Zusammenfassung
Die Aufklärung der Pathogenese entzündlich rheumatischer Erkrankungen, speziell der chronischen Polyarthritis (c. P.), und damit eine an der Pathogenese orientierte Therapie, ist bis heute ein ungelöstes Problem. Grundlage derzeitig weitgehend empirisch begründeter medikamentöser Therapie ist ein am Aktivitätsstadium angepaßter Einsatz von symptomatisch wirkenden nicht-steroidalen Antirheumatika (NSAID) und Kortikosteroiden. Daneben finden Basistherapeutika mit dem Ziel Verwendung, die krankheitstypische Progredienz der Gelenkzerstörung aufzuhalten (Chloroquin [49], Gold [23, 30, 31], D-Penicillamin [60, 103, 113], Sulphasalazin [7, 128, 167], Methotrexat [104, 122, 150, 158], Azathioprin [39, 74,113,117,151,164], Cyclophosphamid [94, 139, 146, 159]). Ob jedoch dieses wesentlichste Therapieziel mit den derzeit zur Verfügung stehenden therapeutischen Mitteln tatsächlich erreicht werden kann, muß auch nach neuesten Ergebnissen weitgehend skeptisch beurteilt werden [119, 120, 131]. Nachgewiesene, therapieinduzierte Remissionen bezüglich der Progredienz ossärer Destruktionen sind eher selten, so daß häufig allenfalls mit einer Verlangsamung des Prozesses gerechnet werden kann [119]. Diese Ergebnisse sind um so ernüchternder, da oben zitierte Langzeitstudien weitgehend an rheumatologisch spezialisierten Zentren durchgeführt wurden, wo Erfahrung und eine die Prognose wesentlich mitbestimmende gute allgemeintherapeutische Infrastruktur eine überdurchschnittlich intensive Behandlung ermöglichte. Wird darüber hinaus noch in Betracht gezogen, daß diese limitierten Erfolgsaussichten durch eine hohe Therapienebenwirkungsquote belastet sind, so wird die insgesamt wenig befriedigende therapeutische Situation offensichtlich.
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Stolzenburg, T., Wilms, K. (1990). Interferone bei rheumatischen Erkrankungen. In: Niederle, N., von Wussow, P. (eds) Interferone. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-93383-7_19
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