Zusammenfassung
Kommen zu den typischen degenerativen, belastungsabhängigen Gelenkbeschwerden im höheren Lebensalter akute Arthritiden, sind diese häufig kristallinduziert. Durch die Kristalle kommt es über die Aktivierung des Immunsystems zum Auftreten von akuten Entzündungen. Neben der Gicht kommt vor allem die Kalziumpyrophosphat-Dihydrat (CPPD-)Ablagerungskrankheit in Betracht. Diagnostisch wegweisend sind bildgebende Verfahren, z. B. zeigen sich früh spezifische Veränderungen des Knorpels mittels Gelenksonographie, später sind CPPD-Kristalle als Knorpelverkalkungen (Chondrokalzinose) in Röntgenaufnahmen sichtbar. Beweisend für die Diagnose der Kristallarthropathien ist der mikroskopische Nachweis der entsprechenden Kristalle in der Synovialflüssigkeit, der den Ausschluss der septischen Arthritis ergänzt. Im Gegensatz zur Arthritis urica (Gicht), die durch die medikamentöse Harnsäuresenkung gut behandelbar ist, existieren für die CPPD-Krankheit bisher keine kausalen Therapieansätze. Da die Kalziumpyrophosphat-Ablagerung sekundär bei metabolischen Erkrankungen, z. B. bei Hyperparathyreoidismus oder Hämochromatose, auftreten kann, erscheint es aber wichtig, nach solchen Ursachen zu fahnden. Im Folgenden sollen aktuelle, praxisrelevante Erkenntnisse zu Pathogenese, Diagnostik und Therapie der CPPD-Erkrankung dargestellt werden.
Abstract
If acute arthritis occurs in the elderly in addition to typical degenerative, load-related joint complaints, this is often induced by crystal deposition. The crystals lead to activation of the immune system resulting in acute inflammation. In addition to gout, calcium pyrophosphate deposition (CPPD) disease in particular must also be taken into consideration. Diagnostically important are imaging techniques, e.g. early specific alterations of cartilage can be shown by joint sonography and later calcium pyrophosphate crystals can be detected as cartilage calcification (chondrocalcinosis) by radiography. Important for the diagnosis of crystal arthropathy is usually the microscopic detection of specific crystals in the synovial fluid and is supported by exclusion of septic arthritis by arthrocentesis. In contrast to gout, which can be well controlled by the pharmaceutical lowering of uric acid levels, there is no causal therapy for CPPD disease so far. As CPPD may occur as a secondary effect in metabolic disorders, such as hyperparathyroidism or hemochromatosis, it seems to be important to search for the underlying disease. The following article presents the current knowledge on clinically relevant aspects of the pathogenesis, diagnosis and therapy of CPPD disease.
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Einhaltung ethischer Richtlinien
Interessenkonflikt. A.-K. Tausche ist als Referentin für die Firma Berlin Chemie Menarini tätig und erhielt Beraterhonorare von Sobi, Novartis, Savient Pharmaceuticals Inc. und Ardea Bioscience Inc. M. Aringer war als Referent für die Firmen Berlin Chemie Menarini und Novartis tätig und erhielt Beraterhonorare von beiden Firmen. Dieser Beitrag beinhaltet keine Studien an Menschen oder Tieren.
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Tausche, AK., Aringer, M. Chondrokalzinose durch Kalziumpyrophosphat-Dihydrat-Ablagerung (CPPD). Z. Rheumatol. 73, 349–359 (2014). https://doi.org/10.1007/s00393-014-1364-5
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DOI: https://doi.org/10.1007/s00393-014-1364-5