Cyclic vulvovaginitis is marked by pain during certain cycle phases (luteal phase, perimenstrual phase), although the local findings are in most cases nonpatholo-gic. In the final analysis, the genesis is again unclear, although the hypothesis of a hypersensitive reaction to Candida albicans is advanced frequently (32).
There have long been indications that the incidence of Candida vaginitis is hormone dependent (2,33). Thus, a Candida infection is observed more frequently in pregnant women than in nonpregnant women. The use of ovulation inhibitors, in particular, those with a high estrogen content, also increases the risk of an infection. In postmenopausal women who do not use estrogen replacement therapy, the incidence is low. Relapses of a Candida infection with pruritus vulvae occur frequently in the luteal phase prior to the onset of menstruation. Kalo-Klein and Witkin demonstrated an inhibition of the cellular immune response to C. albicans during this phase, which they attributed to variations in the progesterone and estradiol levels (33). However, even independent of the menstrual cycle, patients with relapsing Candida vaginitis were shown to have a reduced Candida-specific T cell reaction. In vitro, both a reduced T cell proliferation and a reduced interferon-gamma secretion were demonstrated after stimulation with Candida antigen (10). The immunological effects of progesterone and estrogen discussed previously influence the cycle-dependent occurrence of candida vaginitis. In addition, the presence of an estrogen-binding protein on C. albicans was demonstrated. It is via this estrogen-binding protein that the transformation of C. albicans into the invasive hyphal form is directly stimulated (10).
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