Vulvar Papillomatosis, Aceto-White Lesions, and Normal-Looking Vulvar Mucosa Evaluated by Microscopy and Human Papillomavirus Analysis

Abstract

Background and objectives: To assess the presence of human papillomavirus (HPV) DNA in vulvar papillomatosis, since some women with this complaint have symptoms associated with HPV infection, such as itching, burning, and dyspareunia. Goal: To reassure the patients that they do not have a transmissible viral disease, by excluding a HPV origin of their condition. Study design: Vulvar biopsy specimens from 22 females with vulvar papillomatosis, from 10 females with prominent aceto-white vulvar lesions, and from 14 healthy controls were analyzed histologically for signs of HPV infection and by in situ hybridization and polymerase chain reaction for the presence of HPV DNA. Results: Specimens from women with vulvar papillomatosis showed some histological signs associated with HPV infection, but no koilocytotic atypia or dysplasia and thus resembled normal-looking vulvar mucosa. Aceto-white lesions frequently displayed histological features suggestive of HPV infection, including dysplasia. HPV DNA was detected in 6 of 10 patients with aceto-white lesions, but only in 1 of 22 patients with papillomatosis and in no healthy controls. Conclusions: According to our results, HPV DNA, which is generally found in cervical lesions and subclinical infections, is not present in vulvar papillomatosis even though symptoms associated with HPV infection are frequent complaints.

‘HPV vulvitis’ revisited: frequent and persistent detection of novel epidermodysplasia verruciformis‐associated HPV genotypes

“…26,45,47 These assumptions are in part derived from the colposcopic observation of aceto-whitening of vulva and microscopic findings of koilocytes in the biopsy specimens, incriminating HPV infection as those occurring in the cervical epithelium. Clinicopathologic correlations in these patients were further supported by the demonstration of HPV antigens and/or HPV DNA using immunohistochemical 23,25,26,45 and molecular-based techniques, [19][20][21]23,24,27,29,[32][33][34][36][37][38][39][40][41][42][43][44][45] respectively.…”

“…‘HPV vulvitis’ describes a putative clinical disorder characterized by local symptoms of burning, pruritus, pain and/or dyspareunia, evidence of HPV infection by clinical, colposcopic and/or histologic examination and no other explainable causes 18–47 . The spectrum of clinical findings in HPV vulvitis includes vestibular or vulvar squamous papillomatosis (VSP), vulvar erythema (VE) and/or acetowhite regions of vulva.…”

“…The low prevalence of detectable HPV DNA in the previous vulvitis/VSP studies 19,29–41,46,47 may be in part because of the sensitivity and specificity of the methods employed. The detection of HPV DNA by in situ hybridization or polymerase chain reaction (PCR) using probes and primers specific only for GM genotype may underestimate the prevalence of HPV DNA, particularly the CU and EV genotypes 48,49 .…”

“…The spectrum of clinical findings in HPV vulvitis includes vestibular or vulvar squamous papillomatosis (VSP), vulvar erythema (VE) and/or acetowhite regions of vulva. The validity of this proposed clinical entity has not been readily accepted by most authorities because of the predominately negative or insignificant positive results for HPV in the later studies, 19,[29][30][31][32][33][34][35][36][37][38][39][40][41][42][43]46 high prevalence of VSP, VE and vulvar acetowhite lesions among healthy, sexually active women without vulvar complaints, 29 and the frequent histologic over-diagnosis of HPV by the finding of koilocytes in biopsy specimen. 19 Moreover, many of the vulvar symptoms in this population may be caused by an unrecognized dermatitis rather than HPV infection per se.…”

“…19 Moreover, many of the vulvar symptoms in this population may be caused by an unrecognized dermatitis rather than HPV infection per se. 41 The low prevalence of detectable HPV DNA in the previous vulvitis/VSP studies 19,[29][30][31][32][33][34][35][36][37][38][39][40][41]46,47 may be in part because of the sensitivity and specificity of the methods employed. The detection of HPV DNA by in situ hybridization or polymerase chain reaction (PCR) using probes and primers specific only for GM genotype may underestimate the prevalence of HPV DNA, particularly the CU and EV genotypes.…”