Y染色体微缺失对卵胞浆内单精子注射胚胎发育和妊娠结局的影响

目的探讨Y染色体微缺失对卵胞质内单精子注射(ICSI)胚胎发育和妊娠结局的影响。方法回顾19例Y染色体微缺失患者(研究组)进行的23个治疗周期的胚胎和临床结局资料,与同期无Y染色体微缺失(对照组)的少弱精子症或无精子症的86个治疗周期的相应资料进行比较,分析两组患者在受精率、卵裂率、优质胚胎率、生化妊娠率、临床妊娠率、胚胎种植率、早期流产率的差异。结果研究组和对照组相比,受精率(85.0%vs89.2%)、卵裂率(96.0%vs 95.3%)、优质胚胎率(68.3%vs 66.7%)、生化妊娠率(47.8%vs 50.0%)、临床妊娠率(43.5%vs 41.6%)、胚胎种植率(22.9%vs 20.8%)、早期流产率(10.0%vs 7.5%)差异比较无统计学意义(P0.05)。结论 Y染色体微缺失对胚胎质量和妊娠结局无显著性影响。     

Y染色体微缺失与卵胞浆内单精子注射助孕妊娠结局的相关性分析

目的研究Y染色体微缺失对卵胞浆内单精子注射-胚胎移植(ICSI-ET)助孕妊娠结局的影响。方法回顾性分析2010年1月至2013年12月间因男方严重少精子症为指征在本院行ICSI-ET助孕治疗的夫妇的临床资料,根据Y染色体是否存在微缺失改变将患者分为缺失组和对照组:缺失组167例(共184个ICSI周期):检测显示存在Y染色体微缺失;对照组463例(共528个ICSI周期):检测为无Y染色体微缺失。比较两组患者的一般情况和助孕后的妊娠结局(受精率、优质胚胎率、临床妊娠率等)。结果两组患者的男女方年龄、女方基础FSH、女方体重指数(BMI)、MⅡ卵母细胞数、优质胚胎总数、HCG日内膜厚度、移植胚胎数比较均无显著性差异(P>0.05)。缺失组患者的受精率(62.7%)显著低于对照组(67.8%)(P<0.01);两组患者的优质胚胎率(53.0%vs.50.7%)、临床妊娠率(49.5%vs.51.7%)、异位妊娠率(0.5%vs.0.9%)、早期流产率(5.4%vs.2.8%)、晚期流产率(3.3%vs.3.0%)、早产率(3.8%vs.6.4%)、活产率(40.2%vs.44.9%)、后代男女比例(1.13vs.1.09)比较均无显著性差异(P>0.05)。结论 Y染色体微缺失行ICSI助孕会降低胚胎正常受精率,但不影响临床妊娠率、活产率、后代男女婴比例等妊娠结局。     

不同种类精液异常对辅助生殖临床结局的影响

目的探讨少弱畸精子症患者结合单精子卵细胞浆内显微注射技术(ICSI)后的临床结局及安全性。方法回顾性分析2014年1月到2015年5月来我中心行辅助生殖治疗的508对夫妇经ICSI助孕后的临床结局。排除染色体核型异常、Y染色体微缺失、睾丸发育异常和FSH水平异常的干扰,根据精子来源和精液不同质量参数分为3组:A组,单纯梗阻性无精子症组,即PESA组;B组,少弱畸精子症组;C组,严重少弱畸精子症组。比较3组获卵数,正常受精率、卵裂率、可用胚胎率、种植率、妊娠率、生化妊娠率、流产率以及周期活产率等情况。结果 3组之间受精率、卵裂率、可用胚胎率、临床妊娠率、生化妊娠率、流产率以及周期活产率没有明显差异(P0.05);但与A组相比,B组和C组其种植率显著降低(40.5%vs 50.0%,41.6%vs 50.0%,P0.01);B组和C组之间则无统计学差异(40.5%vs41.6%,P0.05)。结论少弱畸精子症及严重少弱畸精子症显著影响胚胎的种植率。     

