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For mass reproduction, content licensing and permissions contact Dowden Health Media.OBGM ANAGEMENTPhilip J. DiSaia, MDProfessor and DirectorDivision of Gynecologic OncologyDorothy Marsh Chair inReproductive BiologyUniversity of California, IrvineDr. DiSaia is also Chairman of theGynecologic Oncology Group andPast President and Chairman ofthe Board of the American Boardof Obstetrics and GynecologyIN THIS ARTICLE❙ Distinguishingvulvar vestibulitisand dysesthesiaPage 73❙ Paget disease:Not just a breastcomplaintPage 76Noninvasive vulvar lesionsAn illustrated guideto diagnosis and treatmentDystrophies, vulvodynia, and other noncancerous lesionsCopyright ® Dowden Health MediaFor personal use onlyCASEPostmenopausal dyspareuniaA 60-year-old widow who recently remarriedcomplains of dyspareunia. Examination ofthe vulva reveals firm but thin white skinover the periclitoral area and labia minoraand shrinking of the vulvar skin.What is the likely diagnosis?Lichen sclerosus is the probable diagnosis,given her age and the appearanceof the vulva, although it isimpossible to assure the diagnosis withouta biopsy. The preferred treatment is clobetasol,an ultrapotent steroid, applied daily.True, powerful steroids can cause atrophyif applied regularly to other areas ofthe skin, but clobetasol does not causeatrophy of vulvar skin. After several weeksAtrophic labia minora, pale and scarifiedfrom scratching, may be caused by lichensclerosus. The microscopic view shows ahypertrophic keratin layer with an excoriationpenetrating the epithelium.of nightly application, the skin should besofter and more pliable, and dyspareuniashould be resolved. The patient can thenreduce the clobetasol application to twiceweekly—but she must continue the treatmentindefinitely.The vulva over the lifespanThe vulva is sensitive to both physiologicand pathologic changes, as well as to thesex hormones that govern the menstrualcycle. The mucosa on the inner aspects ofthe labia minora is very similar to the skinof the vagina and thus very sensitive toestrogen. The skin of the labia majora andthe outer surface of the labia minora ismore consistent with hair-bearing skin inthe perineal area and more sensitive toandrogens, which help thicken the skin. Atmenopause, the loss of estrogen leads toIMAGE: KIMBERLY MARTENS62 OBG MANAGEMENT • December 2006

atrophy, and the vulvar epithelium isreduced to a few layers of mostly intermediateand parabasal cell types. The labiaminora and majora as well as the clitorisgradually become less prominent with age.The skin of the vulva consists of bothdermis and epidermis, which interact witheach other and respond to different nutritionaland hormonal influences. Forexample, estrogen has little effect on vulvarepidermis, but considerable effect onthe dermis, thickening the skin and preventingatrophy.Postmenopausal atrophic changes canbecome a clinical problem when a womanresumes sexual intercourse after a long periodof abstinence, as in the opening case. Ifatrophy is the main complaint, estrogenreplacement therapy will alleviate symptomsof tightness, irritation, and dyspareunia, butit may take 6 weeks to 6 months to achieveoptimal results. In the interim, women needto be reassured that reasonable function canbe achieved.Hygienic considerationsWith any vulvar irritation, the patientshould discontinue the use of syntheticundergarments in favor of cotton panties,which permit more adequate circulationand do not trap moisture.Sitz baths often help relieve local discomfort,but should be followed by thoroughdrying.❚ Vulvar dystrophies:Think “white”In the past, these diseases have beendefined as non-neoplastic epithelial disordersof the vulva. Although there havebeen many attempts to more accuratelydefine vulvar dystrophies, none have completelydescribed the wide variety of clinicalpresentations.In general, dystrophies are disorders ofepithelial growth and nutrition that oftenresult in a white surface color change. Thisdefinition includes intraepithelial neoplasiaand Paget’s disease of the vulva. TheACOG opinion on vulvodyniaThe new ACOG Committee Opinion reflects recommendationsof the American Society for Colposcopy and Cervical Pathology. 17• Vulvodynia may be localized or generalized. Painlocalized to the vulvar vestibule, formerly termed vulvarvestibulitis, is now classified as localized vulvodynia.