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.

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.

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-␤ (TGF-␤) 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-␤ 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-␤-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-␤. 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-␤-induced COL1A2 transcription. Furthermore, in a cellular context devoid of JNK activity (i.e., JNK Ϫ/Ϫ fibroblasts), 5-FU inhibits neither formation of SMAD/DNA complexes nor SMAD-driven COL1A2 transcription in response to TGF-␤. Together, these results identify 5-FU as a potent inhibitor of TGF-␤/SMAD signaling, capable of blocking TGF-␤-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.

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