Plasma Cell Vulvitis: A Classification Into Two Clinical Phenotypes.

OBJECTIVE: The etiology of plasma cell vulvitis (PCV) is debated. The authors aimed to test the hypothesis that PCV could be divided into 2 clinical phenotypes. METHODS: Patients with a clinico-pathological diagnosis of PCV and with available vulvar photos seen in a vulvar clinic were retrospectively studied. The cases of PCV were divided into 2 groups: non-lichen-associated (primary PCV) and lichen-associated (secondary PCV). The 2 groups were compared in terms of age, menopausal status, location of the PCV, and 12 histologic parameters (Fisher exact test, p < .05). RESULTS: Thirty-five patients (20 primary and 15 secondary PCV) were included. The 2 groups did not differ in terms of age (mean, 65; range, 50-85) or menopausal status. Primary PCV was located exclusively on the vestibule for 19/20 patients, whereas secondary PCV was extravestibular for 14 of 15 patients, either exclusively (2) or both extravestibular and vestibular (12). One patient with secondary PCV had solely vestibular involvement. Five histological features were observed significantly more often in case of secondary PCV: epidermal atrophy, parakeratosis, dermal and epidermal neutrophils, and dermal eosinophils. CONCLUSIONS: Plasma cell vulvitis can be divided clinically into 2 phenotypes. Primary non-lichen-associated PCV is restricted to the vestibule and could be the vulvar counterpart of atrophic vaginitis. Secondary lichen-associated PCV is both extravestibular and vestibular, and its clinical and histological features should be looked for outside the PCV areas. This division of PCV into 2 clinical phenotypes could have therapeutic implications.

Are virtual consultations suitable for patients with vulval disease? A multicentre audit of outcomes in the COVID-19 pandemic.

Background: During the COVID-19 pandemic, virtual consultation (VC) was used to replace in-person consultations. This raises specific questions when dealing with vulval conditions. Objectives: To assess the feasibility and the efficiency of VC with and without supplementary imaging, in patients with vulval conditions, and to evaluate the images provided as an aid to diagnosis. Methods: This prospective multicentre audit took place in three specialized vulval clinics in London and Paris. Anonymized data on patients' clinical characteristics, consultation characteristics (including the number and quality of any supplementary images provided) and consultation outcomes (diagnostic certainty and physician satisfaction) were collected. Characteristics and outcomes in those with or without supplementary imaging were compared amongst both new and follow-up consultations. Results: A total of 316 VCs were included. In total, 18.7% (n = 59) were new patient consultations and 81.3% (n = 257) were follow-up. Supplementary imaging (photographs and/or video recordings) were provided by 28.5% (n = 90) of the total cohort. Median photographic quality was significantly higher on a five-point Likert-type scale when photographs were taken by a third party as opposed to the patient themselves (4 vs. 3, Mann-Whitney U-test, p < 0.0001). There was no association between the provision of supplementary imaging and diagnostic certainty amongst new patient consultations. However, a higher proportion of follow-up patients who provided supplementary imaging received definitive management decisions (χ 2 test, p < 0.001) and physician satisfaction with these consultations, as measured on a five-point Likert-type scale, was significantly higher (Mann-Whitney U-test, p < 0.0001). Furthermore, median physician satisfaction scores ≥4 were observed in follow-up consultations for candidiasis, lichen simplex/eczema and vulvodynia. Conclusions: Although in-person consultation remains the gold standard of care, VC may have a role in the management of selected patients with vulval disease. It is possible to provide good-quality photographs for clinical assessment, particularly with the help of a third party and follow-up patients with an established, cancer-unrelated diagnosis may be best suited for this consultation modality.

Vulvar dermatosis.

Vulvar dermatoses are inflammatory conditions responsible for chronic or recurrent itching and soreness. The lesions are either circumscribed to the vulva or associated with extragenital localizations which may help to assess the diagnosis. They should be differentiated from infectious or neoplastic diseases which may have clinical similarities. As opposed to the majority of all dermatoses that have a benign and regular course, lichen sclerosus or lichen planus could exceptionally foster the occurrence of an epithelial cancer precursor which may evolve to squamous cell carcinoma. Topical corticosteroids are the mainstay treatment of vulvar dermatosis. We do not know if the treatment of vulvar lichen sclerosus and vulvar lichen planus prevents squamous cell carcinoma.

Non-sexually related acute genital ulcers in 13 pubertal girls: a clinical and microbiological study.

