Arrese J E, Dominguez-Soto L, Hojyo-Tomoka M T, Vega-Memije E, Cortés-Franco R, Guevara E, Piérard G E
Department of Dermatopathology, University Medical Center of Liège, Belgium.
J Am Acad Dermatol. 2001 Jun;44(6):957-61. doi: 10.1067/mjd.2001.113477.
Actinic prurigo is a specific familial photodermatosis of uncertain pathogenesis.
Our purpose was to investigate the immunohistologic presentation of actinic prurigo to explore the involved pathomechanisms.
The present immunohistochemical study was performed on biopsy specimens from 20 Mexican patients presenting with a severe and perennial form of the disease.
The dense inflammatory infiltrate was composed predominantly of helper T type 1 lymphocytes admixed with scattered B-cell lymphoid follicles and numerous dermal dendrocytes. Keratinocytes contained abundant tumor necrosis factor-alpha and calprotectin.
In subjects genetically predisposed to actinic prurigo, ultraviolet light may trigger excessive tumor necrosis factor-alpha production by keratinocytes whose sustained release in turn exerts its proinflammatory activity and deleterious epidermal effects. Such a cascade of events is in line with the therapeutic benefit already reported when thalidomide is used to treat actinic prurigo.
光化性痒疹是一种发病机制不明的特殊家族性光皮肤病。
我们的目的是研究光化性痒疹的免疫组织学表现，以探索其相关发病机制。
对20例患有严重且常年性光化性痒疹的墨西哥患者的活检标本进行了本次免疫组织化学研究。
密集的炎性浸润主要由1型辅助性T淋巴细胞组成，混有散在的B细胞淋巴滤泡和大量真皮树突状细胞。角质形成细胞含有丰富的肿瘤坏死因子-α和钙卫蛋白。
在对光化性痒疹具有遗传易感性的个体中，紫外线可能触发角质形成细胞过度产生肿瘤坏死因子-α，其持续释放反过来发挥其促炎活性和有害的表皮效应。这样一系列事件与沙利度胺用于治疗光化性痒疹时已报道的治疗益处相符。
