Artigo Acesso aberto Revisado por pares

Histochemical Responses of Human Skin Following Ultraviolet Irradiation11From the Division of Dermatology, University of Oregon Medical School, Portland, Oregon.Presented at the Twenty-second Annual Meeting of The Society for Investigative Dermatology, Inc., New York, N.Y., June 27, 1961.This work was carried out under U.S. Public Health Service, N.I.H. Grants C-5052(C1) and E-3102(C1).

1961; Elsevier BV; Volume: 37; Issue: 5 Linguagem: Inglês

10.1038/jid.1961.131

ISSN

1523-1747

Autores

Farrington Daniels, Doris Brophy, Walter C. Lobitz,

Tópico(s)

Skin Protection and Aging

Resumo

The earliest clinical evidence of a sunburn reaction in human skin is the development of erythema beginning approximately 4 hours after exposure to sufficient quantity of ultraviolet irradiation between .29 and .32 microns (1-3). The erythema reaches its maximum at approximately 24 hours (1), then gradually fades, being supplanted by a suntan. The earliest histopatho-logical change other than dilatation of dermal vessels is degeneration of scattered individual prickle cells in the outer one-half of the epidermis, first evident 24 hours after exposure (4-6). These individual cells show a shrunken, homogenized, densely-staining glassy cytoplasm, and a hyperchromic condensed pyknotic nucleus. The appearance is somewhat that of individual cell dyskeratosis. The shrunken cytoplasm is surrounded by intracellular edema since the cell margin with prickles is still apparent next to adjacent cells. Thirty to 48 hours after exposure, intercellular edema occurs around these altered prickle cells. In severe sunburn, clinical vesicula-tion appears at this time. The damaged outer one-third gradually shows more homogenization and deep staining on Giemsa and other special stains. This area is then shed without going through a granular layer. By the end of 5 days a new granular layer is beginning to reform underneath the desquamating damaged prickle cells.

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