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Desquamative Inflammatory Vaginitis: Prognosis and Treatment
Abstract & Commentary
By Jeffrey T. Jensen, MD, MPH, Editor, Leon Speroff, Professor and Vice Chair for Research, Department of Obstetrics and Gynecology, Oregon Health and Science University, Portland, is Editor for OB/GYN Clinical Alert.
Synopsis: Desquamative inflammatory vaginitis represents a chronic inflammatory process that responds well to anti-inflammatory treatment and requires long-term maintenance.
Source: Sobel JD, et al. Prognosis and treatment of desquamative inflammatory vaginitis. Obstet Gynecol 2011;117:850-855.
The authors performed a descriptive analysis of all cases of desquamative inflammatory vaginitis (DIV), defined as symptomatic vaginitis (discharge, dyspareunia, pruritus, burning, or irritation) associated with vaginal inflammation (such as focal or linear erosions), a vaginal pH higher than 4.5, and saline microscopy showing an increase in parabasal and inflammatory cells in the absence of an infectious etiology (such as trichomonas, candida, or bacterial vaginosis). A review of clinic charts was conducted to identify women diagnosed with DIV by the lead author between 1996 and 2007 in a referral university-based vaginitis clinic. Clinical findings, laboratory findings, and treatment outcomes were documented during the first 12 months and at 2 and 4 years for subjects with longer follow-up. The authors identified 130 patients who met the case definition, but 32 were excluded (mainly due to a suspicion of erosive lichen planus). All of the patients presented with symptomatic vaginal inflammation and 72% had vestibular findings (e.g., evidence of erythema, erosion, or thinning).
Initial treatments included either topical 2% clindamycin (54%) or 10% hydrocortisone (46%). Both of these treatments relieved symptoms within 3 weeks (median) in the majority (86%) of patients. Among 53 women who discontinued treatment after an initial favorable clinical response, 17/53 (32%) were noted to relapse within 6 weeks. At 1 year, cure was achieved in 25/98 patients (26%) with the initial treatment only, while an additional 57/98 (58%) were asymptomatic but remained dependent on maintenance treatment. Symptoms were only partially controlled in 15/98 (16%). The authors conclude that DIV is an inflammatory condition that typically requires long-term maintenance therapy.
I did not bring this paper to your attention because it was well written (it was not) or great science (single-site case series are the lowest level of medical evidence). However, very little is written about difficult vaginitis, and the problem is highly disruptive to affected women. Vaginitis generally is considered to be a fairly mundane problem for most gynecologists; something for the office nurse to manage over the phone or a midlevel provider to triage in the office. Most cases of common vaginitis are indeed common. We are fortunate to have great treatments for yeast vulvovaginitis, bacterial vaginosis, and trichomoniasis. But, if you've ever seen a patient who presents with recurrent difficult-to-manage inflammatory vaginitis and felt unsure what to do, read on.
Most practitioners recognize a variety of causes of epithelial disorders on the external body surface (including the vulva) due to infectious, allergic, and irritant responses. The immune-based skin disorders, dermatoses (non-neoplastic epithelial disorders such as psoriasis and lichen sclerosus), and neoplastic conditions such as vulvar intraepithelial neoplasia and squamous cancers also generally are recognized by most providers. If not, the presence of a distinct lesion usually leads to the appropriate action (biopsy or referral).
Why then the reluctance to consider that this diversity of disorders also may exist in the vagina? Many clinicians think that vaginal discharge can only mean infection or cancer. When screening tests for these conditions come up empty, the patient often receives yet another round of antifungal or antibiotic treatment. If you haven't found a way to effectively diagnose and manage difficult vaginitis, you may not even know it; these women probably have left your practice.
So what can we learn from this case series? First, the author's practice is a large university referral clinic for vulvovaginal disorders, so the cases represent a substantial accumulation of experience. This case series also comes with long-term follow-up (at least 30 months for most patients), so it provides us with some insight into the natural history of the condition. Finally, the manuscript represents a change in thinking by the author. Although DIV originally was recognized in the 1960s by Gray and Barnes1 and described by Gardner,2 the etiology and approach to therapy have been controversial. Almost 30 years after these initial reports, Sobel published a paper describing DIV as an infectious disease, and suggested that the condition was caused by an uncharacterized anaerobic bacterial overgrowth.3 The absence of protective lactobacillus and clinical response to intravaginal clindamycin provided the basis for this conclusion. Although the science of the 1995 paper was similar to the current manuscript (case series), the lack of competing theories made it influential. The approach to treatment of DIV became antibiotics: usually clindamycin but sometimes penicillin (for the Group B Streptococcus [GBS] culture fans).
How did GBS become a vaginal pathogen? Guilt by association. Some clinicians began culturing difficult vaginitis and not surprisingly GBS was identified. Since GBS is present in about 20% of our obstetrical population, this should not be a surprise, but this colonization was accepted (and treated) as an infection by many providers.
Unfortunately, antibiotic treatment is not without risk. Both penicillin and clindamycin kill lactobacillus, the bacterium we rely on to maintain the normal vaginal ecosystem. Not surprising then that these therapies typically fail to reestablish normal flora. Leclair published an important (but not widely seen) paper last year in the Journal of Lower Genital Tract Disease that considered the question of GBS.4 In this manuscript, non-pregnant reproductive age women with and without vaginitis underwent vaginal culture for GBS. Of the 215 women recruited, 68% showed no evidence of vaginitis, 19% had evidence of a common vaginitis (such as candida, BV, or trich), and 13% showed evidence of inflammatory vaginitis. The overall prevalence rate of GBS was 22.8%. Both common vaginitis (odds ratio [OR] 2.7, 95% confidence interval [CI] 1.1-6.2) and inflammatory vaginitis (OR 2.9, CI 1.1-8.0) were associated with an increased odds of GBS colonization. These findings demonstrate that disruption of the normal vaginal bacterial environment is an important predictor of GBS colonization. In other words, GBS fills a void when lactobacillus became scarce. GBS colonization is a result, and not a cause of disrupted flora, and treatment of gynecologic patients with penicillin for vaginitis is not warranted.
What about clindamycin? It works primarily due to its anti-inflammatory effects through a mechanism similar to macrolides and steroids. This is why clindamycin provides an effective benefit in treating acne as a topical product. It is also why metronidazole was not effective in treating DIV. The current manuscript by Sobel corrects the erroneous conclusions reached in 1995 that DIV has an infectious etiology and firmly establishes an inflammatory (possibly autoimmune) basis.
So how should you manage DIV? At our University Vulvar referral practice, we typical initiate therapy with hydrocortisone 25 mg rectal suppositories (used vaginally) at a dose of ½-1 suppository twice daily. See the patient back in 2 weeks to evaluate response. Usually, the inflammation and discharge (and symptoms) are greatly reduced as are the number of parabasal cells seen on wet smear. When adequate control is achieved, wean the therapy, but recognize that many patients will require long-term maintenance. Consider judicious use of intravaginal tacrolimus or clobetasol to manage difficult-to-treat cases. My personal belief is that most DIV represents a variant of erosive lichen planus, so look for signs of this dermatosis on the vestibule and vulva.