Y染色体AZFc区完全缺失患者ICSI治疗妊娠结局分析

目的探讨Y染色体AZFc区完全缺失患者的精子获得率及AZFc区缺失是否影响卵胞浆内单精子注射(ICSI)的妊娠结局。方法回顾性分析我中心确诊的79例AZFc区完全缺失患者的临床资料,统计其精子获得率。其中行ICSI鲜胚移植的27例患者为研究组,另外选取同期在我中心行ICSI治疗、无Y染色体微缺失的无精子症和严重少弱精子症患者58例为对照组,比较两组患者的一般情况、平均获卵数、注射MⅡ卵数、移植胚胎数、卵裂率、受精率、优胚率、种植率、临床妊娠率及流产率等数据。结果 79例AZFc区完全缺失患者的精子获得率为48.1%。两组患者一般资料、基础内分泌激素水平、男方精液浓度等比较,差异均无统计学意义(P>0.05);两组受精率(65.05%vs.70.07%)、卵裂率(97.34%vs.96.02%)、优胚率(44.81%vs.40.88%)、可用胚胎率(79.23%vs.78.45%)、种植率(39.13%vs.43.27%)、妊娠率(51.85%vs.58.62%)、流产率(7.14%vs.5.88%)及异位妊娠率(0vs.2.94%)比较,差异均无统计学意义(P>0.05)。结论 Y染色体AZFc区完全缺失可能并不影响ICSI的妊娠结局。     

男性不育症伴成人型多囊肾患者ICSI治疗结局分析

目的:成人型多囊肾(ADPKD)可引起少弱精子症和无精子症,从而导致男性不育症。本文总结ADPKD致男性不育症的临床特征与治疗方案,并比较其与先天性双侧输精管缺如(CBAVD)患者的卵细胞胞质内单精子注射(ICSI)及胚胎移植(ET)治疗结局。方法:回顾性分析了2009年4月至2014年1月我中心收治的21例ADPKD不育症患者临床数据,其中15例行ICSI治疗,严格匹配164例CBAVD不育症患者,比较两组第一周期ICSI数据如夫妇双方年龄,ICSI卵子数、受精率、可移植胚胎率、优质胚胎率、胚胎种植率、生化妊娠率、临床妊娠率、早期流产率、单胎率、双胎率。结果:15例行ICSI的ADPKD不育症患者经过28个ICSI周期,10例实现临床妊娠,其中活产7例,自然流产1例,持续妊娠2例。两组患者在男、女方年龄,女方BMI,ICSI卵子数,平均移植胚胎数等基本情况差别无统计学意义(P>0.05)。ADPKD不育症组与CBAVD对照组的ICSI受精率(72.64%vs76.17%)、可移植胚胎率(51.28%vs 63.24%)、优质胚胎率(38.46%vs 49.83%)、胚胎种植率(17.64%vs38.50%)、早期流产率(0%vs 9.23%)、单胎率(50%vs 81.54%)、双胎率(50%vs 18.46%)差别无统计学意义;生化妊娠率(13.33%vs 42.68%,P=0.023<0.05)、临床妊娠率(13.33%vs 39.63%,P=0.032<0.05)差别有统计学意义。结论:ICSI治疗ADPKD致男性不育症同样有效,但单个周期成功率较CBAVD患者低。其后代将会面临遗传风险,应在充分遗传咨询的情况下,遵从患者夫妇意愿选择治疗方案。     

不同来源的精子ICSI治疗周期妊娠结局分析

目的:比较不同来源的精子进行ICSI治疗后受精率、胚胎种植率、临床妊娠率等临床指标有无差异。方法:回顾性分析2006年1月~2008年12月本院生殖中心进行的431个ICSI治疗周期,按精子来源分为A组(重度少弱精子症组)287个周期、B组(梗阻性无精子症附睾穿刺组)109个周期、C组(梗阻性无精子症睾丸穿刺组)35个周期,比较各组女方平均年龄、男方平均年龄、不孕病史、平均MII卵数、受精率、卵裂率、胚胎利用率、平均移植胚胎数量、种植率、妊娠率、流产率等指标的差异。结果:A组与B、C两组在种植率、妊娠率方面差异有统计学意义(18.46%vs25.23%、28.76%;31.23%vs42.16%、39.39%,P<0.05);B、C两组之间各数据差异无统计学意义(P>0.05),受精率、卵裂率、流产率3组之间差异无统计学意义。结论:重度少弱精子症患者射出精子进行ICSI治疗后胚胎种植率、临床妊娠率低于梗阻性无精子症患者。     

