Prevalence and Mechanism for Formation of Varicocele
Defined as the abnormal dilatation of the veins that are responsible for venous return from the testicles, the term varicocele was originally coined by Curling in 1843. Varicocele is the most common treatable pathology of the male infertility.

Studies conducted show that varicocele can occur in 15% of men in general and 40% of men seeking medical help for infertility. According to the Guidelines of the European Association of Urology, varicocele is found in 12% of adult males whereas it is detected in 26% of patients who have impaired sperm values.

It is more common in the left testicle than the right testicle. The frequency of occurrence of varicocele in the left testicle alone is 90% whereas the frequency for the right testicle alone is relatively low, which is around 2%.

There are mainly 3 theories suggested in development of varicocele. These are anatomical differences between the right and left testicular veins, reflux (backflow) of the blood to the vein, and partial obstruction of the testicular veins

Partial obstruction of the testicular vein
Venous drainage of the testicles is obstructed as a result of compression of the left testicular vein that lies between the aorta and the artery that supplies blood the colons.

Impairment mechanisms of varicocele
Numerous studies show that presence of varicocele leads to impaired testicular development. There are various accepted theories to explain testicular impairment in the presence of varicocele.
Impairment caused by elevation of intratesticular temperature: This is the most commonly accepted theory of the varicocele.

Studies conducted have found out that mean intratesticular temperature of 30°C reaches 35-36°C in the presence of varicocele. The increase in temperature, which results from pooling of blood in the veins, leads to stoppage of sperm production. Anatomical structure of the scrotum and the network of veins ensures scrotal thermoregulation. The thin skin structure of the scrotum, absence of subcutaneous fatty tissue, and the muscle of the sac arranging the surface area ensure thermoregulation. The heat exchange between the testicular artery and the pampiniform venous plexus in its adjacency plays one of the main roles in temperature regulation of the testicles. High-temperature blood supplied from the abdominal aorta is cooled by the veins that carry lower-temperature blood. This mechanism works when the temperature of the blood in the vein is lower. ıt is believed that varicocele impairs this mechanism. In studies conducted, it has been observed that intratesticular temperature returns to normal levels after varicocele operation.

Another theory to explain the testicular impairment is the increasing intratesticular pressure. Increasing testicular pressure may lead to oncotic and hydrostatic pressure changes. As a result, the changing intracellular fluid balance affects conveyance of hormones. Additionally, it is suggested that impaired supply resulting from constant contraction of veins impacts sperm production.

The relationship of varicocele with hormones has been evidenced by studies conducted. Detrimental effects of varicocele include Leydig cell (the cells that produce testosterone) dysfunctions, impaired tubular structure, interstitial fibrosis and reduced sperm production. Leydig cell dysfunction might result in reduced testosterone levels. A study conducted show that intratesticular testosterone level must be minimum 20 ng/dl for healthy continuance of sperm production. The same study has found that intratesticular testosterone level is significantly lower in varicocele patients.

Effects of varicocele on testicles and sperm
In presence of varicocele, testicle volume might decrease or testicles might shrink abnormally, depending on the severity of varicocele
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