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Desquamative inflammatory vaginitis (DIV)

Desquamative inflammatory vaginitis (DIV)
Literature review current through: Jan 2024.
This topic last updated: May 25, 2023.

INTRODUCTION — Bacterial vaginosis, vulvovaginal candidiasis, and trichomonas vaginitis are the most common causes of abnormal vaginal discharge in adult females (pre- and postmenopause). When these conditions have been excluded, other less frequent causes of vaginal discharge must be considered, including desquamative inflammatory vaginitis (DIV). DIV is considered a noninfectious cause of inflammatory vaginitis.

This topic will review the presentation, diagnosis, and management of DIV. Related content on the evaluation of vaginitis and cervicitis is presented separately.

(See "Vaginitis in adults: Initial evaluation".)

(See "Acute cervicitis".)

In this topic, when discussing study results, we will use the terms "woman/en" or "patient(s)" as they are used in the studies presented. However, we encourage the reader to consider the specific counseling and treatment needs of transgender and gender-expansive individuals.

PATHOGENESIS AND EPIDEMIOLOGY — First described in the 1950s, DIV is a chronic clinical syndrome of unknown etiology that typically causes copious vaginal discharge and pain [1,2].

Possible mechanisms – Proposed underlying contributory mechanisms include estrogen deficiency, a toxic reaction to Staphylococcus aureus, an immunologic abnormality, or a combination [3,4]. Two cases of DIV that appeared to have been triggered by toxic shock syndrome toxin-1 (TSST-1)-producing Staphylococcus aureus strains have been reported [5].

Inflammation versus infection – The author and most North American investigators believe DIV is an inflammatory vaginitis of noninfectious etiology with secondary bacterial microbiota disruption [6]. In this viewpoint, DIV is believed to be a relatively nonspecific form of immuno-inflammatory or reactive vaginitis that is multifactorial in etiology.

Other investigators believe the disorder is due to altered vaginal flora (eg, Escherichia coli), and have termed the spectrum of findings "aerobic vaginitis" [7-10]. However, no consistent microbiologic pathogen has been identified except for the near absence of lactobacilli in almost all affected individuals [11].

Role of dysbiosis Profound disturbances of vaginal microbiota are uniformly found in DIV and other forms of inflammatory vaginitis. However, to date, advanced vaginal microbiome research has not revealed consistent microbial alterations or new microbial pathogens in these patients. Thus, it is suspected that the characteristic dysbiosis is the result and not the cause of DIV.

Prevalence – In a prospective cohort study of 200 self-reported women with chronic vulvovaginal symptoms, 8 percent (16 out of 200) were diagnosed with DIV [12]. Those with DIV were older than the mean age (44.2 versus 38.4 years) and least likely to be menstruating. As this study group represented patients referred to a subspecialty center, the actual incidence may be higher or lower in the general population.

Overlap with plasma cell vulvitis – Overlapping histopathological features have been described for DIV and plasma cell vulvitis, including epithelial thickness, rete ridge appearance exocytosis, and spongiosis [13]. This finding raises the possibility that they are different manifestations of the same underlying process.

PRIMARY VERSUS SECONDARY DIV — Primary DIV is idiopathic. Increased awareness of DIV has revealed a secondary, nonidiopathic form of inflammatory vaginitis similar to primary DIV, but caused by drugs (rituximab has been reported [14]) or associated with other immune-mediated disorders (eg, Crohn disease [15]). While the clinical presentation is the same for both, secondary DIV manifests in different patient populations and has different prognoses and responses to therapy. Recognizing DIV's existence has emphasized that not all vaginitis is caused by the traditional, more frequent causes of vaginal discharge (vulvovaginal candidiasis, bacterial vaginosis, and trichomoniasis [70 percent only]), and many additional causes of inflammatory vaginitis undoubtedly exist [16].

CLINICAL PRESENTATION — Patients with primary or secondary DIV present with copious vaginal discharge and pain.

Vaginal discharge and pain – The pain and copious vaginal discharge of DIV may be accompanied by vestibular and vulvar inflammatory symptoms and signs. The pain can be described as dyspareunia, vaginal/introital pain, burning, or a combination thereof [11,12]. A diffuse exudative vaginitis and epithelial cell exfoliation results in profuse vaginal discharge (usually yellow but may be gray or green) [3]. In a series of 98 patients diagnosed with DIV (mean age 49.6 years), 70 to 90 percent had purulent vaginal discharge, dyspareunia, and vaginal inflammation [11].

