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4 n, uniformly had clinical evidence of severe vulvovaginal atrophy, dyspareunia (median pain score, 8
13 sseminated candidiasis (HDC) and episodes of vulvovaginal candidiasis (VVC) in humans, we found evide
18 Candida test using a reference standard for vulvovaginal candidiasis (VVC) of yeast culture plus exc
20 s the causative agent of acute and recurrent vulvovaginal candidiasis (VVC), a common mucosal infecti
21 rial vaginosis (BV), 25 acquired symptomatic vulvovaginal candidiasis (VVC), and 7 acquired vaginal t
22 ion with lactobacilli may reduce the risk of vulvovaginal candidiasis (VVC), but supporting data are
25 opharyngeal candidiasis (OPC), as opposed to vulvovaginal candidiasis (VVC), is a common opportunisti
26 ections, including bacterial vaginosis (BV), vulvovaginal candidiasis (VVC), or Trichomonas vaginalis
27 ctions, notably bacterial vaginosis (BV) and vulvovaginal candidiasis (VVC), particularly in the sett
29 anslocation, nor do we implicate the gene in vulvovaginal candidiasis among mice in pseudoestrus.
30 oth clinical studies of women with recurrent vulvovaginal candidiasis and a murine model of experimen
31 24 premenopausal women with acute recurrent vulvovaginal candidiasis and from 21 healthy asymptomati
34 women with non-antibiotic-induced recurrent vulvovaginal candidiasis suffering from acute Candida va
35 e randomly assigned 387 women with recurrent vulvovaginal candidiasis to receive treatment with fluco
36 b-), the relative risk of chronic recurring vulvovaginal candidiasis was 2.41-4.39, depending on the
37 infection, Trichomonas vaginalis infection, vulvovaginal candidiasis, and bacterial vaginosis) in HI
39 chlamydia, bacterial vaginosis, trichomonas, vulvovaginal candidiasis, pelvic inflammatory disease, g
40 e antifungal susceptibility of yeast causing vulvovaginal candidiasis, since cultures are rarely perf
41 ypeptides in both bacterial vaginosis and in vulvovaginal candidiasis, suggesting that the abnormalit
54 patients with recurrent infections, oral and vulvovaginal isolates were identical, in 35% they were h
55 o (1%) of 341 HIV-1-negative women developed vulvovaginal or perianal lesions, resulting in an incide
59 questionnaire was completed and cervical and vulvovaginal samples were collected to detect HPV DNA.
60 necologic examinations included cervical and vulvovaginal specimen collection for Pap and HPV DNA tes
62 that included HPV genotyping of cervical and vulvovaginal swab specimens and collection of colposcopy
64 ting Chlamydia trachomatis in self-collected vulvovaginal-swab and first-catch urine specimens from w
66 I], 93.1 to 99.2%) of infected patients with vulvovaginal-swab specimens and 91.8% (86.1 to 95.7%) wi
69 and behavioral information and cervical and vulvovaginal swabs for HPV DNA assay were obtained at 4-
70 musculoskeletal adverse events (MSAEs), and vulvovaginal symptoms (VVSs) in postmenopausal patients
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