Decreased expression of Fas (APO‐1/CD95) on lesional CD4+ T lymphocytes in cutaneous T cell lymphomas: correlations with blood data
Decreased expression of Fas (APO‐1/CD95) on lesional CD4+ T lymphocytes in cutaneous T cell lymphomas: correlations with blood data
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皮肤 T 细胞淋巴瘤病变 CD4+ T 淋巴细胞上 Fas (APO-1/CD95) 表达降低:与血液数据的相关性
DOI:
10.1046/j.1365-2133.2001.04544.x
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发表时间:
2001
影响因子:
10.3
通讯作者:
J. Guilhou
中科院分区:
文献类型:
--
作者:
O. Dereure;P. Portalès;Jacques Clot;J. Guilhou
Sir, Bowenoid papulosis is a disease presenting with fleshy, usually pigmented papules involving the genitalia of both sexes. In vulvar lesions, the term vulvar intraepithelial neoplasia (VIN3) is also used to describe the same condition. Histological examination reveals a picture consistent with carcinoma in situ, although the course of the disease appears to be benign. Association with oncogenic human papillomavirus (HPV 16, 18, 33) has been demonstrated. In the past, excisional surgery, electrocoagulation, cryotherapy and 5-fluorouracil have been used in the treatment of the condition with varying degrees of success. A 38-year-old woman was referred to our clinic with a 4-year history of pruritic skin lesions on her labia majora. She had previously been treated with podophyllin without any benefit. The molecular biological examination of the vaginal mucosa had been negative in terms of HPV typing (groups 6/11, 16/18, 31/33). However, HPV 31/33 was detected in the cervical smear (Hybrid Capture II test). Previous treatment with erbium laser, KTP 532 mm laser and podophyllin had been unsuccessful. On examination, erythema and numerous small papules were detectable on the labia minora and majora as well as in the clitoral and perianal area, each papule 1±3 mm in diameter (Fig. 1). The dermatohistopathological examination of several biopsies taken from these sites showed a uniform pattern with bowenoid epithelial changes, thus supporting the clinical diagnosis of bowenoid papulosis (Fig. 2). Treatment with imiquimod was initiated with a regimen different from that recommended for the treatment of genital warts. Imiquimod cream 5% was applied to affected areas on alternate days for 10 days until the skin became visibly irritated. The cream was now applied once daily for another 10 days, but washed off after 2 h each time. This treatment led towards complete clinical resolution within 8 weeks (Fig. 3). Histology performed 1 month, 6 months and 18 months after treatment demonstrated the absence of any precancerous epidermal changes (Fig. 4). The lympho histiocytic dermal infiltrate observed 1 month after treatment decreased in density in the control biopsies taken 6 and 18 months after treatment. Colposcopy performed 10 months after treatment showed minor acetic-white areas around the portio. No low-risk or high-risk HPV material was detected on the cervix (Hybrid Capture II test). More than 18 months after treatment the patient continues to be clinically clear. Imiquimod is a topical immune response modifier so far registered for the treatment of condylomata acuminata. Imiquimod directly induces antiviral and immunomodulating cytokines such as interferon-a, tumour necrosis factor-a and different interleukins from monocytes, macrophages and dendritic cells. Its effect on the innate immune response and the activation of Th1-immunity are responsible for its acute