Pathogenic mechanisms.
Causes that may lead to male varicocele may be:
1. a consequence of a mass occupying space in the retroperitoneum or pelvis (benign or malignant tumors in this region) which compresses the venous structures, and that with the mechanism of venous outflow, realize the picture of VARICOCELE 0 SECONDARY symptomatic.
2. A primary or idiopathic form, which hits the left side predominantly (over 98% of cases).


The cause of the latter remains essentially unknown. Also seems able to admit that the genesis may reside in a failure of the valves which lead to a venous reflux with a consequent increase in the retrograde sense in Rio. The most common left varicocele may be largely supported by a reno-spermatic reflux linked to valvular agenesis or incontinence.

SYMPTOMS
Varicocele causes a painful sense tensive corresponding scrotal area. This pain can sometimes be confused with that of a chronic syndrome prostatitica. Increases during standing and sexual restraint. Rapid development of varicocele in a grown man can be an expression of a renal tumor. Even the varicocele, like all other varicosities, may meet with phenomena phlebitic with all the clinical picture related to it. Clinical examination is revealed as a mass of dilated and tortuous veins at the root of the scrotum. It disappears when supine. Sometimes coexisting atrophy of the testis. The increased interest aroused by the varicocele is not the clinical picture, which in most cases and as modest as the correlation between this and the Sub-.fertility male.
CASE OF PATHOGENESIS sub fertility
The most credible hypothesis are:
Thermal alterations of the testis
Venous stasis resulting in hypoxia
Refluenti toxic effects of substances by the kidney.
II venous reflux, which is easily adjustable with a Doppler, could lead to a concentration of harmful substances harm germinal epithelium of the testis. The most accredited pathogenetic mechanism is certainly the increase in local temperatures.
This increase due to changes in seminal acting mainly on spermatocytes undergoing pachitene.
The difference in temperature is usually higher in the varicocele ‘s 0,6-1,4%. This proved sufficient to alter spermatogenesis and maturation epididimaria. In conclusion can say that not all bearers of varicocele are sub-fertile or that there is a correlation between severity of varicocele and severity of testicular dysfunction.
There are still elements that escape in that regard.
One of the critical factors could be related to the hypothetical moment of onset of varicocele in relation to pubertal status. If the venous vascular disease begins before puberty, the immature testis may suffer more than the contralateral creating a greater likelihood of sub-fertility.