OBJECTIVE: To describe the clinical and microbiological features of acute genital ulcers (AGU), which have been reported in virgin adolescents, predominantly in girls. DESIGN: Descriptive study. We collected data on the clinical features, sexual history, blood cell count, biochemistry, microbiological workup, and 1-year follow-up. SETTING: Departments of dermatology of 3 university hospitals in Paris. Patients Thirteen immunocompetent female patients with a first flare of non-sexually transmitted AGU. MAIN OUTCOME MEASURES: Clinical and microbiological data, using a standardized form. RESULTS: Mean age was 16.6 years (range, 11-19 years). Eleven patients denied previous sexual contact. A fever or flulike symptoms preceded AGU in 10 of the 13 patients (77%), with a mean delay of 3.8 days before the AGU onset (range, 0-10 days). The genital ulcers were bilateral in 10 patients. The final diagnosis was Epstein-Barr virus primary infection in 4 patients (31%) and Behçet disease in 1 patient (8%). No other infectious agents were detected in this series. CONCLUSIONS: We recommend serologic testing for Epstein-Barr virus with IgM antibodies to viral capsid antigens in non-sexually related AGU in immunocompetent patients. Further microbiological studies are required to identify other causative agents.

Treatment of undifferentiated vulvar intraepithelial neoplasia with 5% imiquimod cream: a prospective study of 12 cases.

OBJECTIVE: To assess the efficacy of 5% imiquimod cream on undifferentiated vulvar intraepithelial neoplasia (VIN), a disease caused by high-risk human papillomavirus. DESIGN: Prospective, uncontrolled study. SETTING: University hospital vulvar clinic. Patients Twelve consecutive patients treated with 5% imiquimod cream for undifferentiated VIN between March 1, 1999, and May 31, 2001. INTERVENTION: Self-application of 5% imiquimod cream, initially 3 times a week, then adjusted according to tolerance, for up to 7 months according to clinical response. MAIN OUTCOME MEASURES: Therapeutic response, clinically assessed by successive photographs and histologically confirmed for complete responders, was scored as complete, partial (> or =50% decrease in lesion size), or failure. Tolerance was evaluated at each visit. RESULTS: A total of 3, 4, and 5 patients achieved complete response, partial response (> or =75% reduction in lesion size for all such cases), and failure, respectively. Mean duration of treatment was 3.6 months (37.3 applications), 5.0 months (50.7 applications), and 3.4 months (25.2 applications) for complete responders, partial responders, and failures, respectively. Follow-up after treatment was 5 to 18, 14 to 32, and 2 to 28 months, respectively, with 1 partial responder lost to long-term follow-up. No patient developed invasive carcinoma. All but 2 patients experienced vulvar discomfort, resulting in treatment withdrawal for 3. Two patients had flulike symptoms. CONCLUSIONS: Imiquimod cream could be a therapeutic option for undifferentiated VIN. Although poorly tolerated, this self-applied treatment could spare patients, either totally or partially, the classic painful and sometimes mutilating treatments of VIN. Controlled, randomized studies are needed to evaluate its efficacy and tolerance.

5-fluorouracil blocks transforming growth factor-beta-induced alpha 2 type I collagen gene (COL1A2) expression in human fibroblasts via c-Jun NH2-terminal kinase/activator protein-1 activation.

5-Fluorouracil (5-FU), a pyrimidine analog widely used in cancer chemotherapy and in glaucoma surgery, has recently shown some efficacy in the treatment of keloids, scars that overgrow the boundaries of original wounds. Given the physiopathological importance of transforming growth factor-beta (TGF-beta) in keloid and scar formation, we have examined whether the clinical benefits from 5-FU treatment may result from its capacity to interfere with TGF-beta signaling and resulting activation of type I collagen gene expression. Using various molecular approaches to study the mechanisms underlying 5-FU effects, we have demonstrated that 5-FU antagonizes TGF-beta-driven COL1A2 transcription and associated type I collagen production by dermal fibroblasts. In addition, 5-FU inhibits both SMAD3/4-specific transcription and formation of SMAD/DNA complexes induced by TGF-beta. 5-FU induces c-Jun phosphorylation and activates both AP-1-specific transcription and DNA binding. Overexpression of an antisense c-jun expression vector, or that of a dominant-negative form of MKK4 that interferes with c-Jun N-terminal kinase (JNK) activation, blocks the inhibitory activity of 5-FU on TGF-beta-induced COL1A2 transcription. Furthermore, in a cellular context devoid of JNK activity (i.e., JNK-/- fibroblasts), 5-FU inhibits neither formation of SMAD/DNA complexes nor SMAD-driven COL1A2 transcription in response to TGF-beta. Together, these results identify 5-FU as a potent inhibitor of TGF-beta/SMAD signaling, capable of blocking TGF-beta-induced, SMAD-driven up-regulation of COL1A2 gene expression in a JNK-dependent manner. We thus provide a molecular explanation to the observed clinical benefits of 5-FU in the treatment of keloids and hypertrophic scars.