Symptom onset and duration – While primary DIV occurs in both pre- and post-menopausal individuals, it is more common in perimenopausal women [3,11,12]. Secondary DIV can occur in individuals of any age. In addition, those with DIV have often noted symptoms for more than one year and been treated for multiple other causes of vaginitis without relief [12].

DIAGNOSTIC EVALUATION — Individuals with complaints of abnormal vaginal discharge (quantity or quality) are evaluated with a complete history and physical examination as well as appropriate laboratory tests, such as pH and microscopy (algorithm 1). Sexually active patients are evaluated for sexually transmitted infections.

A detailed discussion of the approach to abnormal vaginal discharge is presented in related content. (See "Vaginitis in adults: Initial evaluation".)

History — We obtain detailed symptom and sexual histories. Additional questions include menopause status, contraceptive use, use of topical vulvovaginal therapies, recent treatment (topical or systemic), and sexual practices. While these questions are not specific to diagnosing DIV, the answers can guide the differential diagnosis and help exclude other causes of vaginal discharge and pain. (See "Vaginitis in adults: Initial evaluation", section on 'History'.)

Physical examination and findings

External genitalia – Normal vulvovaginal architecture is maintained. The vestibule is often affected and may be thinned, sensitive, erythematous, and/or edematous. These findings may be a result of irritation from the discharge or, more likely, due to vestibule or mucosa inflammation similar to that of the vagina.

Vagina – Speculum examination of the vagina often reveals a spotty ecchymotic rash or diffuse or focal erythema or linear erosions. Copious vaginal discharge is present (usually yellow but may be gray or green).

Cervix – Submucosal petechiae and erosive lesions, similar to those seen with trichomoniasis infection, may be present [17-19]. In addition, at least one case report has described DIV associated with persistent cervical ectropion [20].

Other systems – There are no extra-genital findings (eg, oral lesions) on examination. No epidermal involvement occurs.

Laboratory tests

Vaginal pH – Increased (>4.5).

Saline wet mount microscopy – Increased number of parabasal and inflammatory cells, and the leukocyte to epithelial cell ratio is greater than 1:1 (picture 1) [3,17,19]. Parabasal cells are immature squamous epithelial cells that are rounded and have a large nucleus-to-cytoplasm ratio; by contrast, mature squamous epithelial cells are larger, cuboidal, with a smaller nucleus-to-cytoplasm ratio, and sometimes folded.

Laboratory tests – Laboratory tests to exclude bacterial vaginosis and vulvovaginal candidiasis are performed in all patients. Those who are sexually active are also tested for gonorrhea, chlamydia, and trichomoniasis. Patients with unilateral or vesicular lesions undergo testing for herpes simplex virus.

Specific tests for these and other genital infections are discussed in detail in related content:

(See "Bacterial vaginosis: Clinical manifestations and diagnosis", section on 'Diagnostic evaluation'.)

(See "Candida vulvovaginitis: Clinical manifestations and diagnosis", section on 'Diagnostic approach'.)

(See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents", section on 'Diagnostic techniques'.)

(See "Clinical manifestations and diagnosis of Chlamydia trachomatis infections", section on 'Diagnosis of chlamydial infections'.)

(See "Trichomoniasis: Clinical manifestations and diagnosis".)

(See "Approach to the patient with genital ulcers", section on 'Diagnostic testing'.)

DIAGNOSIS — The diagnosis of DIV requires all of the following criteria [11,21]:

Vaginal symptoms (at least one must be present) – vaginal discharge, dyspareunia, pruritus, burning, irritation.

Vaginal inflammation (spotted ecchymotic rash, erythema, focal or linear erosion).

Vaginal pH >4.5.

Saline microscopy – Increased numbers of parabasal and inflammatory cells with a leukocyte to epithelial cell ratio greater than 1:1 (picture 1).

Exclusion of other infectious etiologies – Bacterial vaginosis, vulvovaginal candidiasis, and when indicated, Neisseria gonorrhoeae, Chlamydia trachomatis, and Trichomonas vaginalis infection should be excluded as etiologies (algorithm 1).

