Eleonora Carosa

Prevalence of chronic prostatitis in men with premature ejaculation

OBJECTIVES To investigate the prevalence of chronic prostatitis in men with premature ejaculation. The etiology of premature ejaculation is currently considered psychological in nature. However, the possibility that urologic, hormonal, or neurologic factors may contribute to this condition should be considered in its management. METHODS We evaluated segmented urine specimens before and after prostatic massage and expressed prostatic secretion specimens from 46 patients with premature ejaculation and 30 controls by bacteriologic localization studies. The incidence of premature ejaculation in the subjects with chronic prostatitis was also evaluated. RESULTS Prostatic inflammation was found in 56.5% and chronic bacterial prostatitis in 47.8% of the subjects with premature ejaculation, respectively. When compared with the controls, these novel findings were statistically significant (P <0.05). CONCLUSIONS Considering the role of the prostate gland in the mechanism of ejaculation, we suggest a role for chronic prostate inflammation in the pathogenesis of some cases of premature ejaculation. Since chronic prostatitis has been found with a high frequency in men with premature ejaculation, we stress the importance of a careful examination of the prostate before any pharmacologic or psychosexual therapy for premature ejaculation.

Measurement of the Thickness of the Urethrovaginal Space in Women with or without Vaginal Orgasm

INTRODUCTION The physiology and anatomy of female sexual function are poorly understood. The differences in sexual function among women may be partly attributed to anatomical factors. AIM The purpose of this study was to use ultrasonography to evaluate the anatomical variability of the urethrovaginal space in women with and without vaginal orgasm. METHODS Twenty healthy, neurologically intact volunteers were recruited from a population of women who were a part of a previous published study. All women underwent a complete urodynamic evaluation and those with clinical and urodynamic urinary incontinence, idiopathic detrusor overactivity, or micturition disorders, as well as postmenopausal women and those with sexual dysfunction were excluded. The reported experience of vaginal orgasm was investigated. MAIN OUTCOME MEASURE The urethrovaginal space thickness as measured by ultrasound was chosen as the indicator of urogenital anatomical variability. Designated evaluators carried out the measurements in a blinded fashion. RESULTS The urethrovaginal space and distal, middle, and proximal urethrovaginal segments were thinner in women without vaginal orgasm. A direct correlation between the presence of vaginal orgasm and the thickness of urethrovaginal space was found. Women with a thicker urethrovaginal space were more likely to experience vaginal orgasm (r = 0.884; P = 0.015). A direct and significant correlation between the thickness of each urethrovaginal segment and the presence of vaginal orgasm was found, with the best correlation observed for the distal segment (r = 0.863; P < 0.0001). Interobserver agreement between the designated evaluators was excellent (r = 0.87; P < 0.001). CONCLUSIONS The measurement of the space within the anterior vaginal wall by ultrasonography is a simple tool to explore anatomical variability of the human clitoris-urethrovaginal complex, also known as the G-spot, which can be correlated to the ability to experience the vaginally activated orgasm.

Type V phosphodiesterase inhibitor treatments for erectile dysfunction increase testosterone levels.

objective  Lack of sexual activity due to erectile dysfunction (ED) decreases testosterone (T) levels through a central effect on the hypothalamic–pituitary axis. In this paper we studied the effect of different type V phosphodiesterase (PDE5) inhibitor treatments for ED on the reversibility of this endocrine pattern.

