Changes in gonadal steroid receptors in the cardinal ligaments of prolapsed uteri: immunohistomorphometric data.
BACKGROUND
The precise mechanism of uterine prolapse is poorly understood. This immunohistochemical study was performed on paraffin-embedded sections of the cardinal ligaments in an attempt to evaluate the differential expression of gonadal steroid receptors in human cardinal ligaments of prolapsed uteri compared with non-prolapsed controls.


METHODS
Specimens from women with pelvic organ prolapse (POP) stage III (n = 33), together with the appropriate controls (n = 25), were stained for estrogen receptor alpha (ERalpha), ERbeta, progesterone receptor (PR), androgen receptor (AR) and Ki-67. The control materials were samples of the cardinal ligaments obtained from pre- and post-menopausal women with no prolapse, who were not using hormonal therapy. RESULTS The prolapsed ligaments expressed 1.5-2.5 times more ERalpha-positive cells (statistically significant in post-menopausal women not taking HRT, P < 0.001), a 3-4 times greater percentage of AR-positive cells (P = 0.004 and P = 0.008 in pre-menopausal and post-menopausal women not taking HRT, respectively) and twice the percentage of PR-positive cells (statistically significant in the pre-menopausal group, P = 0.03) compared with the no prolapse group. Expression of ERbeta was twice as high in the ligaments of pre-menopausal women with no prolapse compared with those with prolapse (P = 0.02), and no significant difference was found in the post-menopausal groups. The use of HRT was significantly associated with low AR and high PR expression. Ki-67 expression was not detected in these specimens.


CONCLUSIONS
The clearly discernible levels of expression of ERalpha, ERbeta, AR and PR in the prolapsed cardinal ligaments may suggest a relationship to the process of tissue stretch 'trauma', rather than an effect of the menopausal status, HRT use or cell proliferation. The use of HRT in post-menopausal women appears to offset some of the changes observed with the prolapse.
Ewies
Ayman A A
AA
Leicester and Warwick Medical School, UK.
Thompson
John
J
Al-Azzawi
Farook
F
D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D047628:Estrogen Receptor alpha / Q000378:metabolism; D047629:Estrogen Receptor beta / Q000378:metabolism; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000378:metabolism; D008022:Ligaments / Q000378:metabolism*; D008875:Middle Aged; D010053:Ovary / Q000378:metabolism*; D011944:Receptors, Androgen / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D011987:Receptors, Steroid / Q000378:metabolism*; D014596:Uterine Prolapse / Q000378:metabolism*
D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D019394:Ki-67 Antigen; D011944:Receptors, Androgen; D011980:Receptors, Progesterone; D011987:Receptors, Steroid