• The cause is unknown, and therefore it cannot bedetermined whether localized and generalized vulvodyniaare different manifestations of the same disease orcompletely different entities.• Treatment can be difficult, and improvement can takeweeks or months, even with appropriate therapy.– No single agent is successful in all women– Pain may never subside completely– Patients may need us to help them developrealistic expectations for improvement• Some women need psychological support, such assex therapy and counseling.Vulvodynia. American College of Obstetricians and Gynecologists CommitteeOpinion No. 345. Obstet Gynecol. October 2006;108:1049–1052.International Society for the Study ofVulvovaginal Disease has proposed multipleclassifications since 1975. I prefer theclarity of the 1987 classification system. 1 Ialso consider these terms out-of-date:lichen sclerosus et atrophicus, carcinomasimplex, leukoplakic vulvitis, leukoplakia,hyperplastic vulvitis, neurodermatitis,kraurosis vulvae, leukokeratosis, erythroplasiaof Queyrat, and Bowen’s disease.What makes the lesions white?The white appearance of dystrophiclesions is due to excessive keratin, at timesdeep pigmentation, and relative avascularity.All 3 of these characteristics are presentin the spectrum of vulvar dystrophies.Biopsy of the affected skin is the key toaccurate diagnosis and successful therapy.FAST TRACKVulvar dystrophies❙ Lichen sclerosus❙ Squamous cellhyperplasiaFormerly “hyperplasticdystrophy”❙ Other dermatosis❙ Squamous cellcarcinoma in situMay present clinicallyat any age as papulesor macules, coalescent ordiscrete, single or multiple❙ Paget’s diseaseof the vulvaClinicopathologic entitywith a pathognomonichistologic appearanceSource: Modified from Voet RL 1❚ Lichen sclerosusDoes not raise risk of carcinomaThe most common of the 3 groups ofwhite lesions described in the 1987 classificationof dystrophies, lichen sclerosususually occurs in postmenopausal women,but can appear at any age, including childwww.obgmanagement.comDecember 2006 • OBG MANAGEMENT 63

▲Noninvasive vulvar lesions: An illustrated guideFIGURE 1Lichen sclerosus affects all ages3-year-old child. Note the inflammationsecondary to excoriations.20-year-old woman. The glansclitoris has begun the hoodingprocess.70-year-old woman. The introitushas shrunk, making intercourseimpossible.FAST TRACKThere is no goodevidence thatwomen with lichensclerosus facea higher risk forvulvar carcinomahood (FIGURE 1). Despite claims to the contrary,there is no good evidence thatwomen with lichen sclerosus face a higherrisk for vulvar carcinoma.Signs and symptomsIn lichen sclerosus, the skin of the vulvaappears very thin, atrophic, and dry,resembling parchment. It is also white,with loss of pigmentation.Pruritus is the most common symptom andis usually the presenting symptom.Scratching during sleep may create ulcerationsand areas of ecchymosis, and there isgeneralized shrinking of the vulvar skin,with eventual loss of the labia minora.The edema and shrinking that occuraround the clitoris cause a “hooding” ofthe glans clitoris. If the process continuesunchecked, it can involve the labia majoraas well as the skin of the inner thigh andanal region.Prescribe clobetasol ointmentThe patient should be instructed to use clobetasol0.05% ointment on a continuingbasis. This drug is so successful it haseclipsed the use of testosterone propionatefor this indication. Lorenz and colleagues 2found very high success rates in 81 symptomaticpatients with biopsy-proven diseasewho had failed previous therapy.For reasons that are unknown, persistentuse of this steroid on vulvar skin doesnot cause the atrophy commonly seen withprolonged use of high-potency steroids onother areas of the skin.Start with twice-daily application and taperto less frequent use as the symptoms comeunder control. Most patients in remissioncan be maintained with twice-weeklyapplication. Pruritus should disappearcompletely, and the skin itself will becomeless “leathery.”Surgical treatment is not advisedSurgery does not appear to have a rolebecause lichen sclerosus often recurs outsideexcised areas. Several reports haveeven described the return of disease in skingrafts used to replace large diseased areas.I do not recommend surgery except indire circumstances, when symptom relief isessential to the patient’s quality of life andall other therapies have failed.❚ Squamous cell hyperplasiaThis disease is probably the same entity aslichen simplex chronicus. Changes in vulvarskin appear to result from chronicscratching secondary to intense pruritus.This complaint often involves a viciouscycle of scratching, increased pruritus, andmore scratching, until excoriations occur.CONTINUED64 OBG MANAGEMENT • December 2006