Sexual inactivity results in reversible reduction of LH bioavailability

We have recently documented significantly reduced serum testosterone (T) levels in patients with erectile dysfunction (ED). To understand the mechanism of this hypotestosteronemia, which was independent of the etiology of ED, and its reversibility only in patients in whom a variety of nonhormonal therapies restored sexual activity, we measured serum luteinizing hormone (LH) in the same cohort of ED patients (n=83; 70% organic, 30% nonorganic). Both immunoreactive LH (I-LH) and bioactive LH (B-LH) were measured at entry and 3 months after therapy. Based on outcome (ie number of successful attempts of intercourse per month), patients were categorized as full responders (namely, at least eight attempts; n=51), partial responders (at least one attempt; n=20) and non-responders (n=16). Compared to 30 healthy men with no ED, baseline B-LH (mean±s.d.) in the 83 patients was decreased (13.6±5.5 vs 31.7±6.9 IU/L, P<0.001), in the face of a slightly increased, but in the normal range, I-LH (5.3±1.8 vs 3.4±0.9 IU/L, P<0.001); consequently, the B/I LH ratio was decreased (3.6±3.9 vs 9.7±3.3, P<0.001). Similar to our previous observation for serum T, the three outcome groups did not differ significantly for any of these three parameters at baseline. However, outcome groups differed after therapy. Bioactivity of LH increased markedly in full responders (pre-therapy=13.7±5.3, post-therapy=22.6±5.4, P<0.001), modestly in partial responders (14.8±6.9 vs 17.2±7.0, P<0.05) but remained unchanged in non-responders (11.2±2.2 vs 12.2±5.1). The corresponding changes went in the opposite direction for I-LH (5.2±1.7 vs 2.6±5.4, P<0.001; 5.4±2.2 vs 4.0±1.7, P<0.05; 5.6±1.2 vs 5.0±1.2, respectively), and in the same direction as B-LH for the B/I ratio (3.7±4.1 vs 11.8±7.8, P<0.001; 4.2±4.3 vs 5.8±4.2, P<0.05; 2.1±0.7 vs 2.6±1.3, respectively). We hypothesize that the hypotestosteronemia of ED patients is due to impaired bioactivity of LH. This reduced bioactivity is reversible, provided that resumption of sexual activity is achieved regardless of the therapeutic modality. Because biopotency of pituitary hormones is controlled by the hypothalamus, LH hypoactivity should be due to the hypothalamic functional damage associated to the psychological disturbances which unavoidably follow sexual inactivity.

Sexual Symptoms in Endocrine Diseases: Psychosomatic Perspectives

Background: Not only the most frequent causes of endocrine sexual dysfunction, such as hypogonadism and hyperprolactinemia, but almost all extragonadal endocrinopathies (hyper- and hypothyroidism, hyper- and hypocortisolism, steroidal secreting tumors, etc.) may have a greater or lesser effect on sexual function. Methods: We analyzed scientific literature on the correlations between hormones and sexual behavior, analyzing the most important issue from a practical point of view. The aim of this review article was thus to summarize the sexual symptoms that may be observed with endocrine diseases. Results: Hormones directly or indirectly regulate all human sexual functions (desire, erection/lubrication, ejaculation, orgasm). Some sexual symptoms may occur as a psychosomatic consequence of hormonal impairment. However, in other cases, endocrine failure may be generated by the psychosomatic involvement. Conclusions: The endocrinologist, as an expert in body chemistry, is ideally positioned to identify and evaluate the full range of medical, physical, and psychiatric problems disrupting sexual function.

Ontogeny and regulation of variant thyroid hormone receptor isoforms in developing rat testis

High affinity-low capacity nuclear triiodothyronine (T3) receptors (TRs), identified as a product of c-erbAα proto-oncogene, are expressed in prepubertal rat Sertoli cell. At this age, exogenous T3 treatment as well as hypothyroidism affects Sertoli cell functions. We examined the ontogenetic expression pattern of TRs in the rat testis. Northern analysis confirms that TRs are expressed at high level from fetal development until prepubertal period. Rnase protection analysis demonstrates that TRα2, the variant isoform of TRα1, is constitutively expressed at all ages, while TRα3 is absent in the adult gonad. While TRα1 and TRα2 expression declines during development, Rev-erbAα (Rev), the antisense mRNA encoded by the same c-erbAα genomic locus, increases beginning 5 days after birth and maximizing in adulthood. TRα1, TRα2, and Rev mRNAs do not appear to be directly regulated by thyroid hormone in testis; however, short-term neonatal hypothyroidism leads to the expression of TRα1 and its variant in adult testis, which is absent in control coeval animals. Thus, during development of rat testis, the levels of messages of genes encoded in the c-erbAα genomic locus have different ontogenetic control. The ontogenetic profile of TRα1 and its variant isoforms within the seminiferous epithelium suggests that these receptors are involved in the differentiation of the male gonad.

