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 zellulären und humoralen Immunantwort ist. Daher ist die Definition „Autoimmunerkrankung“ treffender. Genetisch liegt offenbar eine Prädisposition vor, insbesondere zum systemischen LE (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.
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Orfanos, C.E., Garbe, C. (2002). Lupus erythematodes und verwandte Immunopathien einschließlich Überlappungssyndromen. In: Blume-Peytavi, U., et al. Therapie der Hautkrankheiten. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-56219-8_21
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