特发性无、少精子症病人精浆中性激素水平的测定及意义

目的 :通过测定特发性无、少精子症病人精浆中的性激素水平 ,比较分析精浆性激素与无、少精子症的关系。　方法 :特发性无、少精子症男性各 5 0例 ,正常对照 5 0例。精液常规分析判断精子密度 ,化学发光技术测定精浆性激素水平。　结果 :特发性无、少精子症组黄体生成素 (LH)分别为 (5 .19± 0 .6 7)IU/L和 (4.77± 0 .6 8)IU/L ,与正常组 (2 .19± 0 .2 2 )IU/L相比 ,特发性无精子症组差异有极显著性 (P <0 .0 1) ,特发性少精子症组与正常组相比差异有显著性 (P <0 .0 5 ) ;卵泡刺激素 (FSH)分别为 (1.90± 0 .79)IU/L和 (2 .2 7± 0 .2 5 )IU/L ,与正常组 (1.6 1± 0 .14)IU/L相比 ,差异均有显著性 (P <0 .0 5 ) ;泌乳素 (PRL)分别为 (6 .2 5± 0 .34 )ng/ml和 (6 .33±0 .5 1)ng/ml,与正常组 (6 .36± 0 .32 )ng/ml相比差异均无显著性 (P >0 .0 5 ) ;睾酮 (T)分别为 (1.5 1± 0 .12 )ng/ml和 (1.6 8± 0 .71)ng/ml,与正常组 (1.83± 0 .0 9)ng/ml相比 ,特发性无精子症组差异有显著性 (P <0 .0 5 ) ,特发性少精子症组差异无显著性 (P >0 .0 5 ) ;T/LH的比值分别为 0 .2 9± 0 .0 4和 0 .35± 0 .0 9,与对照组 0 .84± 0 .2 0相比 ,差异均有显著性 (P <0 .0 5 )。　结论 :特发性无、少精子症病人 ,精浆

Detection of Sexual Hormone in Semen of Patients with Idiopathic Azoospermia or Oligospermia and Its Significance

OBJECTIVES: To detect the sexual hormone level in semen of patients with idiopathic azoospermia and oligospermia, and further analyze the relationship between sexual hormone and idiopathic azoospermia and oligospermia. METHODS: 50 male patients with idiopathic azoospermia, 50 in idiopathic oligospermia and 50 male controls with normal sperm density were selected. The sperm density and sexual hormone in semen were detected respectively by routine semen analysis and chemical luminescence technique. RESULTS: The values of LH were (5.19 +/- 0.67) IU/L and (4.77 +/- 0.68) IU/L, and those of FSH were (1.90 +/- 0.79) IU/L and (2.27 +/- 0.25) IU/L in idiopathic azoospermia and oligospermia respectively, and the values of LH and FSH were (2.19 +/- 0.22) IU/L and (1.61 +/- 0.14) IU/L in normal control group respectively. There were significant differences in the values of LH and FSH between idiopathic azoospermia and normal control group(P < 0.01 or P < 0.05). The values of PRL were (6.25 +/- 0.51) ng/ml and (6.33 +/- 0.34) ng/ml, and those of T were (1.51 +/- 0.12) ng/ml and (1.68 +/- 0.71) ng/ml in idiopathic azoospermia and oligospermia respectively, and the values of PRL and T were (6.36 +/- 0.32) ng/ml and (1.83 +/- 0.09) ng/ml in normal control group respectively. There were no significant difference in the values of PRL between idiopathic azoospermia, oligospermia and normal control group, but there were significant differences of T between idiopathic azoospermia and normal control. Compared with 0.84 +/- 0.20 in normal control, the values of T/LH were 0.35 +/- 0.09 and 0.29 +/- 0.04 in idiopathic oligospermia and azoospermia respectively and there were significant differences(P < 0.05). CONCLUSIONS: The changes of LH, FSH and T values may be one of the reasons that cause the dysfunction of spermatogenesis and sperm maturation in patients with idiopathic azoospermia and oligospermia. The study of semen hormone may lead to new strategies in the treatment to azoospermia and oligospermia.