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.