysfunction could be useful for identification of the condition as that reported with hSMR3A and Vcsa1 in cases of ED.