ABSTRACT
Although elevated prolactin levels have been shown to inhibit penile erection, the relationship between prolactin and erection of the penile tip or base has not been extensively researched. We therefore investigated the prolactin's effects on erection of the penile tip and base, with a cross-sectional study of 135 patients with erectile dysfunction, based on scores of ≤21 on the International Index of Erectile Function-5. All patients were tested for nocturnal penile tumescence, blood pressure, serum glucose, total cholesterol, triglyceride, high-density lipoprotein, low-density lipoprotein, luteinizing hormone, follicle-stimulating hormone, prolactin, estradiol, testosterone, and progesterone. Univariate and multivariate analyses were used to assess the associations between prolactin levels and erection at the penile tip and base. We found no obvious relationship between erection time at penile tip and prolactin levels, but observed a negative correlation between base erection time and prolactin level (hazard ratio: -2.68; 95% confidence interval [CI]: -5.13--0.22). With increasing prolactin concentration, multivariate analysis showed obvious reduction in base erection time among patients with normal Rigiscan results (hazard ratio: -3.10; 95% CI: -7.96-1.77; P < 0.05). Our data indicate that prolactin inhibits penile erection, particularly at the penile base. In addition, when the effective erection time of the penile base lasts longer than 10 min, prolactin has a more obvious inhibitory effect on penile base erection.
Subject(s)
Adult , Humans , Male , Cross-Sectional Studies , Erectile Dysfunction/blood , Penile Erection , Prolactin/blood , Time FactorsABSTRACT
Although elevated prolactin levels have been shown to inhibit penile erection, the relationship between prolactin and erection of the penile tip or base has not been extensively researched. We therefore investigated the prolactin's effects on erection of the penile tip and base, with a cross-sectional study of 135 patients with erectile dysfunction, based on scores of ≤21 on the International Index of Erectile Function-5. All patients were tested for nocturnal penile tumescence, blood pressure, serum glucose, total cholesterol, triglyceride, high-density lipoprotein, low-density lipoprotein, luteinizing hormone, follicle-stimulating hormone, prolactin, estradiol, testosterone, and progesterone. Univariate and multivariate analyses were used to assess the associations between prolactin levels and erection at the penile tip and base. We found no obvious relationship between erection time at penile tip and prolactin levels, but observed a negative correlation between base erection time and prolactin level (hazard ratio: -2.68; 95% confidence interval [CI]: -5.13 - 0.22). With increasing prolactin concentration, multivariate analysis showed obvious reduction in base erection time among patients with normal Rigiscan results (hazard ratio: -3.10; 95% CI: -7.96-1.77; P < 0.05). Our data indicate that prolactin inhibits penile erection, particularly at the penile base. In addition, when the effective erection time of the penile base lasts longer than 10 min, prolactin has a more obvious inhibitory effect on penile base erection.
ABSTRACT
The aim of our study was to investigate the role of platelet parameters including mean platelet volume (MPV) and platelet count (PC) in the pathogenesis of penile arteriogenic erectile dysfunction (ED) and to evaluate the association between the platelet parameters and arteriogenic ED. There were 244 patients with ED (based on the International Index of Erectile Function [IIEF]-5 ≤21) and 60 healthy controls (IIEF-5 >21) enrolled. All participants were asked to undergo a laboratory examination, and penile vascular function was evaluated using penile color Doppler ultrasonography (pDUS). Among these ED patients, 24 patients with no abnormality on nocturnal penile tumescence (NPT) and 84 with normal vasculature or mixed vascular abnormalities were excluded. The other patients were classified into three groups as follows: control (n = 60), arteriogenic ED (n = 99), and venous leakage (n = 37) groups. MPV and PC were significantly higher in the arteriogenic ED group compared with the venous and control groups (P < 0.05). Receiver operating characteristic curve analysis revealed that the area under the curve for MPV to predict arteriogenic ED was 0.707. MPV ≥9.65 fl was recognized as a cut-off value for potential arteriogenic ED (sensitivity: 47.5%; specificity: 91.7%). A significant inverse correlation was detected between MPV and 10-min peak systolic velocity (PSV) (r = -0.34; P < 0.001) in the arteriogenic ED group. These findings suggest that the MPV might be a powerful indicator to predict and diagnose arteriogenic ED, and MPV may be a marker for ED when using pDUS.