Premature ejaculation results in female sexual distress: standardization and validation of a new diagnostic tool for sexual distress.

PURPOSE We measured premature ejaculation related female sexual distress using a new diagnostic tool, the Female Sexual Distress Scale-Revised-Premature Ejaculation questionnaire. MATERIALS AND METHODS In this large-scale, Internet based population study we evaluated 2,109 women in a stable relationship during the last 6 months. The 1,361 women in the premature ejaculation group had no female sexual disorder but the partner had premature ejaculation alone. The 748 controls had no female sexual disorder and a partner without premature ejaculation. We determined questionnaire content and discriminant validity, internal consistency and test-retest reliability. Multivariate logistic regression with propensity score reweighting was done to determine the clinical impact of demographics on the perception of sexual distress. RESULTS The questionnaire was well understood. Internal consistency was greater than 0.90 and 0.84 in the premature ejaculation and control groups, respectively. Test-retest reliability was 0.82 (95% CI 0.72-0.87) and 0.85 (95% CI 0.79-0.92) in the premature ejaculation and control groups, respectively. The questionnaire had a high AUC of 0.90 (95% CI 0.89-0.91). The new cutoff score of 12 or greater had 79.1% sensitivity (95% CI 73.8-82.5), 99.5% specificity (95% CI 98.0-100.0), 99.3% positive predictive value (95% CI 98.7-100.0) and 67.9% negative predictive value (95% CI 64.2-73.2). Median questionnaire scores were significantly higher in the premature ejaculation group than in controls (20, 95% CI 19-21 vs 6, 95% CI 6-7, p <0.0001). Logistic regression adjusted and unadjusted by propensity score indicated that women in the premature ejaculation group had a 7.12 (95% CI 5.98-10.14, p <0.0001) to 9.83 (95% CI 7.94-12.15) greater probability of sexual distress than controls. CONCLUSIONS The Female Sexual Distress Scale-Revised-Premature Ejaculation questionnaire fulfills psychometric requirements for measuring sexual distress related to partner sexual dysfunction.

Differential effects of PXD101 (belinostat) on androgen-dependent and androgen-independent prostate cancer models

Histone deacetylase inhibitors (HDACi) are promising epigenetic cancer chemotherapeutics rapidly approaching clinical use. In this study, we tested using in vitro and in vivo models the differential biological effects of a novel HDAC inhibitor [belinostat (PXD101)], in a wide panel of androgen-sensitive and androgen-independent tumor cells. Belinostat significantly increased acetylation of histones H3 and H4. Belinostat potently inhibited the growth of prostate cancer cell lines (IC50 range from 0.5 to 2.5 µM) with cytotoxic activity preferentially against tumor cells. This agent induced G2/M arrest and increased significantly the percentage of apoptosis mainly in androgen-sensitive tumor cells confirming its growth-inhibitory effects. The cell death mechanisms were studied in three different prostate cancer cell lines with different androgen dependence and expression of androgen receptor; LAPC-4 and 22rv1 (androgen-dependent and expressing androgen receptor) and PC3 (androgen-independent not expressing androgen receptor). Belinostat induced the expression of p21 and p27, acetylation of p53 and G2/M arrest associated with Bcl2 and Bcl-Xl downmodulation and significant reduction of survivin, IAPs and Akt/pAkt and increased caspase-8 and -9 expression/activity. Belinostat effectiveness was dependent on the androgen receptor (AR), since the stable transfection of AR greatly increased the efficacy of this HDAC inhibitor. These observations were correlated using in vivo models. We demonstrated that belinostat preferentially resulted in antitumor effect in androgen-dependent tumor cells expressing AR. Our findings provide evidence that belinostat may be a promising anticancer drug for prostate cancer expressing AR, supporting its clinical role in prostate cancer.

