BackgroundInfertility affects an estimated 15% of couples globally, amounting to 48.5 million couples. Males are found to be solely responsible for 20-30% of infertility cases and contribute to 50% of cases overall. However, this number does not accurately represent all regions of the world. Indeed, on a global level, there is a lack of accurate statistics on rates of male infertility. Our report examines major regions of the world and reports rates of male infertility based on data on female infertility.MethodsOur search consisted of systematic reviews, meta-analyses, and population-based studies by searching the terms “epidemiology, male infertility, and prevalence.” We identified 16 articles for detailed study. We typically used the assumption that 50% of all cases of infertility are due to female factors alone, 20-30% are due to male factors alone, and the remaining 20-30% are due to a combination of male and female factors. Therefore, in regions of the world where male factor or rates of male infertility were not reported, we used this assumption to calculate general rates of male factor infertility.ResultsOur calculated data showed that the distribution of infertility due to male factor ranged from 20% to 70% and that the percentage of infertile men ranged from 2·5% to 12%. Infertility rates were highest in Africa and Central/Eastern Europe. Additionally, according to a variety of sources, rates of male infertility in North America, Australia, and Central and Eastern Europe varied from 4 5-6%, 9%, and 8-12%, respectively.ConclusionThis study demonstrates a novel and unique way to calculate the distribution of male infertility around the world. According to our results, at least 30 million men worldwide are infertile with the highest rates in Africa and Eastern Europe. Results indicate further research is needed regarding etiology and treatment, reduce stigma & cultural barriers, and establish a more precise calculation.

BackgroundLeukocytes contribute directly and indirectly to reactive oxygen species (ROS) production. Although leukocytospermia is defined as the presence of ≥1 × 106 white blood cells/mL (WBC/mL) in a semen sample, the presence of less than 1×106 WBC/mL (low-level leukocytospermia) can still produce a detectable amount of ROS, impairing sperm function and lowering the chances of pregnancy. Our objective was to assess the effect of low-level leukocytospermia on semen quality, ROS levels, and DNA damage in infertile men.MethodsSemen samples were examined from 472 patients and divided into 3 groups: no seminal leukocytes; group 2, men with low-level leukoctyospermia (0.1-1.0 × 106 WBC/mL); and group 3, frank leukocytospermia, (>1.0 × 106. WBC/mL). Semen analysis, leukoctyospermia, reactive oxygen species and DNA fragmentation was tested.ResultsConventional semen parameters between the 3 groups were similar. Group 2 patients had significantly higher levels of ROS and sperm DNA fragmentation (1839.65 ± 2173.57RLU/s; DNA damage: 26.47 ± 19.64%) compared with group 1 (ROS: 1101.09 ± 5557.54 RLU/s; DNA damage: 19.89 ± 17.31%) (ROS: p = 0.002; DNA damage: p = 0.047). There was no significant difference in ROS levels between groups 2 and 3.ConclusionsPatients presenting with low-level leukocytospermia have seminal oxidative stress. Although these patients are not categorized as leukocytospermic by current World Health Organization (WHO) guidelines, these men may benefit by treatment with antibiotics, testing for bacterial cultures, or antioxidant supplements to reduce ROS-induced sperm DNA fragmentation and improve their chances of fertility. The WHO guidelines for leukocytospermia may need to be revised accordingly.

Infertile patients presenting with poor semen concentration, motility, and morphology have significantly higher levels of reactive oxygen species (ROS). In this cross-sectional study, our goal was to: 1) determine how semen parameters such as concentration, motility, morphology, as well as ROS are altered in oligozoospermic men alone and those in combination with poor sperm concentration, motility, morphology, and compare these with three control groups; unproven donors, donors with proven fertility <2 years, and proven donors with fertility established >2 years; 2) establish the cutoff, sensitivity, specificity for ROS, and see how it compared in the three donor groups compared to the patient groups, and 3) establish the reference range for the various semen parameters in these three donor groups compared to the oligozoospermic group by generating receiver operating characteristic (ROC) curves for each parameter. Fifty-six donors and 101 infertile men were included in this study. The patient group included: oligozoospermia: n = 16; oligoasthenozoospermia (OA): n = 12; oligoteratozoospermia (OT): n = 19; oligoasthenoteratozoospermia (OAT): n = 54. The patient group was compared with the three donor groups. Proven donors who had established a pregnancy in the past or recently (<2 years) had significantly improved semen motility and morphology compared to the OAT and OT groups (p < 0.001). In the OAT group, normal morphology was positively correlated with concentration and negatively with levels of ROS. Compared to the three donor groups, oligozoospermic patients in the OAT, OT, and OA groups had significantly elevated ROS levels. The cutoff for ROS in the proven donors < 2 years was significantly lower with a higher sensitivity and specificity compared to the unproven donors and donors who had not established a recent pregnancy. These results indicate a positive association between semen parameters and ROS suggesting a common underlying mechanism in these infertile patient groups.

Background Reports on the feasibility and effectiveness of translating proactive, antitumor necrosis factor (TNF) therapeutic drug monitoring (TDM) for inflammatory bowel disease into practice-wide quality improvement (QI) are lacking. We aimed to determine whether a TDM QI program improved outcomes at a large academic pediatric gastroenterology practice. Methods We instituted local anti-TNF TDM practice guidelines to proactively monitor and optimize drug levels (goal &gt;5 μg/mL). We conducted a retrospective single-center cohort analysis of patient outcomes before (pre-TDM) and after (post-TDM) guideline institution and assessed the independent effect by multivariable regression. Primary outcome was sustained clinical remission (SCR22-52), defined as physician global assessment (PGA) of inactive from 22 to 52 weeks and off corticosteroids at 52 weeks. Results We identified 108 pre-TDM and 206 post-TDM patients. The SCR22-52 was achieved in 42% of pre-TDM and 59% of post-TDM patients (risk difference, 17.6%; 95% CI, 5.4–29%; P = 0.004). The post-TDM group had an increased adjusted odds of achieving SCR22-52 (odds ratio, 2.03; 95% CI, 1.27–3.26; P = 0.003). The adjusted risk of developing high titer antidrug antibodies (ADAs) was lower in the post-TDM group (hazard ratio, 0.18; 95% CI, 0.09–0.35; P &lt; 0.001). Although the risk of anti-TNF cessation for any reason was not significantly different, there was a lower adjusted risk of cessation related to any detectable ADA in the post-TDM group (hazard ratio, 0.45; 95% CI, 0.26–0.77; P = 0.003). Conclusions A practice-wide proactive anti-TNF TDM QI program improved key clinical outcomes at our institution, including sustained clinical remission, incidence of high titer ADA, and anti-TNF cessation related to ADA.