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Aktuelle Rheumatologie 2015; 40(03): 223-226
DOI: 10.1055/s-0035-1550012
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© Georg Thieme Verlag KG Stuttgart · New York

Durch Infektionen ausgelöste Vaskulitiden

Vasculitides Secondary to Infections
W. Graninger
1   Klinische Abteilung für Rheumatologie, Medizinische Universität Graz, Graz, Austria
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Publication History

Publication Date:
18 June 2015 (online)

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Zusammenfassung

Chronische Gefäßwandentzündungen (Vaskulitiden) können durch die mit Infektionen verbundene Immunaktivierung ausgelöst werden, deren eigentliches Ziel ja die Elimination der Erreger ist. Die Vaskulitis kann auch nach der Neutralisierung des infektiösen Agens perpetuiert werden; es ist jedenfalls ratsam, zu Beginn, im Verlauf und während einer immunsuppressiven Therapie von Systemvaskulitiden nach Infektionen zu fahnden. Pathogenetisch bestehen neben der bekannten Verknüpfung von Staphylokokkus aureus und granulomatöser Polyangitis oder Hepatitis B und Panarteritis nodosa für andere „vaskulitogene“ Erreger nur Verdachtsmomente aus serologischen Daten. Neue Erkenntnisse über die Interaktionen zwischen Erregern und dem humanen Abwehrsystem ermutigen zur frühen gezielten antiinfektiven Therapie bei Systemvaskulitiden und bei infektions-getriggerten Exacerbationen unter immunsuppressiver Dauerbehandlung, sodass insgesamt eine niedrigere Gesamtmortalität erzielt wird.

Abstract

Chronic inflammation of the walls of blood vessels (vasculitis) is mediated by the host’s immune system trying to eliminate the infectious element. This reaction can be perpetuated in a destructive manner after the presence of the infectious agent, in which case an immunosuppressive treatment is necessary to avoid damage incurred by the body’s own defense system. However, detection of an infection in time can lead to a cure of the disease or at least to the termination of the erroneous reaction creating organ damage. Thus in all cases of newly proven vasculitis, “causative” or at least “associated” infections should be considered. This applies to all variants of the clinically so diverse forms of vasculitic diseases; there are notorious associations between Staphylococcus aureus and granulomatosis with polyangiitis or between polyangiitis nodosa and hepatitis B. Moreover, the perpetuation or reactivation of chronic systemic vasculitides by trivial infections deserves awareness and prophylactic strategies during immunomodulating therapies. Recent insights into the mechanisms of infection-related pathogenesis of vascular inflammatory disease could lead to better care and outcome in these rare diseases.

Schlüsselwörter

Vasculitis - pathogenese - netose - mimicry

Key words

vasculitis - pathogenesis - netosis - mimicry
 

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