Arthritis und Rheuma 2019; 39(01): 08-14
DOI: 10.1055/a-0822-0133
Schwerpunkt
© Georg Thieme Verlag KG Stuttgart · New York

Labordiagnostik bei entzündlichen Gelenkerkrankungen

Laboratory diagnostics of inflammatory joint diseases
Dr. rer. nat. Rudolf Mierau
1   ehemals: Labor an der Rheumaklinik Aachen
› Author Affiliations
Further Information

Publication History

Publication Date:
13 March 2019 (online)

Zusammenfassung

Das Labor leistet auf mehreren Gebieten Beiträge in der Primärdiagnostik entzündlicher Gelenkerkrankungen und begleitet zudem auch deren Management im Verlauf. Entzündungsparameter helfen, zwischen primär entzündlichen und nicht entzündlichen rheumatischen Erkrankungen zu unterscheiden, sind allerdings sowohl bei der rheumatoiden Arthritis (RA) als auch bei den Spondyloarthritiden nicht in jedem Fall erhöht. Autoantikörper sind bedeutende Diagnostik-Bausteine vor allem bei der RA sowie bei den Kollagenosen. Die Synovia-Analyse hilft bei der Beurteilung der Entzündungsaktivität und liefert ätiologische Hinweise z. B. bei Kristallarthropathien. Genetische Risikofaktoren für Gelenkerkrankungen sind in großer Zahl bekannt; diagnostisch verwertet wird von diesen aber nur die Bestimmung des HLA-B27-Merkmals in der Diagnostik der Spondyloarthritiden.

Abstract

The laboratory contributes in several ways to the primary diagnosis of inflammatory joint diseases and also accompanies their management during disease course. Inflammatory parameters help to distinguish between primary inflammatory and noninflammatory rheumatic diseases, but are not always elevated in both rheumatoid arthritis (RA) and spondyloarthritis. Autoantibodies are important diagnostic elements especially in RA and in connective tissue diseases. Synovial analysis aids in the assessment of inflammatory activity and provides etiologic clues, e. g. in crystal arthropathies. Genetic risk factors for joint diseases are known in large numbers; of these, however, only the determination of the HLA-B27 allele in the context of spondyloarthritides is used for diagnostic purpose.