严重少精子症患者行卵胞浆内单精子注射治疗单个取卵周期累积活产率分析

目的分析严重少精子症患者行卵胞浆内单精子注射(ICSI)治疗的单个取卵周期累积活产率。方法回顾性分析2014年1月至2019年9月在本院生殖医学科因男方严重少精子症为主要指征接受ICSI治疗的187对不育夫妇的临床资料,其中8对夫妇伴有男方染色体异常,单独列出分析。将最终纳入的179对夫妇的240个取卵周期按照女方年龄分为≤35岁、36～39岁、≥40岁组;按照获卵数不同分为≤5枚、6～10枚、11～15枚、≥16枚组,比较各组的移植胚胎情况及累积临床妊娠率和累积活产率。结果 179对夫妇目前的单个取卵周期累积活产率为50.00%(96/192)。≤35岁组、36～39岁组、≥40岁组的获卵数、可利用胚胎数、累积临床妊娠率及活产率比较均有显著性差异(P<0.05),随着女方年龄的增加,获卵数、可利用胚胎数、累积临床妊娠率及累积活产率均呈下降的趋势。不同获卵数组间比较,随着获卵数的增加,可利用胚胎数显著增加(P<0.05)。获卵数≥6枚的各组与≤5枚组比较,女方年龄、无可利用胚胎率、平均移植胚胎数、平均移植优胚数、累积临床妊娠率、累积活产率均显著升高(P<0.05)。获...     

精子DNA碎片指数和精子畸形率对ICSI临床结局的影响

目的:通过评估ICSI治疗前的精子畸形率(SMR)和精子DNA碎片指数(DFI),探讨精子DFI和SMR对卵胞浆内单精子注射(ICSI)助孕结局的影响。方法:共入组79对因少弱精子症实施第一周期ICSI治疗的不孕夫妇,在进入治疗周期前3⁶个月,评价精子浓度、前向运动精子百分率、SMR及DFI。主要观察SMR和DFI与ICSI结局参数的关系。结果:79例少弱精子症患者DFI正常51例,异常28例,异常组的DFI值明显升高(14.18%vs 41.47%);巧合的是,SMR正常组同样为51例,异常组28例,异常组的SMR值亦明显升高(87.88%vs98.46%)。按DFI正常(DFI≤25%)与异常(DFI>25%)分组,或按SMR正常(≤96%)与异常(>96%)分组,组间的双方年龄、女方BMI、获卵数、移植胚胎数等基本情况差异无统计学意义。DFI正常和异常组间,SMR正常和异常组间的受精卵子数、可移植胚胎数、早期流产率无显著差异;异常组生化妊娠率(43.5%vs 61.5%)和临床妊娠率(39.1%vs 56.4%)降低,但差异无统计学意义(P=0.19及0.10)。精子DFI与SMR呈显著正相关(r=0.231,P<0.05)。结论:精子DFI增高(>25%),与按严格标准检测的SMR增高(>96%)男性行ICSI治疗,生化妊娠率和临床妊娠率降低,但与正常者比较未发现有统计学差异,可能与样本量小有关,有必要深入研究。     

梗阻性无精子症患者年龄对配偶卵胞浆内单精子注射结局的影响

将2011年1月至2012年11月在本中心接受卵胞浆内单精子注射(ICSI)治疗的梗阻性无精子症患者81例,按男方年龄分为3组(≤30岁、31~35岁、35岁组),观察男方年龄对无精子症患者配偶ICSI的正常受精率、正常卵裂率、胚胎着床率和临床妊娠率的影响。结果显示,男方年龄≤30岁组正常受精率、胚胎着床率、临床妊娠率均显著高于男方年龄31~35岁组及男方年龄35岁组(P0.05);男方年龄35岁组正常受精率、胚胎着床率数值低于男方年龄31~35岁组,但无显著性差异(P0.05)。结果提示,随着男方年龄的增加,无精子症患者配偶行ICSI治疗时正常受精率、胚胎着床率、临床妊娠率可能受影响而下降。     

严重少弱精子症患者微量精子冻融后行卵胞浆内单精子注射的妊娠结局分析

目的探讨严重少弱精子症患者行自精微量冻融复苏后卵胞浆内单精子注射(ICSI)的妊娠结局。方法回顾性分析2015年1月至2016年6月在本中心行辅助生殖技术助孕的严重少弱精子症患者96例(100个治疗周期)的临床资料,根据所用精子的不同进行分组:43例患者(45个周期)使用冻融精子,即冻融精子组;53例患者(55个周期)使用新鲜精子,即新鲜精子组。比较两组患者的一般资料、受精率、优质胚胎率、妊娠率、流产率等。结果两组患者一般资料、获卵数、移植胚胎数比较无显著性差异(P0.05);两组患者的受精率、优质胚胎率、可利用胚胎率、生化妊娠率、临床妊娠率、流产率等比较亦无显著性差异(P0.05)。结论严重少弱精子症患者微量精子冻融后行ICSI可以获得与新鲜精子ICSI相似的妊娠结局,但仍需后续更大样本量的前瞻性研究加以探讨验证。     