Attachment styles and sexual dysfunctions: A case-control study of female and male sexuality

The aim of this study was to investigate attachment styles in a group of women and men with sexual dysfunction. We recruited 44 subjects (21 women and 23 men) with sexual dysfunction and 41 subjects (21 women and 20 men) with healthy sexual function as the control group. Validated instruments for the evaluation of male and female sexual dysfunctions (M/F SD) and a psychometric tool specifically designed to investigate attachment style were administered. In women, significant differences were found between subjects with sexual dysfunction and healthy controls. The scales indicating an insecure attachment showed: discomfort with closeness (FSD=42.85±11.55 vs CTRL=37.38±8.54; P<0.01), relationship as secondary (FSD=26.76±2.60 vs CTRL=18.42±7.99; P<0.01), and need for approval (FSD=26.38±3.61 vs CTRL=20.76±7.36; P<0.01). Healthy women also had significantly higher scores in secure attachment (confidence: FSD=24.57±3.89 vs CTRL=33.42±5.74; P<0.01). Men with sexual dysfunctions differed from healthy men in confidence (MSD=30±6.33 vs CTRL=36.05±5.26; P<0.01) and in discomfort with closeness (MSD=39.08±8 vs CTRL=34.25±7.54; P<0.05). These results suggest that particular aspects related to insecure attachment have a determinant role in people with sexual dysfunctions. It is therefore fundamental to identify the attachment styles and relational patterns in patients receiving counselling and psychological treatments focussed on sexual problems.

Psychoticism, Immature Defense Mechanisms and a Fearful Attachment Style are Associated with a Higher Homophobic Attitude

INTRODUCTION Homophobic behavior and a negative attitude toward homosexuals are prevalent among the population. Despite this, few researches have investigated the psychologic aspects associated with homophobia, as psychopathologic symptoms, the defensive system, and attachment styles. AIM The aim of this study was to investigate the psychologic factors mentioned earlier and their correlation with homophobia. METHODS Five hundred fifty-one university students recruited, aged 18-30, were asked to complete several psychometric evaluation. MAIN OUTCOME MEASURES In particular, Homophobia Scale (HS) was used to assess homophobia levels, the Symptoms Check List Revised (SCL-90-R) for the identification of psychopathologic symptoms, the Defence Style Questionnaire (DSQ-40) for the evaluation of defense mechanisms and the Relationship Questionnaire (RQ) for attachment styles. RESULTS After a regression analysis, we found a significant predictive value of psychoticism (β = 0.142; P = 0.04) and of immature defense mechanisms (β = 0.257; P < 0.0001) for homophobia, while neurotic defense mechanisms (β = -0.123; P = 0.02) and depressive symptoms (β = -0.152; P = 0.04) have an opposite role. Moreover, categorical constructs of the RQ revealed a significant difference between secure and fearful attachments styles in levels of homophobia (secure = 22.09 ± 17.22 vs. fearful = 31.07 ± 25.09; P < 0.05). Finally, a gender difference to HS scores and a significant influence of male sex was found (β = 0.213; P < 0.0001). CONCLUSIONS We demonstrated the involvement of psychoticism and immature defense mechanisms in homophobic attitudes, while a contrasting role is played by neurotic defense mechanisms and depressive symptoms. Moreover, secure attachment is an indicator of low levels of homophobia compared with the subjects demonstrating a fearful style of attachment. Hence, in the assessment of homophobia and in the relevant programs of prevention, it is necessary to consider the psychologic aspects described earlier.