DIFFERENTIAL DIAGNOSIS — DIV is a diagnosis of exclusion. As there is no confirmatory test for the disorder and the presenting symptoms of vaginal discharge and/or pain are shared with other processes, additional causes of vaginal inflammation and elevated pH, such as atrophic vaginitis, erosive disorders, or infections such as bacterial vaginosis or trichomoniasis, must be considered and excluded. A comparison of common infectious causes of vaginal discharge is presented in the table (table 1).

The evaluation of individuals with persistent vaginal discharge and pain of unclear etiology, after infectious causes have been excluded, is presented in detail separately. (See "Vaginitis in adults: Initial evaluation", section on 'No diagnosis after initial evaluation'.)

The differential diagnosis varies by symptom and finding.

Isolated vaginal discharge – Of individuals who present for evaluation of abnormal vaginal discharge, 9 percent have been reported to have physiologic vaginal discharge (ie, leukorrhea) [12]. Physiologic vaginal discharge, which is also a diagnosis of exclusion, is distinguished from DIV by a vaginal pH of 4.5 or less and normal saline microscopy. (See "Vaginitis in adults: Initial evaluation", section on 'Normal vaginal discharge'.)

Atrophic vaginitis – In hypoestrogenic patients, severe atrophic vaginitis can mimic DIV and microscopy findings are similar for both conditions. Improvement in symptoms with estrogen therapy helps distinguish atrophic vaginitis from DIV. (See "Genitourinary syndrome of menopause (vulvovaginal atrophy): Clinical manifestations and diagnosis".)

Erosive disorders – The differential diagnosis for erosive vaginal lesions includes erosive lichen planus, pemphigus vulgaris, and cicatricial pemphigoid [17]. DIV typically occurs in perimenopausal women, while erosive lichen planus and cicatricial pemphigoid typically occur in menopausal women. (See "Vulvar lesions: Differential diagnosis of vesicles, bullae, erosions, and ulcers", section on 'Erosions, excoriations, and fissures'.)

DIV – For DIV, purulent discharge is a prominent finding, normal vulvovaginal architecture is maintained, and there are no extra genital findings.

Erosive lichen planus – In erosive lichen planus, the vaginal epithelium is friable and easily bleeds upon speculum insertion or with coitus. Small areas of inflammation and increased vaginal discharge may be present, or the vagina may be massively inflamed and denuded with a seropurulent exudate, pseudomembrane, or serosanguineous vaginal discharge. Eroded epithelial surfaces often have a glazed red surface (picture 2 and picture 3). In severe cases, adhesions and synechiae can develop, which can lead to narrowing or obliteration of the vagina. Extragenital mucous membrane disease is common (particularly the mouth (picture 4)). (See "Vulvar lichen planus" and "Vulvar lichen planus", section on 'Erosive lichen planus'.)

Pemphigus vulgaris and cicatricial pemphigoid - Unlike DIV and lichen planus, both pemphigus vulgaris and cicatricial pemphigoid begin as blisters, which soon degenerate into nonspecific erosions. As with lichen planus, women with pemphigus vulgaris and cicatricial pemphigoid are likely to have evidence of extragenital mucous membrane disease (particularly the mouth). Cicatricial pemphigoid, but not pemphigus vulgaris, leads to scarring. (See "Pathogenesis, clinical manifestations, and diagnosis of pemphigus" and "Clinical features and diagnosis of bullous pemphigoid and mucous membrane pemphigoid".)

Biopsy from the edge of an erosion or blister for histopathological examination and immunofluorescence studies are needed to confirm these other diagnoses.

(See "Vulvar lichen planus", section on 'Erosive lichen planus'.)

(See "Pathogenesis, clinical manifestations, and diagnosis of pemphigus".)

(See "Management and prognosis of bullous pemphigoid".)

Dyspareunia or sexual pain – Dyspareunia or pain with sexual activity may result from atrophy related to hypoestrogenism or vaginismus; copious vaginal discharge is not typically present. Improvement in symptoms with targeted therapy (topical estrogen, pelvic floor physical therapy) helps distinguish causes of isolated sexual pain from DIV.

(See "Female sexual pain: Evaluation".)

(See "Female sexual pain: Differential diagnosis", section on 'Vaginismus and myofascial pelvic pain syndrome (MPPS)'.)

Vaginal pain – In the absence of other findings, isolated vaginal pain may represent a centralized pain syndrome similar to that of chronic pelvic pain. (See "Chronic pelvic pain in adult females: Evaluation".)