陕西地区不明原因无精子症和少精子症患者Y染色体长臂微缺失分析

目的: 评估陕西地区不明原因无精子症和少精子症不育男性患者Y染色体长臂微缺失的频率,探讨精子密度与Y染色体微缺失发生率的相关性。　方法: 以Y染色体特异性无精子症因子区STS AZFa、AZFb、AZFc和SRY4个基因 5个片段设计引物,采用PCR方法对 64例无精子症和少精子症患者以及 20例正常生育男性进行微缺失检测,并比较不同精子密度患者Y染色体微缺失的发生率。　结果: 20例精子密度正常的生育男性未检出Y染色体微缺失,而 64例特发性无精子症 /少精子症患者AZFc区的缺失率为17. 2% (11 /64),AZFc和AZFb联合缺失 1例,未发现AZFa区缺失,SRY基因均为阳性。其中无精子症组缺失率为21. 43% ( 3 /14 );精子密度 <1×106 /ml组,缺失率为 20. 0% (2 /10);精子密度 (1 ~5)×106 /ml组缺失率为17. 9% (5 /28);精子密度 (5 ~10 )×106 /ml组缺失率为8. 3% (1 /12)。各组缺失率经卡方检验差异有显著性 (χ2 =70. 144,P<0. 005 )。　结论: 无精子症和少精子症不育患者Y染色体AZFc缺失率明显较高,PCR扩增AZF基因是诊断Y染色体微缺失的简单方法。     

Cytogenetic and molecular analysis of the Y chromosome: absence of a significant relationship between CAG repeat length in exon 1 of the androgen receptor gene and infertility in Indian men

The genetic basis of male infertility remains unclear in the majority of cases. Recent studies have indicated an association between microdeletions of the azoospermia factor a (AZFa)-AZFc regions of Yq and severe oligospermia or azoospermia. Increased (CAG)n repeat lengths in the androgen receptor (AR) gene have also been reported in infertile men. Therefore, in order to assess the prevalence of these genetic defects to male infertility, 183 men with non-obstructive azoospermia (n = 70), obstructive azoospermia (n = 33), severe oligospermia (n = 80) and 59 fertile men were examined cytogenetically and at molecular level for Yq deletions, microdeletions, and AR-CAG repeat lengths along with hormonal profiles [luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone (T)]. We used high resolution cytogenetics to detect chromosome deletions and multiplex polymerase chain reaction (PCR) involving 27 sequence-tagged site (STS) markers on Yq to determine the rate and extent of Yq microdeletions. PCR amplification with primers flanking exon 1 of AR gene was used to determine the AR-(CAG)n repeat lengths. Hormonal profiles (LH, FSH and T levels) were also analysed in infertile and fertile men. Testicular biopsies showed Sertoli cell only (SCO) morphology, maturation arrests (MA) and hypospermatogenesis. No chromosome aberrations were found in infertile men but there was a significant increase (p < 0.001) in the association of acrocentric chromosomes including the Y chromosome. Yq microdeletions were found in 16 non-obstructive azoospermic men (16 of 70; 22%) and seven severe oligospermic individuals (seven of 80; 8.7%) and most of them had deletions in the sY240 locus. No Yq microdeletions were detected in patients with obstructive azoospermia. No statistically significant difference in the mean length of CAG repeats in AR gene was observed between infertile and fertile men (22.2 +/- 1.5 and 21.5 +/- 1.4 respectively). No significant increase or decrease in levels of LH, FSH and T was observed in infertile and fertile men. In some infertile men, significantly elevated levels of FSH alone or in combination with LH were found to be indicative of failure of spermatogenesis and/or suggestive of testicular failure. Y-chromosome microdeletions contribute to infertility in some patients but no relationship could be established with the (CAG)n repeat lengths in exon 1 of the AR gene in infertile Indian men.     

Severe oligospermia associated with a unique balanced reciprocal translocation t(6;12)(q23;q24.3): male infertility related to t(6;12)

The prevalence of chromosome abnormalities is increased in infertile men, the incidence of a chromosomal factor being estimated to be about 8%. We report two brothers, a 38-year-old man with 10 years' primary infertility and severe oligospermia, but otherwise healthy, and a 35-year-old man with primary infertility and a history of mumps during puberty. Semen and karyotype analysis, and investigation of Y-chromosome microdeletions were performed. An apparently unique reciprocal translocation t(6;12)(q23;q24.3) was found in both infertile brothers. Semen analyses showed severe oligospermia. No Y-chromosome microdeletions were found. These two cases support the relationship between both environmental and chromosomal abnormalities, combined or separated, with male infertility. Investigation of genetic alterations in infertile males has to be performed prior to performing any assisted reproduction technique.     

