Stanczyk F Z, Chang L, Carmina E, Putz Z, Lobo R A
Department of Obstetrics and Gynecology, University of Southern California School of Medicine, Los Angeles.
Am J Obstet Gynecol. 1991 Dec;165(6 Pt 1):1837-42. doi: 10.1016/0002-9378(91)90042-p.
To determine whether the adrenal androgen 11 beta-hydroxyandrostenedione is a more sensitive and specific marker than dehydroepiandrosterone sulfate, we compared these serum androgens in 81 women with anovulatory hyperandrogenism before treatment, after corticotropin and corticotropin-releasing-factor stimulation, and after short- and long-term dexamethasone suppression. Of all subjects, 65% and 57% had elevated levels of 11 beta-hydroxyandrostenedione (greater than 2.0 ng/ml) and dehydroepiandrosterone sulfate (greater than 2.8 micrograms/ml), respectively. However, 11 beta-hydroxyandrostenedione and dehydroepiandrosterone sulfate levels did not correlate in either the women with hyperandrogenism (r = 0.12) or the 26 normal women (r = 0.29). After 0.25 mg corticotropin was administered intravenously (n = 16), 11 beta-hydroxyandrostenedione increased by 157% +/- 53% (mean +/- SEM), whereas dehydroepiandrosterone sulfate, androstenedione, dehydroepiandrosterone, and cortisol increased by 6% +/- 2%, 46% +/- 10%, 416% +/- 80%, and 2326% +/- 371%, respectively. After intravenous administration of 100 micrograms corticotropin-releasing factor to eight patients, the percent change from baseline level to peak was 148% +/- 26%, 24% +/- 5%, 61% +/- 15%, 117% +/- 15%, and 116% +/- 18% for 11 beta-hydroxyandrostenedione, dehydroepiandrosterone sulfate, androstenedione, dehydroepiandrosterone, and cortisol, respectively. After 2 mg dexamethasone for 3 days (n = 10), 11 beta-hydroxyandrostenedione, dehydroepiandrosterone sulfate, androstenedione, and testosterone were suppressed by 95% +/- 2%, 74% +/- 3%, 51% +/- 9%, and 32% +/- 9%, respectively. Suppression with 0.5 mg dexamethasone for 3 months lowered 11 beta-hydroxyandrostenedione and dehydroepiandrosterone sulfate levels equally by 50% +/- 14% and 62% +/- 12%, respectively. 11 beta-Hydroxyandrostenedione is a useful marker of adrenal androgen secretion with a calculated sensitivity and specificity greater than that of dehydroepiandrosterone sulfate. The greater sensitivity of 11 beta-hydroxyandrostenedione over dehydroepiandrosterone sulfate to adrenal stimulation and suppression suggests its unique diagnostic use.
为了确定肾上腺雄激素11β - 羟基雄烯二酮是否比硫酸脱氢表雄酮更敏感、更具特异性，我们比较了81名无排卵性高雄激素血症女性在治疗前、促肾上腺皮质激素和促肾上腺皮质激素释放因子刺激后以及短期和长期地塞米松抑制后的血清雄激素水平。在所有受试者中，分别有65%和57%的11β - 羟基雄烯二酮（大于2.0 ng/ml）和硫酸脱氢表雄酮（大于2.8 μg/ml）水平升高。然而，在高雄激素血症女性（r = 0.12）或26名正常女性（r = 0.29）中，11β - 羟基雄烯二酮和硫酸脱氢表雄酮水平均无相关性。静脉注射0.25 mg促肾上腺皮质激素后（n = 16），11β - 羟基雄烯二酮升高了157%±53%（平均值±标准误），而硫酸脱氢表雄酮、雄烯二酮、脱氢表雄酮和皮质醇分别升高了6%±2%、46%±10%、416%±80%和2326%±371%。对8名患者静脉注射100 μg促肾上腺皮质激素释放因子后，11β - 羟基雄烯二酮、硫酸脱氢表雄酮、雄烯二酮、脱氢表雄酮和皮质醇从基线水平到峰值的变化百分比分别为148%±26%、24%±5%、61%±15%、117%±15%和116%±18%。给予2 mg地塞米松3天（n = 10）后，11β - 羟基雄烯二酮、硫酸脱氢表雄酮、雄烯二酮和睾酮分别被抑制了95%±2%、74%±3%、51%±9%和32%±9%。给予0.5 mg地塞米松3个月后，11β - 羟基雄烯二酮和硫酸脱氢表雄酮水平分别同样降低了50%±14%和62%±12%。11β - 羟基雄烯二酮是肾上腺雄激素分泌的一个有用标志物，其计算得出的敏感性和特异性高于硫酸脱氢表雄酮。11β - 羟基雄烯二酮相对于硫酸脱氢表雄酮对肾上腺刺激和抑制更敏感，提示其具有独特的诊断用途。
