Background Military men are at a higher risk of developing sexual dysfunction (SD) as compared to the general population because military deployment exposes soldiers to stressful situations (e.g., death of comrades, combat stress, war inflicted injuries, severe environment, lack of sleep, mental distress, isolation, post-traumatic stress disorder (PTSD), polluted environment and substance abuse, etc.) that may alter their psychological and underlying biological processes. Understanding mechanisms and estimating the burden of SD in military men would also be helpful for the implication in the general population of men exposed to such harsh conditions. Objective To systematically review published reports on SD in military men. Methods Medline was searched for original articles published between 2008 and 2020 by using the search terms “sexual dysfunction in military personnel,” and “sexual dysfunction in veterans”. Quality evaluation and data extraction were done by two authors. Studies that reported the sexual dysfunction in newly inducted or interviewed men in recruitment centres or specific disease cohorts, and that reported the effect of different drugs on sexual health under controlled conditions were excluded. Information related to the sampling duration, sampling method, sample size, methods of diagnosis, cut off values, the prevalence of different sexual dysfunctions and associated factors were extracted. All discrepancies were resolved by discussion. Results A total of 8211 studies were identified initially. After the removal of duplicates, 5186 studies were screened based on titles and abstracts. The full articles were downloaded for 54 studies, of which 27 studies were finally included in the qualitative study. Among the included studies 16 were conducted in North America (US=15 and Canada=01), 4 in Europe (Netherlands=1, France=1 and Croatia=2) and 7 in Asia (Israel=3, Iran=1, South Korea=1 and Taiwan=2). All the studies included in the present review had variable sample sizes (n=53 - 456,340). Sampling methods included mailed questionnaires, in-person interviews, medical chart reviews and secondary data taken from large surveys and patients from outpatient clinics. The studies reported a wide range of prevalence of overall SD (5.6% - 88.7%), erectile dysfunction (ED) (2% - 83.4%), ejaculatory dysfunction (0.1% - 25.5.0%), orgasmic dysfunction (0.2% - 15.4%) sexual desire disorders (0.3% - 74.0%) and sexual dissatisfaction (11.8% - 73.5%). The prevalence of mild ED (16.7% - 30.3%) was highest followed by mild to moderate ED (3.4% - 20.5%), moderate ED (1.1% - 9.3%) and severe ED (0.3% - 10%). Prevalence of premature and delayed ejaculation was 0.1% - 25.5% and 18.0%, respectively. Prevalence of quick orgasms and difficulty in orgasm was reported in 15.4% and 13.8%, respectively. Orgasmic anhedonia was also reported in 11 % of men. The prevalence of SD was positively associated with PTSD, depression and anxiety, using nicotine and antidepressants, physical health (infections, cardiovascular diseases), and being non-white race. However, age, alcohol, body weight and education had no association with SD in military men. Conclusion A considerably variable number of military men had SD due to different factors. Studies in Asian and European countries were limited in number and magnitude. Disclosure Work supported by industry: no.
The objective of the present study was to find out the association of folate genes MTR A2756G and MTRR A66G polymorphisms with the risk of male infertility. The databases of Google Scholar, PubMed, and Science Direct were searched to find relevant studies. Data were extracted from the eligible studies and were analyzed for pooled up odds ratio (OR) with 95% confidence interval (CI). Review Manager 5.4 was used for statistical analysis. Nineteen case-control studies were included in this meta-analysis which comprised 3621 cases and 3327 controls. Pooled analysis revealed that there is a significant association between MTR A2756G polymorphism with male infertility except for the dominant model. The ORs and 95% CI for each genetic model were as follows: 1.21 [1.03–1.42] for the allele model (G vs. A), 2.31 [1.38–3.96] for the additive model (GG vs. AA), 1.17 [0.98–1.38] for the dominant model (GG+AG vs. AA) and 2.10 [1.55–2.86] for the recessive model (GG vs. AG+AA). MTRR A66G has no noticeable association with male infertility. The current meta-analysis suggests that MTR A2756G polymorphism might be a potential risk factor for male infertility. In the future, the sample size should be increased to confirm the present results.
Introduction Sertoli-cell only syndrome (SCOS) is the severe form of non-obstructive azoospermia, in which only the Sertoli cells line the wall of seminiferous tubules. Y chromosome microdeletions are the obvious cause of SCOS in men, but conclusive and summarized data is lacking on the monogenic mutations. Objective To systematically review published data on monogenic mutations causing SCOS. Methods Medline was searched without publication date restriction for all the genetic association studies on SCOS by using keywords: genetics of Sertoli cell-only syndrome, genetics of azoospermia secondary to SCOS and, genes of Sertoli cell-only syndrome. Quality evaluation and data extraction were done by two authors Studies included in the systematic review were presenting original clinical data, human male cases and patients with confirmed SCOS by histopathology or MD-TESE. The genetic evidence of SCOS was included even if the reported case and genetic testing were published separately. Non-English language studies, descriptive reviews, articles of gene expression in SCOS, and articles related to the other chromosomal abnormalities as a cause of SCOS were also excluded. Any dispute on exclusion and inclusion of a study was resolved by discussion and consensus between all authors. Results The initial database search identified 489 articles, after evaluation according to the defined criteria, only 15 studies matched the inclusion criteria for systematic review. Articles included in the systematic review were published from 2005 to 2020. Only 13% (n=2) of articles were published before 2012. From 2012 to 2020, there have been 87% (n=13) publications. Most of the studies (66.7%, n=10) were carried out on Asian populations (Japanese population) and the rest were on Caucasians. The 15 publications included a total of 1513 cases of SCOS, originating from 7 different countries. However, 151 cases appeared in 2 articles. Extracted data show that 40% of studies exclude patients with a history of infections, seminal tract obstruction, pituitary gland disorder or any other cause of testicular damage, and 27% of studies only recruit patients with no chromosomal abnormalities. Approximately 13% of eligible studies exclude the patients based on congenital abnormalities, past cryptorchidism, orchitis, cancer and other systemic illnesses. In addition, 13% of studies included patients who were diagnosed with SCOS. Only 7% of studies include the patient with unknown cause of male infertility. In all the studies only patients with normal karyotype and without Y-chromosome microdeletions were included. In all the studies semen analysis and confirmatory tests MD-TESE or histopathology were for SCOS. Most of the studies used the technique of direct sequencing and only one study performed whole-exome sequencing. Altogether approximately 51 variations in 13 genes (USP26, RAD21L, SEPTIN12, PAPOLB, PLK4, H3t, ETV5, GILZ, SIN3A, CUL4B, DMRT1, SPATA17 and, LRWD1) were identified from which only 7 variations showed a statistically significant association, but others showed rare or no association. Conclusion Comprehensive large-scale studies on monogenic causes of SCOS still lacking. Altogether approximately 51 variations in 13 genes were identified from which only 7 variations showed statistically significant association. Further studies are required to determine the monogenic causes of SCOS. Disclosure Work supported by industry: no.
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