Varicocele and concomitant dilation of the periprostatic venous plexus: effects on semen viscosity sperm parameters.

INTRODUCTION: Since varicocele is often associated with other venous abnormalities, this study was undertaken to evaluate the frequency of dilation of the periprostatic venous plexus (DPVP) in these patients and the effects of this association on sperm parameters before and after varicocelectomy. MATERIALS AND METHODS: Sperm parameters were evaluated using the conventional WHO criteria, and seminal fluid viscosity was further evaluated by quantitative viscometry, in 50 patients (aged 20-38 years) who underwent surgical treatment for grade III bilateral varicocele. RESULTS: Thirty patients with varicocele had also DPVP (DPVP+) (60 %). Sperm concentration and the percentage of spermatozoa with normal morphology did not differ significantly in patients with DPVP- or DPVP+ before or after surgical repair. On the other hand, sperm progressive motility was low in all patients and increased significantly after varicocele repair, but only in DPVP- patients. Before varicocele treatment, a significantly higher number of DPVP+ patients (25/30 = 83.3 %) had seminal fluid hyperviscosity compared to DPVP- patient (2/20 = 10.0 %). Viscosity quantitative measurement was significantly higher in DPVP+ patients both before and after varicocele repair compared to DPVP- patients. These latter showed a statistically significant reduction of sperm viscosity after varicocele surgical repair compared to pretreatment values. Finally, periprostatic venous plexus diameter and seminal fluid viscosity correlated directly in DPVP+ patients. CONCLUSIONS: In conclusion, these results showed that a large number of patients with varicocele had a concomitant DPVP. This subset of patients did not take advantage from varicocele surgical repair since only DPVP- varicocele patients showed a significant improvement of sperm progressive motility and seminal fluid viscosity. These findings suggest the evaluation of the periprostatic venous plexus and seminal fluid viscosity before patients with varicocele undergo surgical repair for asthenozoospemia.

Relevance of genetic investigation in male infertility.

Genetic causes can be directly responsible for various clinical conditions of male infertility and spermatogenic impairment. With the increased use of assisted reproduction technologies our understanding of genetic basis of male infertility has large implications not only for understanding the causes of infertility but also in determining the prognosis and management of such couples. For these reasons, the genetic investigations represent today an essential and useful tool in the treatment of male infertility. Several evidences are available for the clinical practice regarding the diagnosis; however, there are less information relative to the treatment of the genetic causes of male infertility. Focus of this review is to discuss the main and more common genetic causes of male infertility to better direct the genetics investigation in the treatment of spermatogenic impairment.

Cryptorchidism and its long-term complications.

Cryptorchidism is the most frequent defect of the male urogenital tract at birth. It represents a risk factor for primitive testiculopathy associated with long-term complications (infertility, testicular neoplasia, and hormonal changes). An only consensus exists: "children with bilateral cryptorchidism who are not treated in early age are certainly set to become infertile". The majority of Authors agrees that the cryptorchid testicle will be in for structural and functional alterations and the rate of infertility is inversely proportional to the age at the time of orchidopexy. Cryptorchidism causes secretory primitive testicular pathology responsible for infertility. It is correlated to a non-specific severe histopathological pattern that can be useful to predict future infertility at the moment of orchidopexy. Also cryptorchidism represents the major risk factor associated with germ cell testicular neoplasia (5-10 times more probably than a normal testicle) due to genetic, hormonal, environmental factors.

Andrological characterization of the patient with diabetes mellitus.

AIM: In the management of the chronic complications caused by diabetes mellitus, an important role is played to andrological problematics, which require a specialistic evaluation combined in order to concretely contribute to the improvement of quality of life of such patients. The erectile disfunction in the diabetic patient notoriously correlates with the main cardiometabolics risk factors, and recently it has been pointed out how after chronic use of inhibitors of the phospodiesterase-enzyme-5 (PDE5-I) it is possible to improve the vascular response profile, evaluated through ecolor doppler (ECD) penile dynamic. The incidence of the vascular extra-genital pathology in the patients with ED of organic arterial type has also been observed, underlining in particular the correlation with a low value of the systolic peak at penile level. Little attention has been paid to other andrologic pathologies that preliminary clinic evidences or less followed research points have individuated as real emerging problems; among them there are: 1) the hypogonadism in adult age (late onset hypogonadism); 2) the lower urinary tract symptoms (LUTS) correlated to the condition of prostatic hypertrophy; 3) the infections of the male genito-urinary tract with different characterization for imaging respect to the not diabetic population; 4) different sexual disorders; 5) implications over the male reproductive sphere. METHODS: Retrospective analysis of the clinic, laboratory (spermatic, microbiologic and hormonal), ultrasonography integrated data, led on a diabetic population examined during the last 3 years; finalized at the estimation of the distribution of the andrological pathology characterizing such population, with the comparison of the data on the basis of years of duration disease, grade of glicometabolic compensation and levels of total testosterone. RESULTS: ED was present in 16.36% of the examined population; 50% showed vascular arterial form; hypogonadism was present in 10% of the population. A very high prevalence of subfertility was observed 51.82%. The ultrasonographic characterization of the didimo-epididimary and prostatic-vesicular regions showed reduced testicular volume the 16.36% of cases, increase of the prostatic glandular volume in 45.45% of cases, altered thickness of the seminal vesicles in the 24.45% of cases. The microbiologic characterization evidences the contemporary positivity of the 3 prechosen indicators (spermiocolture, urinocolture, leukocytospermia) in 34.55% of patients. CONCLUSIONS: The study has contributed to enrich the data relative to the heterogeneity of the clinic-andrological presentation of the diabetic patient.

