Varicocele and Male Infertility: Evidence in the Era of Assisted Reproductive Technology

Purpose: To evaluate the current literature on the varicocele treatment and impact on fertility. Materials and Methods: Pertinent articles were identified through PubMed search on varicocele repair and male infertility. Discussion: The proposed mechanisms of how varicocele results in impaired spermatogenesis and infertility include an altered or impaired testicular blood flow, increased scrotal temperature and oxidative stress as well as resulting sex hormone changes, reflux of adrenal hormones, and autoimmunity with anti-sperm antibody formation. The repair of varicocele as an infertility treatment is dependent on many factors such as the grade and size of the varicocele, unilateral or simultaneous bilateral repair, female partner’s age, the period during which the couple as failed to conceive and quality of the semen. Summary: Varicoceles can present in up to 40% of men presenting with infertility and published literature support the findings that varicocele adversely affect spermatogenesis. Surgical varicocelectomy is an effective treatment for improving the semen parameters in men and spontaneous pregnancy rate for couples with an infertile male partner who has low semen parameters and a palpable varicocele. Comparative studies favour the microsurgical subinguinal technique as the standard of care with highest rates of success and lowest rates of complications. *Corresponding author: Eric Chung, Department of Urology, Princess Alexandra Hospital, Brisbane QLD Australia, Tel: +617 33242468; Fax: +617 33242546; E-mail: [email protected] Received December 27, 2013; Accepted December 31, 2013; Published January 07, 2014 Citation: Chung E (2014) Varicocele and Male Infertility: Evidence in the Era of Assisted Reproductive Technology. Reprod Syst Sex Disord 3: e114. doi: 10.4172/2161-038X.1000e114 Copyright: © 2014 Chung E. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Introduction Varicocele is defined as dilatation of the pampiniform plexus of the spermatic cord and has long been thought to be associated with male infertility. It is estimated that 10-15% of men and adolescent boys have varicoceles [1], and in men with abnormal semen analysis, the prevalence of varicocele reached 25% [2]. In fact varicocele is the most commonly seen and correctable cause of male factor infertility [1]. The aetiology and pathophysiology of varicocele is complex and likely multifactorial. Contemporary literature suggests that this phenomenon is likely age-dependent, as the incidence in prepubertal boys is extremely rare and increases to about 15% in adolescent [3]. Primary varicocele involves defective venous valves and secondary varicoceles often are a result of external venous compression (e.g., retroperitoneal mass). Most varicoceles are left sided and proposed pathophysiologic mechanisms include anatomical insertion of the left testicular vein in to the renal vein as opposed to a more oblique inlet on the right side. Other proposed mechanism include defective valves, partial compression of the left renal vein between the aorta and superior mesenteric vein (nutcracker syndrome) or extrinsic pressure from retroperitoneal processes on the testicular vein [1]. Varicocele is often asymptomatic and if symptoms do occur, they may include testicular discomfort and presence of varicosities of the scrotal wall. The diagnosis of varicocele is predominantly made by clinical examination. Varicocele can be classified as (1) Grade 3 (visible and palpable at rest), (2) Grade 2 (palpable at rest, but no visible), (3) Grade 1 (palpable during valsalva maneuver but not otherwise), and (4) subclinical (only demonstrable on Valsalva maneuver on imaging studies such as colour-Doppler ultrasound). In general, there is no indication to routinely perform scrotal ultrasound or other imaging for subclinical varicocele (thermography, Doppler, scintigraphy or spermatic venography) as only palpable varicocele has been shown to be associated with infertility [4]. Nonetheless colourDoppler ultrasound can be useful to assess underlying testicular abnormality such as parenchymal lesion and quantify degree of testicular hypotrophy. Pathophysiology of Varicocele and Male Infertility Many studies have established the association between the presence of varicocele and abnormal semen parameters in infertile men. MacLeod was largely credited to first report that sperm in the majority of semen samples obtained from infertile men with varicocele were present at a lower count, decreased motility, and more frequently had abnormal morphologies compared to fertile men [5]. While varicocele has been implicated as a cause in 35-50% of men with primary infertility, it affects up to 80% of men with secondary infertility, suggesting that varicoceles can cause progressive decline in testicular function over time [6]. A study conducted by the World Health Organization found that of the 25.4% of infertile men with abnormal semen, it was often accompanied by decreased testicular volume, lower total sperm count, and a decline in Leydig cell function [2]. The proposed mechanisms of how varicocele results in impaired spermatogenesis and infertility include an altered or impaired testicular blood flow, increased scrotal temperature and oxidative stress as well as resulting sex hormone changes, reflux of adrenal hormones, and autoimmunity with anti-sperm antibody formation through potential breaches in blood-testis barrier [7]. A growing body of literature directly correlates an increase in reactive oxygen species and reduced sperm quality among infertile men with varicocele [8]. Studies in infertile men also showed higher DNA fragmentation, decreased mitochondrial Citation: Chung E (2014) Varicocele and Male Infertility: Evidence in the Era of Assisted Reproductive Technology. Reprod Syst Sex Disord 3: e114. doi: 10.4172/2161-038X.1000e114