Infertility caused by AZF microdeletions. A new case of azoospermia

We report report a case of a man with azoospermia who was studied because of infertility. Between the causes of azoospermia and severe oligospermia, in male patients with infertility evaluations, small deletions in regions of the Y chromosome must be considered, as in our case. Regions for spermatogenesis in the Yq chromosome can be evidenced using PCR analysis. Men with azoospermia are at high risk to have small deletions in that regions. Yq chromosome deletions could be transmitted when ICSI (intracytoplasmic sperm injection) is applied. Thereafter, study of microdeletions would be included in severe infertile men.     

特发性无精子症和严重少精子症患者Y染色体基因微缺失分析

目的：研究Y染色体基因微缺失与特发性无精子症和严重少精子症的关系，并建立一个灵敏、操作简便的分子检测方法。方法：应用实时荧光定量聚合酶链反应(PCR)法对65例特发性无精子症患者、27例严重少精子症患者进行Y染色体YRRM1、DAZ、DYS1基因微缺失的检测。结果：65例特发性无精子症患者中，3例发生YRRM1基因微缺失，发生率为4．6％；5例发生DAZ基因微缺失，发生率为7．7％。27例严重少精子症患者中，1例发生YRRM1基因微缺失，发生率为3．7％；2例发生DAZ基因微缺失，发生率为7．4％。92例患者中均未发现DYS1基因微缺失。结论：YRRM1和DAZ基因位点的微缺失与特发性无精子症和严重少精子症有一定的相关性，DYS1基因缺失与男性生精障碍的相关性仍需进一步研究明确。应用荧光定量PCR法检测Y染色体微缺失具有灵敏、快速、操作简便的特点。     

Uniform testicular maturation arrest: a unique subset of men with nonobstructive azoospermia

PURPOSE: We evaluated the clinical characteristics of men with uniform testicular maturation arrest and nonobstructive azoospermia or severe oligospermia, including the frequency of genetic defects and outcome of intracytoplasmic sperm injection with or without testicular sperm extraction. MATERIALS AND METHODS: We identified a group of 32 men with nonobstructive azoospermia or severe oligospermia, uniform maturation arrest (single spermatogenic pattern on biopsy), and normal follicle-stimulating hormone (7.6 IU/l or less). These patients were identified from 150 intracytoplasmic sperm injection candidates with severe oligospermia (less than 10,000/cc) and 600 men with nonobstructive azoospermia undergoing attempted testicular sperm extraction-intracytoplasmic sperm injection between November 1995 and September 2006. These patients were characterized based on the frequency of genetic anomalies (karyotype or Y chromosome microdeletions). Rates of sperm retrieval by testicular sperm extraction, fertilization and pregnancy after ICSI were measured. RESULTS: Genetic anomalies were more common (45%) in men with uniform maturation arrest and normal follicle-stimulating hormone than other men with nonobstructive azoospermia (17%) undergoing testicular sperm extraction at our center (p <0.001). They had a lower sperm retrieval rate with testicular sperm extraction compared to other nonobstructive azoospermia patients (41% vs 60%, p = 0.05). Fertilization rate (37%) and clinical pregnancy (13%) were significantly less common than in other men with nonobstructive azoospermia (54% and 49%, respectively, p <0.01). CONCLUSIONS: Patients with uniform maturation arrest and normal follicle-stimulating hormone are a clinically definable subgroup of men with nonobstructive azoospermia that have different treatment outcomes. They have a higher incidence of chromosomal abnormalities and Y chromosome microdeletions compared to other men with nonobstructive azoospermia. Despite having normal follicle-stimulating hormone and typically normal testicular volume, sperm retrieval may be difficult and the chance of successful pregnancy is limited.     

