Dtsch Med Wochenschr 2018; 143(16): 1157-1166
DOI: 10.1055/a-0504-5684
Dossier
© Georg Thieme Verlag KG Stuttgart · New York

Gicht und Calciumpyrophosphat-Dihydrat-Arthropathie („Pseudogicht“) – ein Update

Update on Gout and Calcium pyrophosphate deposition (CPPD)
Monika Reuss-Borst
,
Anne-Kathrin Tausche
Further Information

Publication History

Publication Date:
07 August 2018 (online)

Abstract

The metabolic diseases gout and calciumpyrophosphate deposition (CPPD) (formerly: chondrocalcinosis/pseudogout) are crystal arthropathies which are caused by crystals in synovial fluid and in the case of gout also in periarticular structures. Today, in particular gout is considered as an auto-inflammatory process since phagocytosis of monosodium urate crystals by monocytes/macrophages results in the activation of the innate immune system by activation of the NRLP3-Inflammasome and consecutive secretion of the key cytokine interleukin-1ß and other pro-inflammatory cytokines. The prevalence of both crystal arthropathies rises with increasing age of patients. Most often they present clinically as an acute monarthritis of different locations. Beside typical clinical presentation, performance of ultrasonography, conventional X-Ray of joints and under special circumstances dual-energy-computer tomography could be also helpful diagnostic tools. There are EULAR guidelines describing the diagnostic algorithm for making right diagnosis. The arthrocentesis with microscopic detection of crystals is established diagnostic gold standard. Whereas crystals of monosodium urate could be very clearly be seen as relatively large intra- and extracellular needles with a strong birefringence in polarized light microscopy the detection of CPPD-crystals is more difficult. Those crystals are much smaller, showing weaker birefringence and are sometimes only seen with ordinary light microscopy. As both crystal diseases are mediated by IL-1 driven processes, the therapeutic intervention first target the acute inflammation consisting in colchicine, NSAIDs and glucocorticoids. Secondarily, in gout there are well established causal therapies to lower effectively serum urate levels below the target of 6 mg/dL (360 µmol/l). Unfortunately, those causal therapeutic options are still lacking in CPPD.

Der Gichtanfall und die akute Calciumpyrophosphat-Dihydrat (CPPD) -Arthritis (früher als Pseudogicht bezeichnet) sind hochentzündliche, meist akut auftretende Arthritiden. Klinisch manifestieren sie sich überwiegend als akut auftretende Monarthritis, wobei die CPPD-Arthritis eher größere Gelenke betrifft. Da beide Erkrankungen auch koinzident auftreten können, kann die differenzialdiagnostische Unterscheidung schwierig sein.

 
  • Literatur

  • 1 Tausche AK, Aringer M. Die Gicht. Z Rheumatol 2016; 75 (09) 885-898
  • 2 Dalbeth N, Merriman TR, Stamp LK. Gout. Lancet 2016; 388: 2039-2052
  • 3 Pascual E, Sivera F. Time required for disappearance of urate crystals from synovial fluid after successful hypouricaemic treatment relates to the duration of gout. Ann Rheum Dis 2007; 66 (08) 1056-1058
  • 4 Chowalloor PV, Keen HI. A systematic review of ultrasonography in gout and asymptomatic hyperuricemia. Ann Rheum Dis 2013; 72: 638-645
  • 5 Reuss-Borst MA, Pape CA, Tausche AK. Hidden gout – ultrasound findings in patients with musculo-skeletal problems and hyperuricemia. Springerplus 2014; 9: 592
  • 6 Johnson RJ, Gaucher EA, Sautin YY. et al. The planetary biology of ascorbate and uric acid and their relationship with the epidemic of obesity and cardiovascular disease. Med Hypotheses 2008; 71: 22-31
  • 7 Feig DI, Soletsky B, Johnson RJ. Effect of allopurinol on blood pressure of adolescents with newly diagnosed essential hypertension: a randomized trial. JAMA 2008; 300: 924-932
  • 8 Shiozawa A, Szabo SM, Bolzani A. et al. Serum uric acid and the risk of incident and recurrent gout: a systematic review. J Rheumatol 2017; 44: 388-396
  • 9 Köttgen A, Albrecht E, Teumer A. et al. Genome-wide association analyses identify 18 new loci associated with serum urate concentrations. Nat Gen 2013; 45: 145-154
  • 10 Choi HK, Atkinson K, Karlson EW. et al. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med 2004; 350: 1093-1103
  • 11 Choi HK, Atkinson K, Karlson EW. et al. Alcohol intake and risk of incident gout in men: a prospective study. Lancet 2004; 363: 1277-1281
  • 12 Reuss-Borst M, Tausche AK. Stoffwechselkrankheit Gicht. Akt Rheumatol 2018 (in press)
  • 13 Kiltz U, Alten R, Fleck M. et al. Langfassung zur S2e-Leitlinie Gichtarthritis (fachärztlich) – Evidenzbasierte Leitlinie der Deutschen Gesellschaft für Rheumatologie (DGRh). Z Rheumatol 2016; 75: 11-60
  • 14 Janssens HJ. et al. A diagnostic rule for acute gouty arthritis in primary care without joint fluid analysis. Arch Intern Med 2010; 170 (13) 1120-1126
  • 15 Richette P, Doherty M, Pascual E. et al. Updated EULAR evidence-based recommendations for gout. Ann Rheum Dis 2017; 76: 29-42
  • 16 Taylor TH, Mecchella JN, Larson RJ. et al. Initiation of allopurinol at first medical contact or acute attacks of gout: a randomised clinical trial. Am J Med 2012; 125 (11) 1126-1134
  • 17 Zhang W, Doherty M, Bardin T. et al. EULAR recommendations for calcium phyrophosphate deposition. Part 1: terminology and diagnosis. Ann Rheum Dis 2011; 70 (04) 563-570
  • 18 Manger B. Gout and other crystal-induced arthritides. Dtsch Med Wochenschr 2012; 137: 1579-1581
  • 19 Fuerst M, Bertrand J, Lammers L. et al. Calcification of articular cartilage in human osteoarthritis. Arthritis Rheum 2009; 60: 2694-2703
  • 20 Zhang W, Doherty M, Pascual E. et al. EULAR recommendations for calcium pyrophosphate deposition. Part II: management. Ann Rheum Dis 2011; 70 (04) 571-575