Differential characterization of women with vulvar vestibulitis syndrome.
OBJECTIVE
We differentiated women with vulvar vestibulitis syndrome into subgroups on the basis of the time of symptom onset, a history of recurrent vulvovaginal candidiasis, and the interleukin-1 receptor antagonist gene polymorphism.


METHODS
One hundred sixty-two consecutive patients with strictly defined vulvar vestibulitis syndrome were asked to fill out a questionnaire with the assistance of their gynecologist. A buccal sample was collected from each subject for the analysis of interleukin-1 receptor antagonist gene polymorphism; vaginal and vestibular microbial investigations were performed.


RESULTS
Symptoms began with the first act of coitus in 20.4% of patients. A history of a recurrent Candida vulvovaginal infection was reported in 42.6% of patients; 25.9% of the patients were positive for the homozygous interleukin-1 receptor antagonist 2,2 genotype. Women with primary vulvar vestibulitis syndrome differed from women with secondary vulvar vestibulitis syndrome; women with primary vulvar vestibulitis syndrome were younger at the time of the onset of the symptoms (23.8 vs 31.2 years, P <.0001) and had never been pregnant (84.8% vs 61.2%, P <.0001). Women with a history of recurrent Candida vulvovaginitis differed from the other subjects by having a higher frequency of constant vestibular pain (40.6% vs 20.4%, P =.005), a vaginal discharge (79.7% vs 45.2%, P <.0001), and dysuria (62.3% vs 29.0%, P =.0001). Women who were homozygous for interleukin-1 receptor antagonist 2,2 genotype had an earlier onset of symptoms (26 years) than did women who were allele 1 homozygotes (31.3 years, P <.05). They also had a shorter duration of symptoms (4.1 vs 5.9 years, P <.05) and a higher frequency of allergy (47.6% vs 23.4%, P =.002). Human papillomavirus in the vaginal vestibule occurred at a greater frequency in women who were homozygous for interleukin-1 receptor antagonist 2,2 genotype.


CONCLUSIONS
Subgroups of women with vulvar vestibulitis syndrome may be differentiated by symptomatic and genetic variables.
Witkin
Steven S
SS
Division of Immunology and Infectious Diseases, Department of Obstetrics and Gynecology, Weill Medical College of Cornell University, New York, NY 10021, USA. switkin@mail.med.cornell.edu
Gerber
Stefan
S
Ledger
William J
WJ
D000328:Adult; D002181:Candidiasis, Vulvovaginal / Q000150:complications; D005260:Female; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D027383:Papillomaviridae / Q000302:isolation & purification; D011110:Polymorphism, Genetic; D012008:Recurrence; D012795:Sialoglycoproteins / Q000235:genetics*; D013577:Syndrome; D014621:Vagina / Q000382:microbiology; D014847:Vulvitis / Q000188:drug therapy / Q000209:etiology* / Q000235:genetics
C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D012795:Sialoglycoproteins