原因不明性无精症和少精症Y染色体微缺失的筛查分析

目的 探讨原因不明性无精症和少精症不男性与Y染色体微缺失的关系。方法 应用多重PCR技术,对38例原因不明性无精症和少精症者（无精症11例、严重少精症9例、少精症18例）基因组DNA进行Y染色体连锁的18个序列标记位点缺失检测。结果 38例中发现Y染色体微缺失6例,缺失率为16％,其中无精症2例,严重少精症1例,少精症3例。缺失形式前两者为AZFd(DYS 237) AZFc(DAZ DYS240),后者为AZFd(DYS237)。结论 Y染色体微缺失是原因不明性无精症和少精症的重要原因之一。采用多重PCR技术进行缺失检测,是一种非常有效的方法。     

Y-microdeletions: a review of the genetic basis for this common cause of male infertility

The human Y-chromosome contains genetic material responsible for normal testis development and spermatogenesis. The long arm (Yq) of the Y-chromosome has been found to be susceptible to self-recombination during spermatogenesis predisposing this area to deletions. The incidence of these deletions is estimated to be 1/4,000 in the general population but has been found to be much higher in infertile men. Currently, Y-microdeletions are the second most commonly identified genetic cause of male infertility after Klinefelter syndrome. This has led to testing for these deletions becoming standard practice in men with azoospermia and severe oligospermia. There are three commonly identified Y-microdeletions in infertile males, termed azoospermia factor (AZF) microdeletions AZFa, AZFb and AZFc. With increased understanding and investigation of this genetic basis for infertility a more comprehensive understanding of these deletions has evolved, with several other deletion subtypes being identified. Understanding the genetic basis and pathology behind these Y-microdeletions is essential for any clinician involved in reproductive medicine. In this review we discuss the genetic basis of Y-microdeletions, the various subtypes of deletions, and current technologies available for testing. Our understanding of this issue is evolving in many areas, and in this review we highlight future testing opportunities that may allow us to stratify men with Y-microdeletion associated infertility more accurately     

Outcomes of intracytoplasmic sperm injection in oligozoospermic men with Y chromosome AZFb or AZFc microdeletions

We investigated whether the presence of Y chromosome azoospermia factor (AZF) microdeletions impacts upon the outcomes of intracytoplasmic sperm injection (ICSI) using fresh ejaculated spermatozoa. Sixteen oligozoospermia patients with Y chromosome AZFb or AZFc microdeletions and undergoing ICSI cycles between March 2013 and November 2014 were studied. Twenty‐six infertile men with normal Y chromosomes and also undergoing IVF/ICSI in the same time period were used as controls. A retrospective case–control study approach was used. Among the 16 cases, 12 (75%, 12/16) had deletions of AZFc markers (sY152, sY254 and sY255), one (6.25%, 1/16) had a deletion of sY152, and two (12.5%, 2/16) had deletions of sY152, sY254, sY255 and sY157. AZFb microdeletions were found in one patient (6.25%, 1/16). There were no significant differences between groups for cleaved embryo rate, high‐grade embryo rate, blastocyst formation rate, embryo implantation rate, clinical pregnancy rate and delivery rate. The clinical outcomes of ICSI for oligozoospermic patients with Y chromosome AZF microdeletion are comparable to those of infertile patients with normal Y chromosomes. Our findings indicate that ICSI should be offered to patients with an AZFc deletion and that oligozoospermia patients with AZFb microdeletions are likely to father children.     

Chromosomal and Y‐chromosome microdeletion analysis in 1,300 infertile males and the fertility outcome of patients with AZFc microdeletions

The present study investigated the frequency of chromosome aberrations and AZF microdeletions in infertile patients with nonobstructive azoospermia (NOA) or severe oligozoospermia. Additionally, the effect of the AZFc microdeletions on the success of microdissection testicular sperm extraction (microTESE) and intracytoplasmic sperm injection (ICSI) methods were evaluated. Peripheral blood samples were received from 1,300 infertile men with NOA and severe oligozoospermia. Karyotyping and FISH analysis were performed according to standard methods. AZF microdeletions were analysed using multiplex polymerase chain reaction or GML Y‐chromosome Microdeletion Detection System consisting of 14 markers. The chromosomal aberrations and the AZF microdeletions frequency among 1,300 infertile men were 10.6% and 4.0% respectively. Either ejaculated spermatozoa or microTESE was performed on only in 19 out of 26 patients with AZFc deletions. Of the 19 patients, four had severe oligozoospermia and 15 had NOA. In eight out of 15 NOA patients, testicular mature spermatozoa were obtained (53.3%) and then ICSI was applied to mature oocytes. After undergoing ICSI treatment, clinical pregnancy and live birth outcome rates were found to be 37.5% and 25% respectively. These results suggest that infertile patients with AZFc microdeletion could achieve successful fertilisation pregnancies with the help of assisted reproductive technology.