Testosterone therapy improves the clinical response to conventional treatment for male patients with metabolic syndrome associated to late onset hypogonadism.

AIM: Recently, the clinic characterization of the gonadic male function has been put in tight correlation on the pathogenetic level with the main variables forming the condition of metabolic syndrome (MS); probably the serum testosterone (T) concentration in males is to be considered as an additional parameter completely related to the traditional clinical-metabolic findings. Currently the matter of the substitutive hormonal therapy with androgens is apparently influenced by some important unresolved aspects: 1) who really benefits from the T therapy? 2) are the actual dosage methods of T reliable? 3) which vascular and metabolic targets are to be monitored during the T therapy? METHODS: In an analytical longitudinal study, carried out 12 months long on 60 men (average age 58 years, range 54-63 years) affected by metabolic syndrome (MS) and combined hypogonadism late onset (LOH), authors have evaluated the clinical response (androgenic asset, non-invasive hospital monitoring of the arterial pressure, lipidic asset study, body composition and the biologic resistance to the insulinic action) after conventional medical therapy (insulin-sensibilizing and anti-hypertensive) and after substitutive hormonal therapy with testosterone (T) by transdermic way. A group of five patients with MS and LOH, not treated, was used as group of control. RESULTS: The group of patients treated with T showed a profile of clinical response better than the group of controls. CONCLUSIONS: In conclusion, the seric determination of T is useful to better characterize the dismetabolic patient at the moment of the first level active medical therapy planning on the controls of the main risk factors constituting MS, expressing a potential role of conditioning.

Development of an image analysis system to monitor the retention of residual cytoplasm by human spermatozoa: correlation with biochemical markers of the cytoplasmic space, oxidative stress, and sperm function.

A method has been developed for quantifying the residual cytoplasm present in the midpiece of human spermatozoa, based upon the imaging of NADH oxidoreductase activity. This procedure used NADH and nitroblue tetrazolium as electron donor and acceptor, respectively, and resulted in the discrete staining of the entire midpiece area, including the residual cytoplasm. Image analysis techniques were then used to generate binary images of the midpiece, from which objective measurements of this cellular domain could be undertaken. Such data were found to be highly correlated with biochemical markers of the cytoplasmic space, such as creatine kinase (CK) and glucose-6-phosphate dehydrogenase (G-6-PDH), in sperm populations depleted of detectable leukocyte contamination. Morphometric analysis of the sperm midpiece was also found to reflect semen quality in that it predicted the proportion of the ejaculate that would be recovered from the high-density region of Percoll gradients and was negatively correlated with the movement and morphology of the spermatozoa in semen. Variation in the retention of excess residual cytoplasm was also associated with differences in the functional competence of washed sperm preparations, both within and between ejaculates. Thus, within-ejaculate comparisons of high- and low-density sperm subpopulations revealed a relative disruption of sperm function in the low-density fraction. This disruption was associated with the presence of excess residual cytoplasm in the midpiece, high concentrations of cytoplasmic enzymes, and the enhanced-generation reactive oxygen species (ROS). Functional differences between individual high-density Percoll preparations were also negatively correlated with the area of the midpiece and the corresponding capacity of the spermatozoa to generate ROS. These findings suggest that one of the factors involved in the etiology of defective sperm function is the incomplete extrusion of germ cell cytoplasm during spermiogenesis as a consequence of which the spermatozoa experience a loss of function associated with the induction of oxidative stress.

Pharmacological stimulation of sperm motility.

The treatment of male factor infertility is a rapidly developing field. The introduction of microsurgical fertilization techniques allows assisted conception units to treat couples who previously would not have benefited from in-vitro fertilization techniques. However, these techniques are only used for the minority of subfertile men in andrological practice. Many subfertile men are still treated pharmacologically or by sperm selection methods to enhance sperm fertilizing ability. Numerous pharmacological compounds have been described that enhance sperm motility and thus, potentially, sperm fertilizing capacity. This paper attempts to review these compounds and assess their role in treatment of the subfertile male.