Serum levels of Anti-Mullerian Hormone (AMH) have been shown to be biomarker for prediction of the quantitative aspects of ovarian reserve. On the male side, sperm chromatin structure assay (SCSA) DNA fragmentation index (DFI) has been demonstrated to be an important predictor of outcomes in standard IVF procedures but to less degree in intracytoplasmic sperm injection procedures (ICSI). The purpose of this study was to investigate whether the combination of female AMH serum levels and sperm DFI adds to prediction of the outcome of assisted reproduction. A total of 352 couples was included (ICSI-148: IVF-204) A venous blood sample was drawn for AMH analysis before IVF/ICSI treatment. DFI was measured in the ejaculate used for assisted reproduction. Regression models for the following odds ratio calculations were constructed: for obtaining at least one Good Quality Embryo; for live birth in all procedures; for pregnancy in procedures where embryo transfer was performed; for miscarriage. For DFI increase by 10 percentage points (not increased DFI as reference) odds ratio for Good Quality Embryo was statistically significantly lower when AMH was at lower quartile (AMH <12 pmol/L; OR = 0.29, 95% CI: 0.14–0.59,) but not when AMH was at upper quartile (AMH ≥ 36 pmol/L; OR = 0.95, 95% CI: 0.43–2.13,). The marginal effect of an increase in DFI by 10 percentage points was statistically significant only when AMH < 25.2 pmol/L. Similar results were obtained as considers live birth following standard IVF. No interactions were seen for standard IVF in relation to the risk of miscarriage and for any of the outcomes when ICSI was used as method of treatment. We conclude that the impact of high DFI on the outcome of standard IVF is most pronounced if the female partner has relatively low AMH levels. This finding may help in defining the role of sperm DNA integrity testing in management of infertile couples. It may also explain some of the heterogeneity in results of studies focusing on predictive value of DFI measurements in assisted reproduction.

Objective: During androgen ablation in prostate cancer by the standard GnRH agonist treatment, only LH is permanently suppressed, while circulating FSH rebounds. We explored direct prostatic effects of add-back FSH, after androgen ablation with GnRH antagonist, permanently suppressing both gonadotropins. Methods: The effects of recombinant human (rFSH) were examined in mice treated with vehicle (controls), GnRH antagonist degarelix (dgx), dgx + rFSH, dgx + flutamide, or dgx + rFSH + flutamide for four weeks. Prostates and testes sizes and expression of prostate-specific and/or androgen-responsive genes were measured. Additionally, 33 young men underwent dgx-treatment. Seventeen were supplemented with rFSH (weeks 1-5), and all with testosterone (weeks 4-5). Testosterone, gondotropins, PSA, and inhibin B was measured. Results: In dgx and dgx + flutamide treated mice, prostate weight/body weight was 91% lower than in controls, but 41% and 11%, respectively, was regained by rFSH treatment (p=0.02). The levels of Svs6, Pbsn, Nkx3-1, Msmb and Inhibin b were elevated in dgx + rFSH treated animals compared with only dgx treated (all p<0.05). In men, serum inhibin B rose after dgx treatment but was subsequently suppressed by testosterone. rFSH add-back had no effect on PSA levels. Conclusions: These data provide novel evidence for direct effects of FSH on prostate size and gene expression in chemically castrated mice. However, in chemically castrated men, FSH had no effect on PSA production. Whether FSH effects on prostate in humans also requires suppression of the residual adrenal-derived androgens and/or a longer period of rFSH stimulation, remains to be explored.

Dose–response association between level of impairment of semen quality and risk of morbidity or premature death has been reported. Therefore, it can be presumed that men utilizing donated spermatozoa, i.e. patients with non-obstructive azoospermia, are at highest risk for adverse health outcomes. To evaluate the risks of prescription of medications for common metabolic disturbances and testosterone replacement therapy (TRT) among men who father children with donated spermatozoa—who presumably do it due to severe impairment of fertility. We used Swedish nationwide register data on all fathers who had a live-born child between 2007 and 2014 in order to compare men who fathered children with donated spermatozoa to the ones who became fathers by using own gametes. Cox regression analysis was used in order to estimate the post-conception incidence of prescription of medicines for hypertension (HT), diabetes (type 1 and 2), dyslipidaemia (DLE) or TRT. Starting the follow up at time of conception, models were adjusted for age, educational level, and previous cancer treatment. In total 410,119 childbirths were included in the analysis. Among them, for 390 fathers donated spermatozoa were utilized. Fathers to children conceived with donated spermatozoa had higher risk for having TRT prescribed (HR: 18.14; 95%CI: 11.71–28.10; p ≪ 0.001). Same was true for DLE (HR: 2.08; 95%CI: 1.27–3.39; p = 0.003) but not diabetes. Fathers to children conceived by use of donated spermatozoa are at significantly increased risk for testosterone treatment and dyslipidaemia, necessitating stringent follow up and inclusion in prevention programs.

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