 
  • Literatur

  • 1 Combe B, Landewé R, Daien CI. et al. 2016 update of the EULAR recommendations for the management of early arthritis.. Ann Rheum Dis 2017; 76: 948-959.
  • 2 Sokka T, Pincus T. Erythrocyte sedimentation rate, C-reactive protein, or rheumatoid factor are normal at presentation in 35 %-45 % of patients with rheumatoid arthritis seen between 1980 and 2004: analyses from Finland and the United States.. J Rheumatol 2009; 36: 1387-1390.
  • 3 Aletaha D, Neogi T, Silman AJ. et al. 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative.. Arthritis Rheum 2010; 62: 2569-2581.
  • 4 Ritchlin CT, Colbert RA, Gladman DD. Psoriatic Arthritis.. N Engl J Med 2017; 376: 957-970.
  • 5 Taylor W, Gladman D, Helliwell P. et al. Classification criteria for psori-atic arthritis: development of new criteria from a large international study.. Arthritis Rheum 2006; 54: 2665-2673.
  • 6 Rudwaleit M, van der Heijde D, Khan MA, Braun J, Sieper J. How to diagnose axial spondyloarthritis early.. Ann Rheum Dis 2004; 63: 535-543.
  • 7 Kiltz U, Rudwaleit M, Sieper J, Braun J. Evidenzbasierte Empfehlung zur Diagnostik und Therapie der axialen Spondyloarthritis.. Z Rheumatol 2017; 76: 111-117.
  • 8 Rudwaleit M, van der Heijde D, Landewé R. et al. The development of Assessment of SpondyloArthritis international Society classification criteria for axial spondyloarthritis (part II): validation and final selection.. Ann Rheum Dis 2009; 68: 777-783.
  • 9 Poddubnyy D, Rudwaleit M, Haibel H. et al. Rates and predictors of radiographic sacroiliitis progression over 2 years in patients with axial spondyloarthritis.. Ann Rheum Dis 2011; 70: 1369-1374.
  • 10 Felson DT, Smolen JS, Wells G. et al. American College of Rheumatology/European League against Rheumatism provisional definition of remission in rheumatoid arthritis for clinical trials.. Ann Rheum Dis 2011; 70: 404-413.
  • 11 Smolen JS, Landewé R, Bijlsma J. et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2016 update.. Ann Rheum Dis 2017; 76: 960-977.
  • 12 Machado P, Landewé R, Lie E. et al. Ankylosing Spondylitis Disease Activity Score (ASDAS): defining cut-off values for disease activity states and improvement scores.. Ann Rheum Dis 2011; 70: 47-53.
  • 13 Waaler E. On the occurence of a factor in human serum activating the specific agglutination of sheep blood corpuscles.. Acta Pathol Microbiol Scand 1940; 17: 172-178.
  • 14 Shmerling RH, Delbanco TL. The rheumatoid factor: an analysis of clinical utility.. Amer J Med 1991; 91: 528-534.
  • 15 Aggarwal R, Liao K, Nair R. et al. Anti-citrullinated peptide antibody assays and their role in the diagnosis of rheumatoid arthritis.. Arthritis Rheum 2009; 61: 1472-1483.
  • 16 Saraux A, Berthelot JM, Chales G. et al. Value of laboratory tests in early prediction of rheumatoid arthritis.. Arthritis Rheum (Arthritis Care Res ) 2002; 47: 155-165.
  • 17 Schellekens GA, deJong BAW, van den Hoogen FHJ. et al. Citrulline is an essential constituent of antigenic determinants recognized by rheumatoid arthritis-specific autoantibodies.. J Clin Invest 1998; 101: 273-281.
  • 18 Schellekens GA, Visser H, deJong BAW. et al. The diagnostic properties of rheumatoid arthritis antibodies recognizing a cyclic citrullinated peptide.. Arthritis Rheum 2000; 43: 155-163.
  • 19 Salvador G, Gomez A, Vinas O. et al. Prevalence and clinical significance of anti-cyclic citrullinated peptide and antikeratin antibodies in palindromic rheumatism.. An abortive form of rheumatoid arthritis? Rheumatology (Oxford) 2003; 42: 972-975.
  • 20 Cabrera-Villalba S, Gomara MJ, Canete JD. et al. Differing specificities and isotypes of anti-citrullinated peptide/protein antibodies in palin-dromic rheumatism and rheumatoid arthritis.. Arthritis Res Ther 2017; 19: 141.
  • 21 Nishimura K, Sugiyama D, Kogata Y. et al. Meta-analysis: diagnostic accuracy of anti-cyclic citrullinated peptide antibody and rheumatoid factor for rheumatoid arthritis.. Ann Intern Med 2007; 146: 797-808.
  • 22 Jansen ALMA, van der Horst Bruinsma IE, van Schaardenburg D. et al. Rheumatoid factor and antibodies to cyclic citrullinated peptide differentiate rheumatoid arthritis from undifferentiated polyarthritis in patients with early arthritis.. J Rheumatol 2002; 29: 2074-2076.
