Sexual function of patients who underwent surgery for hypospadias in general is not affected. However, there is clearly a difference in certain aspects of sexual behavior between patients with hypospadias and controls. Followup and adequate counselling of patients who underwent surgery for hypospadias in adult life is necessary.

ObjectiveTo compare patient-reported outcomes (PROs) of surgical correction of Peyronie's disease (PD) with the Nesbit procedure, plaque incision and grafting, and the insertion of a malleable penile implant after surgical correction of penile curvature. Patients and MethodsWe performed a retrospective review of men who underwent surgical correction of PD between January 2010 and December 2012 at six international centres. Treatment-related PROs and satisfaction were evaluated with a non-validated questionnaire. ResultsThe response rate to the questionnaire was 70.9%, resulting in a study cohort of 206 patients. The Nesbit procedure, plaque incision with grafting, or implantation of a malleable penile prosthesis was performed in 50, 48, and 108 patients, respectively. Overall, 79.1% reported a subjective loss of penile length due to PD preoperatively (range 2.1-3.2 cm). Those patients treated with a malleable penile implant reported the greatest subjective penile length loss, due to PD. A subjective loss of penile length of >2.5 cm resulted in reduced preoperative sex ability. Postoperatively, 78.0%, 29.2% and 24.1% patients in the Nesbit, grafting, and implant groups reported a postoperative, subjective loss of penile length (range 0.4-1.2 cm), with 86.3%, 78.6%, and 82.1% of the patients in each group, respectively, being bothered by the loss of length. ConclusionsPenile length loss due to PD affects most patients. Further penile length loss due to the surgical correction leads to bother among the affected patients, irrespective of the magnitude of the loss. The Nesbit procedure was associated with the highest losses in penile length. In patients with PD and severe erectile dysfunction, a concomitant lengthening procedure may be offered to patients to help overcome the psychological burden caused by the loss of penile length.

Background: Autism spectrum disorders (ASD) are complex psychiatric disorders, with gene environment interaction being in the basis of their etiology. The association of perinatal complications and ASD is well established. Recent findings suggested that oxidative stress and polymorphism in genes encoding antioxidant enzymes might be involved in the development of ASD. Glutathione transferases (GSTs) have an important role in the antioxidant defense system. We aimed to establish whether the predictive effects of prenatal and perinatal complications (as possible oxidative stress inducers) on ASD risk are dependent on GST polymorphisms. Methods: The study included 113 ASD cases and 114 age- and sex group-matched healthy controls. All participants were genotyped for GSTA1, GSTM1, GSTT1, and GSTP1 polymorphisms. The questionnaire regarding prenatal and perinatal risk factors and complications was administered for all the subjects in the study. Results: The evaluated perinatal complications as a group significantly increased the risk of ASD [odds ratio (OR) = 9.415; p = 0.000], as well as individual perinatal complications, such as prematurity (OR = 11.42; p = 0.001), neonatal jaundice (OR = 8.774; p = 0.000), respiratory distress syndrome (OR = 4.835; p = 0.047), and the use of any medication during pregnancy (OR = 2.413; p = 0.03). In logistic regression model, adding GST genotypes did not modify the significant effects found for prematurity and neonatal jaundice as risk factors in ASD. However, there was a significant interaction of GST genotype with medication use during pregnancy and the use of tocolytics during pregnancy, which was predictive of ASD risk only in carriers of GSTM1-null, as opposed to carriers of GSTM1-active genotype. Conclusion: Specific perinatal complications may be significant risk factors for ASD. GSTM1 genotype may serve as a moderator of the effect of some prenatal factors on the risk of ASD such as using medication during pregnancy. It may be speculated that different oxidative stress-related genetic and environmental factors could lead to development of ASD. Apart from etiological mechanisms, possible therapeutic implications in ASD are also discussed.

Autism spectrum disorders (ASD) are a group of complex psychiatric disorders, with a proposed gene-environment interaction in their etiology. One mechanism that could explain both the genetic and environmental component is oxidative stress. The aim of our study was to investigate the potential role of common polymorphisms in genes for glutathione transferase A1, M1, T1 and P1 in susceptibility to ASD. We also aimed to explore the possible oxidative stress - specific gene-environment interaction, regarding GST polymorphisms, maternal smoking tobacco during pregnancy (TSDP) and the risk of ASD. This case-control study included 113 children with ASD and 114 age and sex-matched controls. The diagnosis was made based on ICD-10 criteria and verified by Autism Diagnostic Interview – Revised (ADI-R). We investigated GSTA1 , GSTM1 , GSTP1 and GSTT1 genotypes and explored their individual and combined effects in individuals with ASD. Individual effect of GST genotypes was shown for GSTM1 active genotype decreasing the risk of ASD (OR = 0.554, 95%CI: 0.313–0.983, p = 0.044), and for GSTA1 CC genotype, increasing susceptibility to ASD (OR = 4.132, 95%CI: 1.219–14.012, p = 0.023); the significance was lost when genotype-genotype interactions were added into the logistic regression model. The combination of GSTM1 active and GSTT1 active genotype decreased the risk of ASD (OR = 0.126, 95%CI: 0.029–0.547, p = 0.006), as well as combination of GSTT1 active and GSTP1 llelle (OR = 0.170, 95%CI: 0.029–0.992, p = 0.049). Increased risk of ASD was observed if combination of GSTM1 active and GSTP1 llelle was present (OR = 11.088, 95%CI: 1.745–70.456, p = 0.011). The effect of TSDP was not significant for the risk of ASD, neither individually, nor in interaction with specific GST genotypes. Specific combination of GST genotypes might be associated with susceptibility to ASD, while it appears that maternal smoking during pregnancy does not increase the risk of ASD.