1) Ipsilateral reperfusion injury causes contralateral reflectory sympathetic mediated vasoconstriction [32] leading to hypoxia

1) Ipsilateral reperfusion injury causes contralateral reflectory sympathetic mediated vasoconstriction [32] leading to hypoxia. of the torsed testis. The evidence is, however, limited as most human GW 542573X studies are small case-series. Theories as to what causes contralateral damage mainly derive from animal studies making it difficult to interpret GW 542573X the results in a human context. Large long-term follow-up studies are needed to clearly uncover changes in testicular function after TT and to determine the clinical impact of such changes. 99.3 million/mL in the control group (p=0.46 and p=0.10, respectively). Overall, it seems that at long-term follow-up after TT some patients experience decreased sperm GW 542573X motility and reduced overall sperm counts possibly rendering them subfertile. However, high quality studies are lacking and available studies are limited by selection bias, as they often include men with proven fertility as controls instead of unselected healthy controls with unknown Rabbit Polyclonal to ZNF134 fertility status. Furthermore, studies lack evaluating the clinical consequences of reduced semen quality after TT. For these reasons a definitive conclusion on the long-term effects of TT on fertility cannot be made. Only one study investigated pregnancy rates among 63 couples where the men had been treated for TT. They found no decrease in paternity rates among TT men when compared to the general population [30]. To more clearly determine the endocrine and exocrine function after TT there is a need for larger prospective long-term follow-up studies using unselected control groups and reporting on future paternity rates. THE IMPACT OF TESTICULAR TORSION ON THE CONTRALATERAL TESTIS Evidence is contradictory regarding how the torsed testis should be surgically managed. Removing it or leaving it in the scrotum after detorsion both seem to have a negative effect on testicular function, perhaps indicating that torsion causes bilateral damage or that the contralateral testis does not have sufficient capacity to increase spermatogenesis and testosterone production. Possible contralateral damage after TT is debated and three main hypotheses exist as to what would cause the abnormality (Fig. 1). 1) Ipsilateral reperfusion injury causes contralateral reflectory sympathetic mediated vasoconstriction [32] leading to hypoxia. 2) The torsion of the ipsilateral spermatic GW 542573X cord breaks down the blood-testis barrier. This initiates an immunological process where immunoglobulins have antibody activity against sperm antigens [33]. These immunoglobulins, also called anti-sperm antibodies (ASA), GW 542573X will in turn reduce sperm motility and sperm concentration [34]. 3) The contralateral testicular function is compromised before TT due to pre-existing congenital testicular dysgenesis [19]. Open in a separate window Fig. 1 Testicular torsion is managed by either orchiectomy or orchiopexy. Detorsion during orchiopexy may cause reperfusion injury and combined with ischemic damage due to arterial constriction spermatogenesis might be altered resulting in reduced sperm concentration, reduced motility and reduced morphologically normal sperm. Studies have also demonstrated a negative impact of testicular torsion on the contralateral testis. This has been hypothesized to be caused by the formation of anti-sperm antibodies (ASA) and contralateral vasoconstriction resulting in hypoxia and subsequent reperfusion damage. 1. Animal studies Evaluating the impact on the contralateral testis in humans can be difficult and is often unethical in the acute phase. Performing extra analyses might prolong the time of torsion potentially further damaging the torsed testis. Animal studies have been valuable in understanding the various hypotheses as to what causes potential contralateral testicular damage after TT. The effect of ipsilateral reperfusion injury after detorsion is thought to manifest itself bilaterally and simultaneously result in a contralateral reflectory sympathetic mediated vasoconstriction of the testicular blood vessels. This reduces the contralateral blood flow causing a period of potential ischemia and subsequent reperfusion damage when blood flow increases again. The hypothesis of contralateral vasoconstriction after TT mainly derives from animal studies which have shown that contralateral microvascular changes occur after TT [35]. In rabbits.