  • 23 Raza K, Breese M, Nightingale P. et al. Predictive value of antibodies to cyclic citrullinated peptide in patients with very early inflammatory arthritis.. J Rheumatol 2005; 32: 231-238.
  • 24 Kastbom A, Strandberg G, Lindroos A, Skogh T. Anti-CCP antibody test predicts the disease course during 3 years in early rheumatoid arthritis (The Swedish TIRA project).. Ann Rheum Dis 2004; 63: 1085-1089.
  • 25 van der Helm-van Mil AHM, Verpoort KN, Breedveld FC. et al. Antibodies to citrullinated proteins and differences in clinical progression of rheumatoid arthritis.. Arthritis Res Ther 2005; 7: R949-R958.
  • 26 Pratt AG, Isaacs JD, Mattey DL. Current concepts in the pathogenesis of early rheumatoid arthritis.. Best Pract Res Clin Rheumatol 2009; 23: 37-48.
  • 27 van der Helm-van Mil AHM, Huizinga TWJ. Advances in the genetics of rheumatoid arthritis point to subclassification into distinct disease subsets.. Arthritis Res Ther 2008; 10: 205.
  • 28 Padyukov L, Seielstad M, Ong RTH. et al. A genome-wide association study suggests contrasting associations in ACPA-positive versus ACPA-negative rheumatoid arthritis.. Ann Rheum Dis 2011; 70: 259-265.
  • 29 Pedersen M, Jacobsen S, Klarlund M. et al. Environmental risk factors differ between rheumatoid arthritis with and without auto-antibodies against cyclic citrullinated peptides.. Arthritis Res Ther 2006; 8: R133.
  • 30 Källberg H, Padyukov L, Plenge RM. et al. Gene-gene and gene-environment interactions involving HLA-DRB1, PTPN22, and smoking in two subsets of rheumatoid arthritis.. Am J Hum Genet 2007; 80: 867-875.
  • 31 Di Giuseppe D, Discacciati A, Orsini N, Wolk A. Cigarette smoking and risk of rheumatoid arthritis: a dose-response meta-analysis.. Arthritis Res Ther 2014; 16: R61.
  • 32 Scott IC, Tan R, Stahl D, Steer S, Lewis CM, Cope AP. The protective effect of alcohol on developing rheumatoid arthritis: a systematic review and meta-analysis.. Rheumatology (Oxford) 2013; 52: 856-867.
  • 33 Fiehn C, Holle J, Iking-Konert C. et al. S2e-Leitlinie: Therapie der rheu-matoiden Arthritis mit krankheitsmodifizierenden Medikamenten.. Z Rheumatol 2018; 77: 35-53.
  • 34 Duftner C, Dejaco C, Klauser A. et al. High positive predictive value of specific antibodies cross-reacting with a 28-kDa Drosophila antigen for diagnosis of ankylosing spondylitis.. Rheumatology (Oxford) 2006; 45: 38-42.
  • 35 Ravelli A, Varnier GC, Oliveira S. et al. Antinuclear antibody-positive patients should be grouped as a separate category in the classification of juvenile idiopathic arthritis.. Arthritis Rheum 2011; 63: 267-275.
  • 36 Bacquet-Deschryver H, Jouen F, Quillard M. et al. Impact of three anti-TNFa biologics on existing and emergent autoimmunity in rheumatoid arthritis and spondylarthropathy patients.. J Clin Immunol 2008; 28: 445-455.
  • 37 Jacob N, Jacob CO. On anti-tumor necrosis factor-induced systemic lupus erythematosus.. J Rheumatol 2010; 37: 3-5.
  • 38 Okada Y, Wu D, Trynka G. et al. Genetics of rheumatoid arthritis contributes to biology and drug discovery.. Nature 2014; 506: 376-381.
  • 39 Kirino Y, Remmers EF. Genetic architectures of seropositive and seronegative rheumatic diseases.. Nat Rev Rheumatol 2015; 11: 401-414.
  • 40 Rudwaleit M. Spondyloarthritiden.. Z Rheumatol 2017; 76: 889-903.
  • 41 Robinson WP, van der Linden SM, Khan MA. et al. HLA-Bw60 increases susceptibility to ankylosing spondylitis in HLA-B27+ patients.. Arthritis Rheum 1989; 32: 1135-1141.
  • 42 Jaakkola E, Herzberg I, Laiho K. et al. Finnish HLA studies confirm the increased risk conferred by HLA-B27 homozygosity in ankylosing spondylitis.. Ann Rheum Dis 2006; 65: 775-780.
  • 43 Kim TJ, Na KS, Lee HJ. et al. HLA-B27 homozygosity has no influence on clinical manifestations and functional disability in ankylosing spondylitis.. Clin Exp Rheumatol 2009; 27: 574-579.
  • 44 van Gaalen FA, Verduijn W, Roelen DL. et al. Epistasis between two HLA antigens defines a subset of individuals at a very high risk for ankylosing spondylitis.. Ann Rheum Dis 2013; 72: 974-978.