Noninvasive vulvar lesions: An illustrated guide▲The aim of therapy is to eliminate the pruritus(FIGURE 2).Signs and symptomsVulvar skin is typically white or pink.Biopsy will confirm the diagnosis, revealinga markedly thickened keratin layer(hyperkeratosis) and irregular thickeningof the Malpighian ridges (acanthosis).Inflammatory changes are also present,especially when there are areas ofexcoriation.FIGURE 2Squamous cell hyperplasiaTreatment is similarto therapy for lichen sclerosusPotent topical corticosteroids are the backboneof treatment; clobetasol is the preferreddrug. The frequency of application isidentical to that described for lichen sclerosus,and response to therapy usually takes 2months. In the interim, it is advisable to prescribeother medications for the pruritus.Lichen sclerosus and squamous cell hyperplasiasometimes coincide. Fortunately, thetherapies are quite similar and both conditionstend to respond.75-year-old woman. The skin isthickened and may be leathery.• History of yeast infection, 64%• Vulvar burning, 57%• Vulvar itching, 46%• Problems with sexual response, 33%Women with vulvar dysesthesia whoappear to have urinary tract symptomsshould undergo a urine culture, though itwill often be negative and antibiotic therapywill have little effect.Intense pruritus and aggressivescratching lead to excoriations.❚ VulvodyniaThis disorder consists of chronic vulvardiscomfort due to itching, burning, and/orpain that causes physical, sexual, and psychologicaldistress. 3,4 Once referred to asessential vulvodynia, it now is defined asgeneralized vulvar dysesthesia.Signs and symptomsWomen with this condition tend to havedifficulty localizing their pain. They oftenpresent with a complaint of recurrent yeastinfection or constant irritation at theintroitus. Dyspareunia may or may not bea presenting symptom, although intercourseoften triggers this condition. Tightpants or rough undergarments also maytrigger symptoms.Common symptoms. In a study bySadownik, 5 women with vulvar dysesthesiareported the following symptoms:• Dyspareunia, 71%A diagnosis of exclusionThe pain of dysesthesia appears to be neuropathicin origin in that it mimics pain ofthe sensory nervous system. It may be diffuseor focal, unilateral or bilateral, constantor sporadic. Thus, it is a diagnosis ofexclusion.Recommended therapiesVulvar dysesthesia should be regarded as achronic pain syndrome and treated accordingly,with emphasis on generalizedimprovements in health and attitude ratherthan single-therapy approaches.Potent topical corticosteroids are usuallyof no benefit. Nor does topical estrogenproduce long-term relief.Once all possible causes of symptomsare excluded, refer the patient for education,support, and treatment of depression,if present. Occasionally, topical anestheticswill provide short-term relief.At least 2 vulvar pain societies—theNational Vulvodynia Association and theCONTINUEDFAST TRACKVulvodynia painmay never subsidecompletelywww.obgmanagement.com December 2006 • OBG MANAGEMENT 69

Noninvasive vulvar lesions: An illustrated guide▲Vulvar Pain Foundation—have newsletters,outreach programs, and Web sites.❚ Vulvar vestibulitisA more readily definable condition in thesame category as vulvodynia is so-calledvulvar vestibulitis, also known as localizedvulvodynia (as classified by the new ACOGCommittee Opinion on vulvodynia).Signs and symptomsThe defining presentation is severe pain onvestibular touch (eg, entry at intercourse),with tenderness to pressure localized withinthe vulvar vestibule in a horseshoe distributionpattern encompassing 3, 6, and 9o’clock on the vestibule. Erythema is oftenpresent, especially at the 5 and 7 o’clockpositions (FIGURE 3).Patients have no symptoms during normaldaily activities, but complain of dyspareuniaand an inability to use tampons.TABLE 1Distinguishing vulvar vestibulitis and dysesthesiaVULVAR VESTIBULITISPain is usually not constantErythema in sensitive areasLidocaine quells sensitivityCause is dermal inflammationESSENTIAL VULVAR DYSESTHESIAPain is a constant burning sensationNo erythema or abnormal appearanceLidocaine has no effectCause is allodynia (heightenednerve sensitivity)TABLE 