Pache T D, Hop W C, de Jong F H, Leerentveld R A, van Geldorp H, Van de Kamp T M, Gooren L J, Fauser B C
Department of Obstetrics and Gynaecology, Dijkzigt University Hospital, Rotterdam, The Netherlands.
Clin Endocrinol (Oxf). 1992 Jun;36(6):565-71. doi: 10.1111/j.1365-2265.1992.tb02266.x.
The aim was to monitor carefully follicular growth arrest in polycystic ovaries by assay of hormones in individual follicles.
Fluid from follicles less than or equal to 10 mm was obtained from ovaries of 16 regularly cycling women between days 1 and 12 of the follicular phase (controls, n = 120 follicles), polycystic ovaries of five women with polycystic ovary syndrome (n = 43), and polycystic ovaries from 14 long-term testosterone treated female to male transsexuals (n = 120).
Fluid was assayed for oestradiol, androstenedione, and immunoactive inhibin. Luteinizing hormone, follicle-stimulating hormone, and testosterone levels were estimated in serum.
Median serum LH was lower in transsexuals than in controls (P less than 0.05), and in polycystic ovary syndrome (P less than 0.01). Median serum testosterone was not significantly different between polycystic ovary syndrome and transsexuals, and was elevated in both groups as compared to controls (P less than 0.01). Oestradiol was present in all follicles obtained from polycystic ovaries of polycystic and transsexual patients, in which no follicle greater than 10 mm could be detected. In the three groups, between-patient differences in mean oestradiol, androstenedione, inhibin, and androstenedione/oestradiol ratio were significantly larger than expected in view of the variation between follicles within individuals. Taking into account this between-patient difference, no significant differences could be established between the three groups for all endocrine parameters. The percentage of presumed healthy follicles (androstenedione/oestradiol ratio less than or equal to 4) was 12% in controls, 17% in polycystics, and 14% in transsexuals, and was not significantly different between groups.
The results may indicate that (1) abnormally high circulating androgen concentrations with or without elevated LH levels disturb the process of selection, and could therefore play a role in the pathogenesis of polycystic ovaries; (2) in polycystic ovaries from polycystic ovary syndrome and transsexual patients, aromatase activity is present in vivo in small antral follicles, and the proportion of presumed healthy follicles is not different from that encountered in normal ovaries; (3) oestradiol levels are not different between non-dominant follicles of normal and polycystic ovaries, suggesting that only enhancement of aromatase activity by FSH may be disrupted in polycystic ovaries, (4) because androstenedione levels are not different comparing follicles of normal and polycystic ovaries, hyperandrogenaemia in the syndrome seems to originate from the abnormally high number of cystic atretic follicles generally observed in polycystic ovaries; (5) marked variation in the endocrine follicular microenvironment within and between-women precludes pooling fluid from several follicles.
通过检测单个卵泡中的激素来仔细监测多囊卵巢中的卵泡生长停滞情况。
从16名月经周期正常的女性卵泡期第1至12天的卵巢中获取直径小于或等于10毫米的卵泡液（对照组，n = 120个卵泡），5名多囊卵巢综合征女性的多囊卵巢（n = 43个卵泡），以及14名长期接受睾酮治疗的女变男变性者的多囊卵巢（n = 120个卵泡）。
检测卵泡液中的雌二醇、雄烯二酮和免疫活性抑制素。测定血清中的促黄体生成素、促卵泡生成素和睾酮水平。
变性者的血清促黄体生成素中位数低于对照组（P < 0.05），也低于多囊卵巢综合征患者（P < 0.01）。多囊卵巢综合征患者和变性者的血清睾酮中位数无显著差异，且两组与对照组相比均升高（P < 0.01）。从多囊卵巢综合征患者和变性者的多囊卵巢中获取的所有卵泡中均存在雌二醇，且未检测到直径大于10毫米的卵泡。在三组中，考虑到个体内卵泡间的差异，患者间雌二醇、雄烯二酮、抑制素以及雄烯二酮/雌二醇比值的差异显著大于预期。考虑到患者间的这种差异，三组所有内分泌参数之间未发现显著差异。对照组中假定健康卵泡（雄烯二酮/雌二醇比值小于或等于4）的比例为12%，多囊卵巢患者中为17%，变性者中为14%，组间无显著差异。
结果可能表明：（1）无论促黄体生成素水平是否升高，循环雄激素浓度异常升高都会干扰选择过程，因此可能在多囊卵巢的发病机制中起作用；（2）在多囊卵巢综合征患者和变性者的多囊卵巢中，小窦状卵泡体内存在芳香化酶活性，假定健康卵泡的比例与正常卵巢中无差异；（3）正常卵巢和多囊卵巢的非优势卵泡中的雌二醇水平无差异，表明多囊卵巢中可能仅促卵泡生成素对芳香化酶活性的增强作用受到破坏；（4）由于正常卵泡和多囊卵泡中的雄烯二酮水平无差异，该综合征中的高雄激素血症似乎源于多囊卵巢中普遍观察到的异常大量的囊性闭锁卵泡；（5）女性个体内和个体间卵泡内分泌微环境的显著差异使得无法将多个卵泡的液体汇集在一起。
