Baranda L, Torres-Alvarez B, Cortes-Franco R, Moncada B, Portales-Perez D P, Gonzalez-Amaro R
Department of Immunology, School of Medicine, University of San Luis Potosí, Mexico City, Mexico.
Arch Dermatol. 1997 Mar;133(3):325-9.
To assess the expression of several cell adhesion and lymphocyte activation molecules in erythema dyschromicum perstans lesions, and to evaluate the effect of clofazimine therapy on the expression of these molecules.
A prospective study. Skin biopsy samples were obtained from patients before and after 3 months of clofazimine therapy, and the expression of cell adhesion and activation molecules was assessed by an immunohistochemical technique.
This study was performed in a clinical referral center and an immunology research laboratory.
We studied 6 patients with erythema dyschromicum perstans. A diagnosis was made on the basis of clinical and histological criteria. Two patients discontinued participation in the study: one because of adverse effects and the other for unknown reasons.
Patients were treated with clofazimine, 100 mg/d, for 3 months.
Expression of cell adhesion and lymphocyte activation molecules in skin biopsy specimens before and after clofazimine therapy.
Before clofazimine therapy, we detected a noticeable expression of intercellular adhesion molecule 1 and major histocompatibility complex class II molecules (HLA-DR) in the keratinocyte basal cell layer. In addition, CD36, a thrombospondin receptor that is not expressed by normal skin, was detected in the strata spinosum and granulosum. The dermal cell infiltrate expressed the activation molecule AIM/CD69 and the cytotoxic cell marker CD94. After clofazimine therapy, the expression of intercellular adhesion molecule 1 and HLA-DR disappeared, as well as the mononuclear cell infiltrate.
Our results suggest that some cell adhesion and activation molecules are involved in the pathogenesis of erythema dyschromicum perstans. Clofazimine appears to have an important effect on the inflammatory phenomenon of erythema dyschromicum perstans.
评估持久性色素异常性红斑皮损中几种细胞黏附分子和淋巴细胞活化分子的表达情况,并评价氯法齐明治疗对这些分子表达的影响。
一项前瞻性研究。在氯法齐明治疗3个月前后获取患者的皮肤活检样本,采用免疫组化技术评估细胞黏附分子和活化分子的表达。
本研究在一家临床转诊中心和一个免疫学研究实验室进行。
我们研究了6例持久性色素异常性红斑患者。根据临床和组织学标准做出诊断。两名患者退出研究:一名因不良反应,另一名原因不明。
患者接受氯法齐明治疗,100mg/d,持续3个月。
氯法齐明治疗前后皮肤活检标本中细胞黏附分子和淋巴细胞活化分子的表达。
在氯法齐明治疗前,我们在角质形成细胞基底层检测到细胞间黏附分子1和主要组织相容性复合体II类分子(HLA-DR)有明显表达。此外,在棘层和颗粒层检测到正常皮肤不表达的血小板反应蛋白受体CD36。真皮细胞浸润表达活化分子AIM/CD69和细胞毒性细胞标志物CD94。氯法齐明治疗后,细胞间黏附分子1和HLA-DR的表达消失,单核细胞浸润也消失。
我们的结果表明,一些细胞黏附分子和活化分子参与了持久性色素异常性红斑的发病机制。氯法齐明似乎对持久性色素异常性红斑的炎症现象有重要影响。