2Impressive track recordfor surgical treatment of vestibulitis% RESPONSESTUDY COMPLETE PARTIAL NONEBornstein et al 7 76 24 0Bergeron et al 12 63 37 0Kehoe and Luesley 13 60 29 11Mann et al 14 66 21 13Schover et al 15 47 37 16Marinoff and Turner 16 82 15 3Adapted from Bornstein et al 7Diagnostic strategiesVulvar vestibulitis can be diagnosed usinga moistened cotton-tip applicator. Pressureapplied in the area of the urethral meatuswill result in minimal discomfort, but pressurein the horseshoe area of the vestibulewill cause exquisite discomfort.Careful inspection at 5 and 7 o’clockin the vestibule usually uncovers intenseerythema over an area of 4 or 5 mm. Todistinguish vestibulitis from dysesthesia,see the comparison in TABLE 1.Recommended therapiesTreatment of vulvar vestibulitis is complex.It is important to see the patientoften to ensure that this syndrome is trulypresent rather than vulvar dysesthesia.Xylocaine jelly should be given in anattempt to relieve symptoms; topicalsteroid ointments are another option.Women with persistent symptoms aredifficult to treat medically. Earlier theoriespointing to infection as the cause ofvestibulitis have been discounted.Some experts believe that foods containingoxalates precipitate these symptoms.It may be advisable to have the patientreduce the content of oxalates in her diet inan effort to address all possible remedies.For refractory cases, consider surgeryConsider surgical removal of the tendervestibule if all other therapies fail to provideadequate relief. Surgery for this indicationhas a high success rate (TABLE 2). 7Some surgeons have attempted treatmentwith laser ablation, but most havefound excision more satisfactory, withfaster recovery and excellent cosmesis.Schneider and colleagues 8 had 69women complete a questionnaire 6 monthsafter surgery, 54 (78%) of whom replied.Moderate to excellent improvement wasreported by 45 women (83%); 7 had repeatsurgery, after which 4 improved.❚ Pigmented lesionsAre they cancer precursors?Precursors of malignant melanoma of theFAST TRACKHallmark ofvestibulitis: Severepain on touch,with tendernesslocalized withinthe vestibulein a horseshoepatternWEB RELATEDSee the Web version of this articleat www.obgmanagement.comfor a list of selected foodsand their oxalate contentwww.obgmanagement.com December 2006 • OBG MANAGEMENT 73

FIGURE 3Vestibular adenitisIntense erythema at the 5 o’clockposition in the vestibule.FIGURE 4Basal cell carcinomaAn uncommon type of vulvar cancer,this tumor rarely metastasizes.Assessing malignant potentialOnly a small number of dysplastic neviprogress to malignant melanoma, but thefrequency increases when the dysplasticnevus is familial and not acquired.In general, the more severe the dysplasia,the greater the likelihood it willprogress to malignancy. In dysplasticnevi, the pattern and appearance of themelanocytic cells are atypical. Bridging ofmelanocytic clusters of atypical cells mayoccur. Often, the atypical melanocytes arevaried in size and shape, increasing in celland nuclear size as severity increases. Inthe most severe cases, nucleoli are veryprominent.Many pigmented lesions of the vulvaare lentigines, similar to freckles. Distinguishingone pigmented lesion fromanother is difficult even with magnification,and the clinician often must decidewhether or not to biopsy. One set ofguidelines recommends excisional biopsyof vulvar nevi when there is a change in:• surface area of the nevus,• elevation of a lesion, ie, it becomesraised, thickened, or nodular,• surface, from smooth to scalyor ulcerated, or• sensation, including itching or tingling. 10Note that a reddish lesion may bebasal cell hyperplasia, which has beenassociated with the development of basalcell carcinoma (FIGURE 4).FAST TRACKVIN lesionsare hyper- orpseudopigmentedin about 30%of casesvulva have yet to be clearly defined. Themajority of these melanomas appear toarise de novo; however, some are associatedwith precursor nevi, especially junctionalnevi. The 3 most common types of nevithat appear on the vulva are:• Junctional—located in the basal layer;most likely to develop into melanoma.• Compound—melanocytes at the epidermal–dermalinterface and withinthe dermal layer.• Intradermal—Compound nevus whenneval cells in the junctional zone ceaseto be active. Intradermal nevi have lowmalignant potential.