男方畸形精子症对胚胎植入前遗传学筛查患者胚胎非整倍体及胚胎发育指标的影响

Influence of teratozoospermia on embryonic aneuploidy and embryonic development in patients of preimplantation genetic screening

目的探讨胚胎植入前遗传学筛查（preimplantation genetic screening, PGS）患者中男方畸形精子症对胚胎的发育及染色体非整倍性率的影响。方法采取回顾性队列研究,对2011年12月至2016年12月就诊于空军军医大学第二附属医院生殖中心进行PGS的患者进行分析,排除梗阻性无精症、严重少弱精子症的患者,共纳入91例患者,计98个周期。收集基本资料及助孕相关指标,按照WHO第5版规范,以男方畸形精子症诊断标准为分组标准,将患者分为精子畸形率≤96%及〉96%两组,采用单因素及多因素分析男方精子畸形率对PGS患者胚胎非整倍体性发生率、胚胎发育指标的影响。结果单因素分析显示,精子畸形率96%和〉96%组患者受精率[（0.73±0.16）%,（0.68±0.20）%]、优胚率[（0.49±0.24）%,（0.46±0.16）%]、囊胚形成率[（0.53±0.29）%,（0.65±0.25）%]、种植率[（0.70±0.45）%,（0.56±0.44）%]和胚胎染色体非整倍体发生率[（0.64±0.26）%,（0.68±0.31）%]比较,差异均无统计学意义（P〉 0.05）。进一步调整混杂因素,建立多元线性回归方程显示,随男方精子畸形率的增加,上述结局指标比较,差异均无统计学意义（P〉0.05）。对精子畸形率≥99%患者应用倾向性评分与精液参数正常患者的基线资料进行匹配,与精液参数正常患者比较,重度畸形精子症患者上述指标比较,差异均无统计学意义（P〉0.05）。结论男方精子畸形率对PGS患者胚胎非整倍体性发生率无明显影响。男方精子畸形率的高低不能作为PGS的单一指征。

Objective To investigate the effects of teratozoospermia on embryonic aneuploidy and embryonic development in patients of preimplantation genetic screening（PGS）. Methods A retrospective cohort study was conducted to analyze the PGS and transplant in the Reproductive Medicine Center of Second Affiliated Hospital of Air Force Military Medical University from December 2011 to December 2016. Patients with obstructive azoospermia and severe oligozoospermia were excluded. 91 patients and 98 PGS cycles were identified. According to the fifth version of WHO, the diagnostic criteria for male teratospermia were used as the grouping criteria, the patients were divided into two groups： sperm abnormality rate ≤ 96% and 96%. Univariate analysis and multivariate linear regression models were used to assess the influence of teratozoospermia on embryonic aneuploidy as well as embryonic development. Results Univariate analysis showed that the rate of fertilization in rate of teratosperm ≤ 96% and 96%[（0.73±0.16）%,（0.68±0.20）%], excellent embryo [（0.49±0.24）%,（0.46±0.16）%], blastocyst formation [（0.53±0.29）%,（0.65±0.25）%], implantation [（0.70±0.45）%,（0.56±0.44）%] and embryonic aneuploidy [（0.64±0.26）%,（0.68±0.31）%] were not statistically significant between groups（P〈0.05）. Further adjustment of confounding factors, multivariate linear regression models showed the difference of the outcomes between groups were of no significant（P〈0.05）. Further propensity score matching（PSM） was used to match control groups with patients of sperm abnormality rate of ≥ 99%. Compared with patients with normal sperm parameters, the outcome of patients with severe deformity sperm was of no significant difference（P〈0.05）. Conclusion The rate of male sperm malformation had no significant effect on the incidence of embryo aneuploidy in PGS patients. Male sperm deformity rate should not be an unique indicators of PGS.