机构地区:[1]国家卫生与计划生育委员会计划生育药具重点实验室,上海市计划生育科学研究所,上海200032 [2]上海交通大学医学院附属仁济医院,上海200001
出 处:《生殖与避孕》2013年第12期811-815,共5页Reproduction and Contraception
基 金:上海市科委基金项目(09411964200);上海市卫生与计划生育委员会局管基金项目;上海市重点学科"人体解剖与组织胚胎学"开放课题(S30201)资助
摘 要:目的:探讨非梗阻性无精子症和隐匿精子症与睾丸体积、血FSH和AZF基因微缺失的相关性。方法:161例男性不育患者分为非梗阻性无精子症(A组,n=86)、隐匿精子症(B组,n=49)、严重少精子症(C组,n=13)和其它患者(D组,n=13,包括死精子症4例,梗阻性无精子症3例,正常精子1例,其他少弱精子症5例),进行睾丸体积、血FSH水平和AZF基因微缺失检测,AZF基因微缺失检测位点包括AZFa(sY84、sY86)、AZFb(sY127、sY134)、AZFcd(sY254、sY255、sY157、sY145和sY152)。结果:4组睾丸体积<12 ml的比例分别为73.26%(63/86)、34.69%(17/49)、7.69%(1/13)、30.77%(4/13);4组FSH水平升高1倍以上的比例分别为67.44%(58/86)、32.65%(16/49)、15.38%(2/13)和0.00%(0/13),组间均有极显著统计学差异(P<0.001);4组AZF基因微缺失率分别为15.12%(13/86)、18.37%(9/49)、0.00%(0/13)和0.00%(0/13),组间均无统计学差异(P>0.05),其中A组AZFa基因缺失1例,AZF(b+c+d)缺失5例,AZF(c+d)基因缺失7例,B组9例均为AZFc和(或)AZFd基因缺失,C组和D组均未见AZF基因缺失。结论:随着生精功能障碍程度的加重,血FSH水平升高和睾丸体积缩小趋势明显,而与AZF缺失几率无高度相关性;但在非梗阻性无精子症和隐匿精子症组中AZF基因缺失几率仍然偏高,AZFa和AZFb缺失大多出现在非梗阻性无精子症组中,而隐匿精子症组以AZFc和AZFd缺失为主。Objective: To explore the relationship oftesticular volume, follicle-stimulating hormone (FSH) and azoospermia factor (AZF) deletion gene microdeletion in patients with non-obstructive azoospermia (NOA) and cryptozoospermia. Methods: Totally 161 male infertility patients were drawn, and testicular volumes, FSH level and AZF microdeletion were recorded. The examination of AZF microdeletion includes AZFa (sY84, sY86), AZFb (sY127, sY134), AZFc (sY254, sY255, sY157), AZFd (sY145, sY152). All patients were divided into four groups. Group A: 86 patients were NOA; group B: 49 patients were cryptozoospermia; group C: 13 patients were severe oligozoospermia patients; group D: 13 cases were enrolled, including 4 necrospermia patients, 3 obstructive azoospermia patients, 1 normal sperm patient and 5 oligoasthenozoospermia patients. Results: The proportions of the testicular volume less than 12 ml were 73.26% (63/86) in group A, 34.69% (17/49) in group B, 7.69% (1/13) in group C, 30.77% (4/13) in group D with significant differences (P〈0.001); the proportions of increasing FSH level with value increased more than 1 fold in 4 groups were 67.44% (58/86), 32.65% (16/49), 15.38% (2/13) and 0.00% (0/13), respectively, with significant differences (P〈0.001); the AZF gene microdeletion of four groups were 15.12% (13/86), 18.37% (9/49), 0.00% (0/13) and 0.00% (0/13), respectively (P〉0.05). In group A, one patient was AZFa gene microdeletion, 5 were AZF(b+c+d) gene microdeletion, 7 were AZF(c+d) gene microdeletion and in group B, 9 patients were AZFc and/or AZFd gene microdeletion. Conclusion: With development of spermatogenesis dysfunction, there was a significant higher level of FSH and lower volume of testes, additionally, no difference was found when comparing the incidence ofAZF gene microdeletion. However, incidence ofAZF gene microdeletion was still high in patients with NOA or cryptozoospermia. Moreover
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