❚ Premalignant lesionsof squamous epitheliumThe variable appearance of vulvarintraepithelial neoplasia (VIN) necessitatesthe liberal use of diagnostic biopsies,particularly when lesions persist orrecur. VIN can present as a white lesion,or as pseudopigmented, pink, or raisedand eroded.Cigarette smoking is a risk factor.Clinical appearanceMacroscopically, VIN lesions are oftenmultiple and appear slightly raised andpapular. Hyper- or pseudopigmentedlesions are seen in about 30% of cases.A confluence of VIN can create anappearance of diffuse plaques. In VIN, asfor CIN, carcinoma in situ involves a fullthicknessabnormality.TerminologyIf the abnormal parabasal layer extends toone half to two thirds of the epithelium,moderate dysplasia is present. A lowerdegree of involvement is called mild dysplasia,and full-thickness involvement issevere dysplasia or carcinoma in situ.High rate of persistence, recurrenceHerod and colleagues 9 reported on a 15-year follow-up of VIN and found that dis-74 OBG MANAGEMENT • December 2006

Noninvasive vulvar lesions: An illustrated guide▲FIGURE 5VIN III lesions: A trio of presentationsWhite lesion. Pseudopigmented lesions. Pink lesion.ease persisted or recurred in 48% ofwomen managed surgically, and 7% ofpatients progressed to frankly invasive carcinoma.These investigators used the followingclassification system:• VIN I—mild dysplasia (formerly mildatypia)• VIN II—moderate dysplasia (formerlymoderate atypia)• VIN III—severe dysplasia (formerlysevere atypia)• VIN IV—carcinoma in situJoura et al 10 strongly suggested that theincidence of this condition is increasing,especially in women prior to the 7thdecade of life. Whether this increase is dueto better recognition or a true rise in prevalencehas been debated.Diagnostic strategiesApplication of 5% acetic acid to the vulvarskin will, after 3 to 5 minutes, allow areasof involvement to be readily seen with ahandheld magnifying glass. Colposcopycan be used, but is slower and not as efficientas a simple magnifying lens. Most clinicianshave abandoned the use of toluidineblue to identify multicentric lesions, sinceacetic acid appears to be less cumbersomeand just as efficient.White or pseudopigmented lesions(FIGURE 5) can be seen anywhere on thevulva and represent 2 of the 3 presentationsof VIN. Pink lesions (FIGURE 5) are usuallyseen on moist surfaces near mucous membranes,whereas the white or pseudopigmentedlesions are usually seen on thedrier, hair-bearing areas of the vulva.Biopsy reveals similar histology.The cause of the pseudopigmentedlesions is unclear, but is unrelated to a disturbanceof the melanin cells. As withother vulvar lesions, biopsy is essential fora correct diagnosis.Recommended therapiesVIN is treated by destroying or excisingthe epithelium involved. When the area islimited in size, simple excision or laservaporization is preferred. A 2- to 3-mmmargin is adequate, because these lesionshave sharp borders.Laser therapy warrants extra care becausethe epithelium is rarely thicker than 0.5mm. For this reason, vaporization of thevulva should be limited to the followingdepths:• Labia minora (hair-free): 0.5 mm• Labia majora (hair-containing): 1.5 to2 mmThese limits will speed healing andprevent the unnecessary destruction ofdermis.Also be aware that the depth of hairfollicleinvolvement rarely exceeds 1 mm.Vaporization of the full thickness of thedermis will lead to alopecia and vulvardryness.When disease is multifocal or confluent, treatmentis more challenging. Several decadesFAST TRACKBiopsy is essentialfor correctdiagnosis of vulvarintraepithelialneoplasiawww.obgmanagement.com December 2006 • OBG MANAGEMENT 75

▲Noninvasive vulvar lesions: An illustrated guideFIGURE 6Paget disease: Not just a breast complaintPaget disease of the nipple withunderlying ductal adenocarcinoma.Vulvar Paget disease: lesion (left) and photomicrograph of the lesion.FAST TRACKPaget’s diseaseof the vulva oftenrecurs, especiallywhen the initiallesion is largeago, simple vulvectomy was performed, butthe patient was left a sexual cripple.Since then, laser therapy has beenattempted in these cases, and has provedto be effective when the area treated doesnot exceed 25% of the total area of thevulva. Extensive laser therapy leads toconsiderable postoperative pain and anunhappy result.Extensive involvementmay necessitatelaser treatment by quadrant to achievethe best results. Another option is “skinningvulvectomy” using a skin graft. Thisprocedure, first described by FelixRutledge, 11 requires a 7- or 8-day hospitalization,but allows for complete therapyin 1 session.