273POINT / COUNTERPOINT I t is reported that 35% to 40% of infertile men have a palpable varicocele (dilated testicular veins), whereas the prevalence of a varicocele in the general male population is about 15%.1-3 Although varicoceles have been associated with impaired male fertility potential, it is also clear that a significant proportion of men with a varicocele (about 75%) are fertile. 2,4,5 As such, a cause and effect relationship between varicocele and male infertility has not been conclusively established. 6 The effect of varicocelectomy on male fertility is also controversial.6-10 Uncontrolled studies have generally shown improved semen quality and pregnancy outcome after surgery.11 On the other hand, the results of randomized controlled studies of varicocelectomy for clinical varicocele (only a few such studies are published) are equivocal. [12][13][14][15] Despite the absence of clear evidence for a positive effect of varicocelectomy, many clinicians consider the data sufficient to support the practice of this surgery, and varicocele is the most commonly treated condition in men with infertility in North America. 8 The benefit of varicocele repair must be balanced by the risk associated with the procedure itself. As such, it is important to select the procedure with the highest success and lowest complication rate. Also, it is important to consider assisted reproductive technologies (ARTs) as an alternative to varicocelectomy in infertile couples.
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Etiology of varicoceleThe etiology of varicocele is multifactorial. The anatomic differences between the left and right internal spermatic vein (accounting for the predominance of left-sided varicocele), the incompetence of venous valves resulting in reflux of venous blood and increased hydrostatic pressure are the most popular theories. 17,18 Increased intraabdominal pressure during childhood and early adolescence may be a predisposing factor in the development of a varicocele.
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Mechanisms of varicocele-induced pathologyScrotal and intratesticular temperatures are elevated in humans and in experimental animal models with varicocele, and varicocelectomy may reduce testicular temperature. [20][21][22][23][24] Scrotal hyperthermia likely represents the primary factor by which a varicocele affects endocrine function and spermatogenesis, both sensitive to temperature elevation (testicular proteins exhibit a reduced thermal stability compared with proteins from other organs). [25][26][27] The detrimental effect of hyperthermia may also be exerted on the epididymis. 28 Experimental elevations in epididymal temperature reduce the storage capacity of this organ, resulting in decreased sperm count and quality in the ejaculate.
28Increased hydrostatic pressure in the internal spermatic vein from renal vein reflux may also be responsible for varicocele-induced pathology.
Pathophysiology of varicoceleThe adverse effect of varicocele on male fertility is most clearly manifested by the testicular atrophy generally associated with this condition. 4 Using scrota...