Ive et al. in 1969 (13) first described actinic reticuloid (AR) as a chronic dermatosis associated with severe photosensitivity and bearing a clinical and histological resemblance to malignant lymphoma, especially to Sezary syndrome. Nowadays, AR
Figure 6 Eczema-like red and scaly infiltration of the sun-exposed skin.
belongs to the group of so-called chronic actinic dermatitis. The clinical presentation is an eczematous and infiltrative dermatitis on light exposed areas with marked thickening and ridging of the skin (Fig. 6). In contrast to Sezary syndrome, nonex-posed and palmoplantar areas are not involved.
Histologically, there is a dense infiltrate of lymphocytes mixed with many polyclonal plasma cells, eosinophils, and macrophages. Pathogenetically, AR in most cases primarily is a photoallergic process due to various photosensitizers activated over a wide spectrum of wavelengths. The process persists in typical cases even after removal of the photosensitizer possibly due to the generation of self-antigens. Gene rearrangement analysis, in combination with immunohistochemistry, may be an important adjunct in differentiating between AR and cutaneous T-cell lymphoma (14).
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