Abstract

Varicocele, a pathological dilation of the scrotal veins, is thought to be the cause of infertility in up to 41% of male factor infertility and is the most common cause of secondary infertility. Men with clinically significant varicocele are found to have reduced sperm counts, impaired motility, and abnormal morphology when compared to men without varicocele. Studies have found that men treated for varicocele show improvement in semen analysis as well as improvement in pregnancy rate. The pathophysiology of varicocele is multifactorial with resulting hyperthermia of the testis, which is believed to be the greatest contributing factor to infertility. Other theories of how varicoceles cause damage include buildup of metabolic waste and reflux of renal and adrenal metabolites. Varicoceles have been found to cause damage to the Leydig cells of the testicle, resulting in decreased serum testosterone levels. Varicocele is also associated with direct damage to the Sertoli cells and germ cells. The damaging effects to these cell types has been found to be reversed when clinical varicoceles are treated by varicocelectomy. Varicoceles not only damage the testes but also the epididymis, affecting the storage and maturation of newly developed sperm. Damage to the epididymis can be quantified by measurement of alpha-glucosidase, and the effect of such damage is seen by decreased transit time through the epididymis, impaired motility, and decreased sperm storage viability. These effects can be reversed with appropriate treatment.

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