TREATMENT — The two most common treatments are intravaginal clindamycin or glucocorticoids [11,17,22,23]. No randomized trials of treatment approaches have been reported. Options for initial therapy include either of the following:

Medication for DIV — Treatment with topical medication is the same for individuals with primary or secondary DIV. Treatment choice is based on patient preference, drug availability, and, for those who have previously been treated for DIV, prior treatment response. Metronidazole does not treat DIV [19].

Topical clindamycin – We use 2% clindamycin cream, to fill a typical applicator (approximately 5 grams containing approximately 100 mg clindamycin) intravaginally at night for four to six weeks [11]. The next steps are determined by treatment response after four to six weeks of therapy. (See 'Treatment response and follow-up' below.)

Others use 2% clindamycin cream 4 to 5 grams (approximately one full typical applicator) intravaginally at night for one to three weeks followed by maintenance therapy once or twice a week for two to six months [19].

OR

Topical hydrocortisone – Ten percent hydrocortisone cream, 3 to 5 grams (dosed by typical vaginal applicator) intravaginally at night for four to six weeks. Ten percent hydrocortisone cream is not commercially available but can be compounded by a pharmacist. For mild disease, twice daily vaginal insertion of either hydrocortisone cream 0.5% (base) or one 25 mg rectal suppository is an option, particularly if 10% hydrocortisone cream is not available [23].

OR

Topical clobetasol gel – Clobetasol gel 0.05%, 5 gram dosed by typical applicator, applied intravaginally at night for one week [19]. In our experience, intravaginal clobetasol gel needs to be continued for several weeks to achieve treatment response and is often more expensive than the above drugs. The maximum total dose should be below 50 g per week.

Treat concomitant disorders — Patients with DIV often have additional clinical diagnoses. The order and timing of treatment of these commonly associated processes relative to the timing of DIV therapy is unknown and individualized to the patient's issues and desire/ability to address more than one process at a time.

Vulvovaginal atrophy – Vulvovaginal atrophy, one component of genitourinary syndrome of menopause, is typically treated with low-dose topical estrogen but other treatments are available. (See "Genitourinary syndrome of menopause (vulvovaginal atrophy): Treatment".)

Low-dose vaginal estrogen – Data to inform the timing of treatment start, selection of estrogen formulation (cream, tablet, or ring), and treatment duration for patients with DIV are lacking. We prescribe the vaginal estrogen product preferred by the patient and start it at the second or third clinical visit; the rationale for the timing is to minimize the number of treatments given to a patient in one visit. Some clinicians prescribe compounded products that combine estrogen and cortisone to simplify the regimen. Starting low-dose topical estrogen earlier in the treatment of DIV is also reasonable. (See "Genitourinary syndrome of menopause (vulvovaginal atrophy): Treatment", section on 'Vaginal estrogen therapy'.)

Ospemifene – Oral treatment for vulvovaginal atrophy with ospemifene may be an option in appropriate patients although supporting data are lacking. (See "Genitourinary syndrome of menopause (vulvovaginal atrophy): Treatment", section on 'Ospemifene'.)

Vulvovaginal candidiasis – Patients with documented vulvovaginal candidiasis at the time of DIV diagnosis are treated. We prefer oral fluconazole 150 mg given once to minimize the use of topical treatments that may increase skin irritation. We have found that individuals with a history of confirmed frequent vulvovaginal candidiasis may also benefit from prophylaxis with oral fluconazole 150 mg given once a week. Additional supporting data are lacking.

(See "Candida vulvovaginitis in adults: Treatment of acute infection", section on 'Non-albicans Candida species'.)

(See "Candida vulvovaginitis in adults: Recurrent infection", section on 'Azole-resistant infection'.)

Address underlying cause — For individuals with secondary DIV, every effort should also be made to treat the underlying cause (eg, treat Crohn disease) or stop the drugs responsible (rituximab has been associated with DIV [14]). Failure to control identified causes is likely to result in disease chronicity. Topical medical therapy is the same for primary and secondary DIV.

TREATMENT RESPONSE AND FOLLOW-UP

Response – Treatment response is seen in three weeks in most (over 80 percent) of patients [11].

Follow-up – The patient is re-evaluated approximately four weeks after starting therapy. Based on our experience, we advise the patient to stop using the vaginal maintenance medication approximately two to three days before evaluation; trial-based data are lacking.

