Relationship between serum mullerian-inhibiting substance and other reproductive hormones in untreated women with polycystic ovary syndrome and normal women

被引:214
作者
Cook, CL
Siow, Y
Brenner, AG
Fallat, ME
机构
[1] Univ Louisville, Dept Obstet & Gynecol, Louisville, KY 40292 USA
[2] Univ Louisville, Dept Surg, Louisville, KY 40292 USA
关键词
mullerian-inhibiting substance (MIS); polycystic ovary syndrome (PCOS);
D O I
10.1016/S0015-0282(01)02944-2
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Objective: To examine the relationship of serum mullerian-inhibiting substance (MIS), E-2, free-T, LH, and FSH in untreated women with polycystic ovary syndrome (PCOS) and in women with normal menstrual cycles. Design: A prospective study. Setting: University Departments of Obstetrics and Gynecology and Surgery. Patient(s): Twenty-seven women with PCOS and 20 women with normal menstrual cycles. Intervention(s): Serum was collected from women with PCOS and from normal women during the early follicular phase of the menstrual cycle, stored frozen until assayed. Main Outcome Measure(s): Serum levels of MIS, E-2, free-T, TSH. LH, and FSH were measured. Result(s): Serum mullerian-inhibiting substance levels in PCOS patients were significantly higher compared with normal women (+/- SE; 5.3 +/- 0.7 and 1.4 +/- 0.2 ng/mL, respectively). An inverse correlation (r = -0.5965) was found between serum levels of MIS and E-2 in PCOS women, but not in normal women. Women with PCOS had higher serum LH levels than those of normal women (15.2 +/- 1.2 and 5.0 +/- 0.7 mIU/mL). Conclusion: In this study, women with PCOS have significantly higher serum MIS levels than normal women. The inverse relationship between mullerian-inhibiting substance and E-2 levels suggests that MIS may modulate ovarian E-2 synthesis and have a role in the disordered folliculogenesis characteristic of PCOS. (Fertil Steril(R) 2002;77:141-6. (C) 2002 by American Society for Reproductive Medicine).
引用
收藏
页码:141 / 146
页数:6
相关论文
共 43 条
[1]   A mechanism for the suppression of estrogen production in polycystic ovary syndrome [J].
Agarwal, SK ;
Judd, HL ;
Magoffin, DA .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1996, 81 (10) :3686-3691
[2]  
ANDREANI CL, 1991, J BIOL CHEM, V266, P6761
[3]  
ANTTILA L, 1991, FERTIL STERIL, V55, P1057
[4]   ENZYMIC INADEQUACIES OF HUMAN POLYCYSTIC OVARIES [J].
AXELROD, LR ;
GOLDZIEHER, JW .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1961, 95 (03) :547-&
[5]  
BEZARD J, 1987, J REPROD FERTIL, V80, P509, DOI 10.1530/jrf.0.0800509
[6]   PRESENCE OF TRANSFORMING GROWTH-FACTOR-BETA AND THEIR SELECTIVE CELLULAR-LOCALIZATION IN HUMAN OVARIAN TISSUE OF VARIOUS REPRODUCTIVE STAGES [J].
CHEGINI, N ;
FLANDERS, KC .
ENDOCRINOLOGY, 1992, 130 (03) :1707-1715
[7]   Serum mullerian-inhibiting substance levels during normal menstrual cycles [J].
Cook, CL ;
Siow, Y ;
Taylor, S ;
Fallat, ME .
FERTILITY AND STERILITY, 2000, 73 (04) :859-861
[8]  
DICLEMENTE N, 1992, DEVELOPMENT, V114, P721
[9]  
EHRMANN DA, 2001, ENDOCRINOLOGY, V3, P2122
[10]   CORRELATION OF THE ULTRASONIC APPEARANCE OF THE OVARIES IN POLYCYSTIC OVARIAN DISEASE AND THE CLINICAL, HORMONAL, AND LAPAROSCOPIC FINDINGS [J].
ELTABBAKH, GH ;
LOTFY, I ;
AZAB, I ;
RAHMAN, HA ;
SOUTHREN, AL ;
ALEEM, FA .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1986, 154 (04) :892-895