Desquamative vaginitis is a condition that resembles atrophic vaginitis, except that the individual does not have estrogen deficiency. The condition was described in 1965 by Gray and Barnes, who termed it desquamative inflammatory vaginitis because of the large numbers of white blood cells (WBC) and squamous epithelial cells present in the vaginal discharge. In 1968, Gardner described eight cases of vaginitis that resembled atrophic vaginitis, but the patients had an estrogen deficiency. Lynch, in 1975, suggested that desquamative vaginitis is a variety of lichen planus because the patient also had buccal and gingival plaque similar to that seen in lichen planus patients. Edwards and Friedrich reported five cases of desquamative vaginitis in patients with oral lesions similar to those seen with lichen planus, then suggested that desquamative vaginitis is caused by erosive lichen planus.
Clinical Presentation And Diagnosis
Desquamative inflammatory vaginitis presents with erythema of the vaginal epithelium, especially the posterior fornix and portio of the cervix. Typically the areas of erythema are a deep, fiery red with well-defined borders. Superficial ulcerations and bleeding also accompany this condition. Occasionally, a gray pseudomembrane develops over the inflamed tissue, which can be easily removed. A characteristic of these ulcerations is the development of a narrow reticulated border at the periphery of the ulcers and the presence of non-erosive lichen planus lesions found elsewhere on the skin or mucus membranes (Table Clinical characteristics of desquamative inflammatory vaginitis).
Table Clinical characteristics of desquamative inflammatory vaginitis
|Erosive diffuse vaginitis|
|Areas of hemorrhage|
|Areas of a white reticulated pattern|
|Copious green discharge|
|Vaginal adhesions might be present|
|Negative whiff tests|
|Large numbers of squamous cells and parabasal cells|
|A large number of white blood cells|
|The noticeable absence of a significant decrease in the number of lactobacilli present|
|The absence of Trichomonas vaginalis and Candida albicans|
In an attempt to determine the microbiologic etiology, Gardner cultured a variety of pathogens from patients in his case study (Table Pathogens isolated from the vagina of patients with desquamative inflammatory vaginitis in a study by Gardner). He concluded that desquamative inflammatory vaginitis was not caused by an infection because no common bacterium was isolated. However, Gardner did not have the ability to culture and identify obligate anaerobic bacteria. Sobel reported that 51 patients with desquamative inflammatory vaginitis had a diffuse exudative vaginitis, exfoliation of squamous epithelial cells, and purulent discharge. Sobel did not find a common bacterium but did note a significant decrease in Lactobacillus. These patients all had a diffuse exudative purulent vaginal discharge, an increase in the number of parabasal cells, an elevated vaginal pH, and the presence of a large number of Gram-positive cocci. The increase in vaginal pH to 5 or more is inhibitory to the growth of Lactobacillus and favors growth of the non-lactobacilli pathogenic bacteria. The presence of an overgrowth, in some patients, by Gram-positive cocci suggests that Streptococcus agalactiae might possibly be an etiologic agent.
Table Pathogens isolated from the vagina of patients with desquamative inflammatory vaginitis in a study by Gardner
|Number of patients||Pathogen|
|4||Haemophilus vaginalis iCardnerella)|
|2||Staphylococcus coagulase negative|
|7||Non-group A streptococci|
Treatment for Desquamative Vaginitis
The treatment for desquamative inflammatory vaginitis has been the use of intravaginal corticosteroids: 12.5 mg vaginal suppositories inserted twice a day for 2 months. This is followed by the administration of 12.5 mg vaginal suppositories once a day for 2 months and then maintenance therapy of 12.5 mg intravaginal suppositories one to three times a week. When Sobel treated 51 patients with 2% clindamycin intravaginal suppositories, more than 95% of his patients achieved improvement but 30% relapsed.
It appears that the etiology of desquamative vaginitis is still unknown, but the basic underlying alteration is an increase in pH that results in a decrease in the growth and presence of lactobacilli. The net result is that bacterial growth within the vagina is reduced and there is a large number of WBC. Thus, it appears that the best approach to treatment is the administration of steroids intravaginally. The steroids need to be administered for a prolonged period and tapered down once there is noticeable improvement. The patient will be required to remain on a maintenance dose for a further prolonged period. When vaginal steroids are discontinued, the patient may experience a relapse. If this occurs, steroid therapy should be reinstituted.
Selections from the book: “Vaginitis: Differential Diagnosis and Management” (2003).