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[Update on Gout and Calcium pyrophosphate deposition (CPPD)].
Dtsch Med Wochenschr. 2018 Aug; 143(16):1157-1166.DM

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-1β 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.

Authors

No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

ger

PubMed ID

30086561

Citation

Reuss-Borst, Monika, and Anne-Kathrin Tausche. "[Update On Gout and Calcium Pyrophosphate Deposition (CPPD)]." Deutsche Medizinische Wochenschrift (1946), vol. 143, no. 16, 2018, pp. 1157-1166.
Reuss-Borst M, Tausche AK. [Update on Gout and Calcium pyrophosphate deposition (CPPD)]. Dtsch Med Wochenschr. 2018;143(16):1157-1166.
Reuss-Borst, M., & Tausche, A. K. (2018). [Update on Gout and Calcium pyrophosphate deposition (CPPD)]. Deutsche Medizinische Wochenschrift (1946), 143(16), 1157-1166. https://doi.org/10.1055/a-0504-5684
Reuss-Borst M, Tausche AK. [Update On Gout and Calcium Pyrophosphate Deposition (CPPD)]. Dtsch Med Wochenschr. 2018;143(16):1157-1166. PubMed PMID: 30086561.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Update on Gout and Calcium pyrophosphate deposition (CPPD)]. AU - Reuss-Borst,Monika, AU - Tausche,Anne-Kathrin, Y1 - 2018/08/07/ PY - 2018/8/8/entrez PY - 2018/8/8/pubmed PY - 2018/8/21/medline SP - 1157 EP - 1166 JF - Deutsche medizinische Wochenschrift (1946) JO - Dtsch Med Wochenschr VL - 143 IS - 16 N2 - 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-1β 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. SN - 1439-4413 UR - https://www.unboundmedicine.com/medline/citation/30086561/[Update_on_Gout_and_Calcium_pyrophosphate_deposition__CPPD_]_ DB - PRIME DP - Unbound Medicine ER -