Remission – Remission is defined as complete resolution of microscopic findings in addition to resolution of clinical signs and symptoms. When the patient's symptoms are gone, prior physical examination findings have resolved, and microscopy shows no increase in leukocytes or parabasal cells, treatment can be stopped.

-For patients using topical corticosteroids, vaginal pH will return to normal as soon as remission is achieved.

-For patients using topical clindamycin, the drug reduces colonization by lactobacilli and thus treatment alters vaginal pH. Normal vaginal pH will return approximately one to two weeks after stopping clindamycin.

We continue to evaluate the patient monthly, for several months, to ensure that remission is maintained. Patients who do not relapse within a few months are likely to be cured, but late relapse is possible. (See 'Relapse and recurrent disease' below.)

Improvement but not remission – If the patient's symptoms and/or physical examination findings have improved but not completely resolved, treatment is continued until complete remission is achieved. Complete remission may take an additional two or more weeks of treatment. The patient is reassessed at 6- to 12-week intervals; follow-up is performed more frequently for patients with more severe symptoms or microscopy findings.

Limited or no improvement – If there has been no or minimal improvement after the initial four weeks of therapy, other diagnoses in the differential diagnosis should be reconsidered. If alternate diagnoses are again excluded, we switch to the other therapy (eg, from clindamycin to hydrocortisone or vice versa) for a four- to six-week course and then reassess for improvement.

RELAPSE AND RECURRENT DISEASE — Recurrent disease (symptomatic or not) can result from relapse of the original inflammatory process, re-exposure to triggering drugs (ie, secondary DIV), newly acquired infection (eg, bacterial vaginosis or trichomoniasis), or new or worsening vaginal atrophy.

For patients with a relapse of symptoms confirmed to be DIV, drug treatment, maintenance, and taper schedules are individually tailored as evidence-based regimens to address recurrence are lacking. Recognizing that there is no one formula, our general approach is:

Retreatment – Patients who have a relapse of disease are retreated. In our experience, the following is helpful:

Alternate therapy – The patient is treated with whichever drug was not used for the initial therapy (clindamycin instead of hydrocortisone or vice versa). The drug is used intravaginally every night and continued until complete remission is achieved. Remission typically requires four to six weeks, but longer duration may be needed. Once remission is achieved, nightly drug dosing is continued for another two to three months. As with primary treatment, remission is defined as absence of symptoms, signs, and resolution of microscopy findings.

OR

Combined therapy – For patients with refractory disease or who have multiple recurrences, another option is to use both hydrocortisone and clindamycin. Those with access to a compounding pharmacy may be able to have both compounded into a single preparation.

Remission followed by reduction of drug frequency – If remission is sustained for two to three months with nightly dosing, we then reduce the medication frequency to every other night for six to eight weeks and reassess the patient.

If remission is maintained, the dosing frequency is reduced to two nights a week for six to eight weeks and the patient is again reassessed.

If the patient continues without symptoms and there is no increase in leukocytes and/or parabasal cells on microscopy, we continue to slowly space out the dosing interval in this manner.

Symptom recurrence or microscopic evidence of disease – If symptoms occur or there is an increase in leukocytes and parabasal cells (even if the patient is asymptomatic), we increase the dosing frequency to the prior level that achieved the most recent remission. Once remission is again achieved, we then slowly taper, again at six- to eight-week intervals, to the lowest dose at which the patient remains in remission. The patient then continues at that dosing frequency and is reassessed. Follow-up visits are essential; the timing is variable and depends on disease response and patient amenability to the plan. In general, we initially assess the patient's response at 6- to 12-week intervals and then space out visits to three to six months.

Long-term suppressive therapy – Some patients require use of suppressive therapy for months or years before it is possible to discontinue therapy without relapse. Prolonged use of intravaginal clindamycin has not been associated with colitis and 10% hydrocortisone does not cause adrenal suppression. However, as safety data specific to patients with a history of C. difficile infection are lacking, we favor hydrocortisone treatment rather than clindamycin for these individuals [24]. We do not suggest routine prophylaxis against vulvovaginal candidiasis in these patients.