❚ Paget’s disease of the vulvaThis disease is most frequently seen in thebreast nipple (FIGURE 6), where it is usuallyassociated with an underlying infiltratingductal carcinoma. Extramammary sitesinclude the vulvar, perianal, and axillaryregions. The disease has also been seen inthe ear canal.Paget’s disease is an intraepithelial adenocarcinomaof eccrine or apocrine origin.Clinical appearancePaget’s disease of the vulva appears as asuperficial, red to pink, velvety, eczematoidlesion (FIGURE 6), which is very pruritic andoften associated with exfoliation. Marginsare difficult to identify grossly.On rare occasions, a nodular tumorcan be found in the middle of the skininvolvement, but in most cases no invasivemalignancy is found at extramammarysites on the vulva.Diagnostic strategiesMicroscopic appearance of Paget cells(FIGURE 6) are pathognomonic of thedisease.Older textbooks suggest that 10% to20% of patients have an associated, underlying,invasive carcinoma of a skinappendage, Bartholin’s gland, urinarytract, or bowel or rectal site, but laterexperience has not confirmed this. Rather,the likelihood of concomitant invasive diseaseis much lower than 10%.Excision is the treatment of choiceAny attempt to achieve negative marginsmust utilize frozen section. Some studieshave suggested that negative margins are notassociated with a reduced rate of recurrence,but these findings have been inconsistent.Recurrence is commonPaget’s disease of the vulva often recurs,especially when the initial lesion is large.Close monitoring will detect these recurrenceswhen they’re quite small and easilyC ONTINUED76 OBG MANAGEMENT • December 2006

Noninvasive vulvar lesions:An illustrated guide▲removed via local excision. Occasionally, theinitial disease is so extensive that skin graftingmay be necessary to cover the defect. ■REFERENCES1. Voet RL. Classification of vulvar dystrophies and premalignantsquamous lesions. J Cutan Pathol. 1994;21:86–90.2. Lorenz B, Kaufman RH, Kutzner SK. Lichen sclerosus. Therapywith clobetasol propionate. J Reprod Med. 1998;43:790–794.3. Proceedings of the XVth World Congress. International Societyfor the Study of Vulvovaginal Disease, Santa Fe, NM;September 26–30, 1999. International Society for the Study ofVulvovaginal Disease Newsletter, Summer 2000.4. Masheb RM, Nash JM, Brondolo E, Kerns RD. Vulvodynia: anintroduction and critical review of a chronic pain condition.Pain. 2000;86–93.5. Sadownik A. Clinical profile of vulvodynia patients. J ReprodMed. 2000;45:679–684.6. Edwards A, Wojnarowska F. The vulvar pain syndromes. Int JSTD AIDS. 1998;9:74–78.7. Bornstein J, Zarfati D, Goldik Z, Abramovici H. Vulvar vestibulitis:physical or psychosexual problem? Obstet Gynecol.1999;93(5 Pt 2):876–880.8. Schneider D, Yaron M, Bukovsky I, Soffer Y, Halpern R.Outcome of surgical treatment for superficial dyspareunia fromvulvar vestibulitis. J Reprod Med. 2001;46:227–231.9. Herod JJ, Shafi MI, Rollason TP, Jordan JA, Luesley DM. Vulvarintraepithelial neoplasia: long-term follow-up of treated anduntreated women. Br J Obstet Gynaecol. 1996;103:446–452.10. Joura EA, Lösch A, Haider-Angeler M-G, Breitenecker G,Leodolter S. Trends in vulvar neoplasia. J Reprod Med.2000;45:613–615.11. Rutledge F, Sinclair M. Treatment of intraepithelial carcinoma ofthe vulva by skin excision and graft. Am J Obstet Gynecol.1968;102:807–818.12. Bergeron S, Bouchard C, Fortier M, Binik YM, Khalife S. Thesurgical treatment of vulvar vestibulitis syndrome: a follow-upstudy. J Sex Marital Ther. 1997;23:317–325.13. Kehoe S, Luesley D. An evaluation of modified vestibulectomyin the treatment of vulvar vestibulitis: preliminary results. ActaObstet Gynecol Scand. 1996;75:676–677.14. Mann MS, Kaufman RH, Brown D Jr, Adam E. Vulvar vestibulitis:significant clinical variables and treatment outcome. ObstetGynecol. 1992;79:122–125.15. Schover LR, Youngs DD, Cannata R. Psychosexual aspects ofthe evaluation and management of vulvar vestibulitis. Am JObstet Gynecol. 1992;167:630–636.16. Marinoff SC, Turner ML. Vulvar vestibulitis syndrome: anoverview. Am J Obstet Gynecol. 1991;165:1228–1233.17. Haefner HK, Collins ME, Davis GD, et al. The vulvodynia guideline.J Low Genit Tract Dis. 2005; 9:45–51.The author reports no financial relationships relevant to this article.Care to commenton an article in this issue?Email us at OBG@dowdenhealth.comOBG MANAGEMENT 79