Marked papillary dermal edema - An unreliable discriminator between polymorphous light eruption and lupus erythematosus or dermatomyositis
Department of Pathology, University of California, San Francisco, San Francisco, CA 94115, USA. Journal of Cutaneous Pathology
(Impact Factor: 1.58).
04/2010; 37(4):416-25. DOI: 10.1111/j.1600-0560.2010.01516.x
The clinical differential diagnosis of photo-distributed papules and plaques includes polymorphous light eruption (PMLE) and lupus erythematosus (LE). These entities share many histopathological features. However, in most contemporary textbooks, a broad band of papillary dermal edema is reported to be characteristic of PMLE and not seen in LE. Nonetheless, older reports describe papillary dermal edema in LE, including acute cutaneous LE (ACLE) in patients with systemic LE (SLE) and early lesions of discoid lupus erythematosus (DLE). Older reports also describe papillary dermal edema in microscopic sections of dermatomyositis (DM).
Nine cases of LE (including two patients with acute lesions of SLE, six with DLE and one unclassifiable) and three cases of DM were identified in which sections showed striking papillary dermal edema. Attributes of chronicity, such as epidermal atrophy, follicular plugging and basement membrane thickening, were present concurrently in many sections.
Marked papillary dermal edema does not reliably distinguish PMLE from LE as it can be seen in ACLE, early and late lesions of DLE and DM. This phenomenon has been underemphasized in recent reports and textbooks. Furthermore, papillary dermal edema in chronic lesions of DLE has not been previously reported.
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ABSTRACT: Skin lesions are the most visible and frequent symptoms in lupus erythromatosus (LE). These lesions vary greatly in their clinical as well as microscopic features, which difficults the understanding and study of LE. Most of the patients that express skin disease do not suffer from serious systemic complications, but from important morbidity given the extension, chronicity, chances of scarring and disfigurement that skin lesions may cause. The exact pathogenic mechanisms that induce the development of skin lesions in LE are unknown at present; however, ultraviolet (UV) radiation could play an important role. UV- induced keratinocyte apoptosis as well as proinflammatory stimuli release because of uncomplete apoptotic cell clearance may be the pillars of the etiology of this skin disease. Nonetheless, there are still many questions to answer. The treatment consists of photoprotection, topical administration of corticoids as well as oral administration of antimalarial drugs.
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