Lack of response – For individuals whose symptoms or microscopic findings do not respond to either clindamycin or hydrocortisone, treatment with the immunosuppressant tacrolimus is an option. Tacrolimus 0.03% (prescribed as 30 or 60 g tube) is applied sparingly into the vagina with a finger twice daily. Alternately, clobetasol 0.05% applied twice daily may be useful [23]. Once clinical remission has been achieved, the patient is reassessed in six- to eight-week intervals and the drug frequency is slowly tapered as above.

LONG-TERM PROGNOSIS — Recurrence is common after discontinuation of therapy. In one study, only one-fourth of patients remained cured at one year after a single course of therapy, and one-third of patients relapsed within six weeks of discontinuing initial treatment [11]. Treatment of these patients is discussed above. (See 'Relapse and recurrent disease' above.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Gynecologic infectious diseases (non-sexually transmitted)".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Beyond the Basics topics (see "Patient education: Vaginal discharge in adult women (Beyond the Basics)" and "Patient education: Chlamydia (Beyond the Basics)" and "Patient education: Gonorrhea (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Etiology – Desquamative inflammatory vaginitis (DIV) appears to be an inflammatory vaginitis of noninfectious etiology with secondary bacterial microbiota disruption. However, some investigators have attributed the primary defect to altered vaginal flora (eg, E. coli) and have termed the spectrum of findings "aerobic vaginitis." No consistent microbiologic pathogen has been identified except for the near absence of lactobacilli in almost all patients. (See 'Pathogenesis and epidemiology' above.)

Clinical presentation – Patients with DIV present with nonspecific findings of purulent vaginal discharge, vulvovaginal burning or irritation, dyspareunia, and vulvar and vaginal erythema. Affected individuals are often in the perimenopausal or menopausal periods. The clinical presentation is the same for primary (ie, idiopathic) and secondary (drug or immune-mediated) DIV.

(See 'Clinical presentation' above.)

(See 'Primary versus secondary DIV' above.)

Diagnostic evaluation – Individuals who present with an alteration in vaginal discharge (qualitative or quantitative) are evaluated with a history, physical examination, and appropriate laboratory tests, such as pH and microscopy. Other causes of vaginal discharge and pain, particularly infectious etiologies (eg, bacterial vaginosis and trichomoniasis), need to be excluded (algorithm 1). (See 'Diagnostic evaluation' above.)

Diagnosis – The diagnosis requires all of the following criteria (see 'Diagnosis' above):

At least one of the following symptoms: vaginal discharge, dyspareunia, pruritus, burning, irritation

Vaginal inflammation (spotted ecchymotic rash, erythema, focal or linear erosion)

Vaginal pH >4.5

Saline microscopy showing increased parabasal and inflammatory cells (ie, leukocyte to epithelial cell ratio greater than 1:1)

Differential diagnosis – DIV is a diagnosis of exclusion. The differential diagnosis includes severe atrophic vaginitis, erosive lichen planus, pemphigus vulgaris, and cicatricial pemphigoid. (See 'Differential diagnosis' above.)

Treatment – The two most common treatments are intravaginal clindamycin or glucocorticoids. Trials evaluating treatment approaches are lacking.

Medication – Treatment choice is based on patient preference, drug availability, and, for those who have previously been treated for DIV, prior treatment response. (See 'Medication for DIV' above.)

Patients with DIV are initially treated with either 2% clindamycin, 4 to 5 grams intravaginally, or 10% hydrocortisone cream, 3 to 5 grams intravaginally, at bedtime for four to six weeks. Both medications are dosed using a vaginal applicator. Some clinicians prefer clobetasol gel 0.05% 5 grams applied intravaginally at night for one week, although longer treatment is typically required in our experience.

Treat concomitant disorders – Patients with DIV may also have vulvovaginal atrophy or candidiasis; each is treated accordingly. (See 'Treat concomitant disorders' above.)

Address underlying cause – For individuals with secondary DIV, every effort should also be made to treat the underlying cause (eg, treat Crohn disease) or stop the drugs responsible (eg, rituximab). (See 'Address underlying cause' above.)

Relapse – For patients who relapse after discontinuation of primary treatment, we treat with the drug that was not used for their initial treatment (clindamycin instead of hydrocortisone or vice versa). This drug is continued until complete remission is again achieved and then tapered gradually. While the approach to taper is individualized, the process involves assessing the patient at regular intervals and reducing the dosing frequency for those in remission. (See 'Relapse and recurrent disease' above.)

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References

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