Plasma homocysteine, fasting insulin, and androgen patterns among women with polycystic ovaries and infertility

被引:40
作者
Sills, ES
Genton, MG
Perloe, M
Schattman, GL
Bralley, JA
Tucker, MJ
机构
[1] Georgia Reprod Specialists, Atlanta, GA USA
[2] MIT, Dept Math, Cambridge, MA 02139 USA
[3] Cornell Univ, Ctr Reprod Med & Infertil, Weill Med Coll, New York Presbyterian Hosp, New York, NY 10021 USA
[4] Metametrix Clin Lab, Norcross, GA USA
关键词
homocysteine; polycystic ovary; hyperandrogenism; risk factors;
D O I
10.1111/j.1447-0756.2001.tb01241.x
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Objective: To measure plasma homocysteine, androgen, and insulin concentrations in women with normal and polycystic-appearing ovaries in an infertility setting. Methods: Among women referred for infertility evaluation (n = 54), homocysteine, androstenedione, DHEAS, total testosterone, fasting insulin/glucose and methyltetrahydrofolate reductase (MTHFR) polymorphism status (C677T mutation) were studied. Ovaries were examined via transvaginal sonogram by one observer and scored as either normal (n = 18) or polycystic (n = 36). Results: When polycystic ovaries were identified, mean total testosterone was significantly higher than when non-polycystic ovaries were present (p = 0.01), although no measured androgen was outside the normal reference range in either group. Average BMI was higher in the polycystic group, but the difference was not significant (p = 0.10). We observed a trend toward higher mean fasting insulin levels in women with polycystic ovaries, but this increase did not reach statistical significance (p = 0.07). Median plasma homocysteine was identical (7.0 mmol/1) in both populations, and no study subject exceeded the current recommended maximum reference value. Conclusions: In this population, the presence of polycystic ovaries was associated with higher serum androgens (especially total testosterone) although none of the measured androgens were above the normal range. While fasting insulin levels were also higher in this group, median plasma homocysteine levels were similar irrespective of ovarian morphology. Concomitant plasma homocysteine derangements in this population of young, lean patients with polycystic-appearing ovaries seem unlikely. Further studies are needed to clarify the role(s) of homocysteine in human reproductive physiology.
引用
收藏
页码:163 / 168
页数:6
相关论文
共 18 条
[1]   A QUANTITATIVE ASSESSMENT OF PLASMA HOMOCYSTEINE AS A RISK FACTOR FOR VASCULAR-DISEASE - PROBABLE BENEFITS OF INCREASING FOLIC-ACID INTAKES [J].
BOUSHEY, CJ ;
BERESFORD, SAA ;
OMENN, GS ;
MOTULSKY, AG .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1995, 274 (13) :1049-1057
[2]   Development of a health-related quality-of-life questionnaire (PCOSQ) for women with polycystic ovary syndrome (PCOS) [J].
Cronin, L ;
Guyatt, G ;
Griffith, L ;
Wong, E ;
Azziz, R ;
Futterweit, W ;
Cook, D ;
Dunaif, A .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1998, 83 (06) :1976-1987
[3]   The TT genotype of the methylenetetrahydrofolate reductase C677T gene polymorphism is associated with the extent of coronary atherosclerosis in patients at high risk for coronary artery disease [J].
Gardemann, A ;
Weidemann, H ;
Philipp, M ;
Katz, N ;
Tillmanns, H ;
Hehrlein, FW ;
Haberbosch, W .
EUROPEAN HEART JOURNAL, 1999, 20 (08) :584-592
[4]   OXYGEN CONCENTRATION GRADIENT ACROSS THE OVARIAN FOLLICULAR EPITHELIUM - MODEL, PREDICTIONS AND IMPLICATIONS [J].
GOSDEN, RG ;
BYATTSMITH, JG .
HUMAN REPRODUCTION, 1986, 1 (02) :65-68
[5]   Plasma homocysteine as a risk factor for vascular disease - The European concerted action project [J].
Graham, IM ;
Daly, LE ;
Refsum, HM ;
Robinson, K ;
Brattstrom, LE ;
Ueland, PM ;
PalmaReis, RJ ;
Boers, GHJ ;
Sheahan, RG ;
Israelsson, B ;
Uiterwaal, CS ;
Meleady, R ;
McMaster, D ;
Verhoef, P ;
Witteman, J ;
Rubba, P ;
Bellet, H ;
Wautrecht, JC ;
deValk, HW ;
Luis, ACS ;
ParrotRoulaud, FM ;
Tan, KS ;
Higgins, I ;
Garcon, D ;
Medrano, MJ ;
Candito, M ;
Evans, AE ;
Andria, G .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1997, 277 (22) :1775-1781
[6]   FAMILIAL POLYCYSTIC OVARIES - A GENETIC-DISEASE [J].
HAGUE, WM ;
ADAMS, J ;
REEDERS, ST ;
PETO, TEA ;
JACOBS, HS .
CLINICAL ENDOCRINOLOGY, 1988, 29 (06) :593-605
[7]  
Hull M G, 1987, Gynecol Endocrinol, V1, P235, DOI 10.3109/09513598709023610
[8]   Polycystic ovary syndrome: a new direction in treatment [J].
Kidson, W .
MEDICAL JOURNAL OF AUSTRALIA, 1998, 169 (10) :537-540
[9]   Recurrent miscarriage: Screening for polycystic ovaries and subsequent pregnancy outcome [J].
Liddell, HS ;
Sowden, K ;
Farquhar, CM .
AUSTRALIAN & NEW ZEALAND JOURNAL OF OBSTETRICS & GYNAECOLOGY, 1997, 37 (04) :402-406
[10]  
Mitwally MF, 2000, MIDDLE E FERTIL SOC, V5, P2