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.

Ontogenetic pattern of thyroid hormone receptor expression in the human testis.

We studied the spatiotemporal distribution of thyroid hormone nuclear receptors (TRs) alpha1 and alpha2 and beta messenger RNA (mRNA) levels in normal human testicular tissue during development and in adulthood. Nonpathological specimens from five aborted fetuses (17 and 23 weeks of gestation, three and two cases, respectively) and from four patients undergoing orchiectomy (18 months old and 38-, 42-, and 52-yr-old, respectively) were analyzed by Northern blot, semiquantitative RT-PCR amplification using DNA sequences or specifically designed primers for the TR isoforms, and in situ hybridization. By using PCR amplification, we found that TRalpha1 and TRalpha2 are both expressed at different levels in fetal and adult testis. At all ages TRalpha2 is found at higher levels. Northern analysis showed hybridization signals corresponding to the expression of TRalpha2 and TRalpha in a ratio that increased from 2.6 at 17 weeks of gestation to 12.0 in adulthood. In fact, the expression of TRalpha1 dramatically decreased throughout development, being faintly detectable in the adult testis. Expression of TRbeta was not detected at any age studied. This finding was further confirmed by PCR, which did not amplify TRbeta either in fetal or in adult testis mRNAs. In situ hybridization studies showed the absence of TRbeta and that TRalpha1 and TRalpha2 colocalized in Sertoli cells of prepubertal testis, whereas germ and interstitial cells appeared devoid of TR mRNA signals. From these results it can be concluded that the human testis exclusively expresses TRalpha, which is localized in Sertoli cells, TRbeta being always undetectable. Fetal and prepubertal ages represent the period of maximal expression of TRalpha1 and TRalpha2. The alpha2/alpha1 ratio rises dramatically after development. These results confirm a critical window for the action of thyroid hormone in human testis, in the period of maximal expression of T3 binding isoform TRalpha1, and may account for the macroorchidism without virilization occurring when hyposecretion of thyroid hormones occurs before puberty.

Lack of sexual activity from erectile dysfunction is associated with a reversible reduction in serum testosterone.

The role of androgenic hormones in human sexuality, in the mechanism of erection and in the pathogenesis of impotence is under debate. While the use of testosterone is common in the clinical therapy of male erectile dysfunction, hypogonadism is a rare cause of impotence. We evaluated serum testosterone levels in men with erectile dysfunction resulting either from organic or non-organic causes before and after non-hormonal impotence therapy. Eighty-three consecutive cases of impotence (70% organic, 30% non-organic, vascular aetiology being the most frequent) were subjected to hormonal screening before and after various psychological, medical (prostaglandin E1, yohimbine) or mechanical therapies (vascular surgery, penile prostheses, vacuum devices). Thirty age-matched healthy men served as a control group. Compared to controls, patients with impotence resulting from both organic and non-organic causes showed reduced serum levels of both total testosterone (11.1 +/- 2.4 vs. 17.7 +/- 5.5 nmol/L) and free testosterone (56.2 +/- 22.9 vs. 79.4 +/- 27.0 pmol/L) (both p < 0.001). Irrespective of the different aetiologies and of the various impotence therapies, a dramatic increase in serum total and free testosterone levels (15.6 +/- 4.2 nmol/L and 73.8 +/- 22.5 pmol/L, respectively) was observed in patients who achieved normal sexual activity 3 months after commencing therapy (p < 0.001). On the contrary, serum testosterone levels did not change in patients in whom therapies were ineffective. Since the pre-therapy low testosterone levels were independent of the aetiology of impotence, we hypothesize that this hormonal pattern is related to the loss of sexual activity, as demonstrated by its normalization with the resumption of coital activity after different therapies. The corollary is that sexual activity may feed itself throughout the increase in testosterone levels.

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-erbAalpha 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 TRalpha2, the variant isoform of TRalpha1, is constitutively expressed at all ages, while TRalpha3 is absent in the adult gonad. While TRalpha1 and TRalpha2 expression declines during development, Rev-erbAalpha (Rev), the antisense mRNA encoded by the same c-erbAalpha genomic locus, increases beginning 5 days after birth and maximizing in adulthood. TRalpha1, TRalpha2, 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 TRalpha1 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-erbAalpha. genomic locus have different ontogenetic control. The ontogenetic profile of TRalpha1 and its variant isoforms within the seminiferous epithelium suggests that these receptors are involved in the differentiation of the male gonad.

[Cryptorchidism: current views]. / Il criptorchidismo: attuali orientamenti.

Cryptorchidism is a pathological condition which affects up to 6% of newborns. Main etiopathogenetic hypotheses are the hormonal and the dysgenetic one. Ultrasonography is useful in locating testis in the inguinal canal, while in the management of intraabdominal testis, laparoscopy is considered the best diagnostic technique and, in many cases, can be coupled with surgical management. Medical treatment with LH-RH or with hCG or, better, combined (LH-RH+hCG) is recommended before the second year. Impairment of fertility is a complication mainly in subjects with a history of bilateral cryptorchidism. Undescended testis has a risk of malignant degeneration ranging from 3% to 18% and for this reason some authors suggest a gonadal biopsy after puberty.