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Therapie der Hautkrankheiten pp 459–481Cite as

Lupus erythematodes und Varianten (einschließlich Überlappungssyndrome)

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Zusammenfassung

Der Lupus erythematodes (LE) ist eine Multisystemerkrankung unbekannter Ätiologie, die früher zu den sog. Kollagenosen gerechnet wurde. Grund dafür ist die fibrinoide Degeneration des Kollagens, die man histologisch häufig bei LE-Läsionen sieht. Diese Einordnung ist jedoch heute von historischer Bedeutung, da der LE keine Erkrankung des kollagenen Bindegewebes, sondern eine gegen verschiedene körpereigene Zellantigene gerichtete Regulationsstörung der zelluldren und humoralen Immunantwort ist. Daher ist die Definition „Autoimmunerkrankung“ treffender. Genetisch liegt offenbar eine Prädisposition vor, insbesondere zum SLE; angeborene Komplementdefekte (C2-, C4-Mangel bzw. Polymorphismen) gehen häufig mit einem LE einher. Histologisch findet man mittels Immunfluoreszenz die Ablagerung von Immunkomplexen an der Dermoepidermalgrenze (sog. Lupusband) oder um die dermalen Gefäße. Serologisch nachweisbar und z. T. meßbar ist die immunologische Regulationsstörung durch das Vorhandensein der diversen zirkulierenden Antikörper (s. Tabelle 19.1). Diese immunhistologischen und immunserologischen Parameter werden zur Diagnosesicherung eines LE genutzt. Darüber hinaus können sie unter Umständen auch auf den Verlauf der Erkrankung hinweisen und somit prognostischen Wert haben (s. S. 474).

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  1. Universitäts-Hautklinik und Poliklinik, Klinikum Benjamin Franklin der Freien Universität Berlin, Hindenburgdamm 30, 12200, Berlin, Deutschland

    Prof. Dr. Prof. h.c. Constantin E. Orfanos & Prof. Dr. Claus Garbe

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  1. Prof. Dr. Prof. h.c. Constantin E. Orfanos
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  2. Prof. Dr. Claus Garbe
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Orfanos, C.E., Garbe, C. (1995). Lupus erythematodes und Varianten (einschließlich Überlappungssyndrome). In: Therapie der Hautkrankheiten. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-97602-5_19

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