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[Update on Gout and Calcium pyrophosphate deposition (CPPD)].

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    Deutsche Medizinische Wochenschrift (1946)
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    Gout and CPPD are crystal-induced inflammatory arthritis. Gout involves monosodium urate crystals activating the NLRP3-Inflammasome, while CPPD crystals are harder to detect. Both are treated with anti-inflammatories, but only gout has causal therapies.

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    Area of Science:

    • Rheumatology
    • Immunology
    • Crystal Arthropathies

    Background:

    • Gout and calcium pyrophosphate deposition (CPPD) are crystal arthropathies causing joint inflammation.
    • Gout is increasingly viewed as an autoinflammatory process driven by monosodium urate crystal-induced NLRP3-Inflammasome activation and IL-1ß secretion.
    • Both conditions increase with age and often present as acute monarthritis.

    Purpose of the Study:

    • To review the pathogenesis, diagnosis, and treatment of gout and CPPD.
    • To highlight diagnostic challenges, particularly for CPPD crystals.
    • To discuss current therapeutic strategies for acute inflammation and underlying causes.

    Main Methods:

    • Review of current literature and EULAR diagnostic guidelines.
    • Discussion of diagnostic tools including ultrasonography, X-ray, dual-energy CT, and arthrocentesis.
    • Microscopic crystal identification using polarized and ordinary light microscopy.

    Main Results:

    • Monosodium urate crystals are large, needle-shaped, and strongly birefringent.
    • CPPD crystals are smaller, weakly birefringent, and more challenging to detect.
    • Both conditions involve IL-1 driven inflammation, treated with colchicine, NSAIDs, or glucocorticoids.

    Conclusions:

    • Effective causal therapies exist for gout to lower serum urate levels.
    • Causal therapeutic options for CPPD remain limited.
    • Further research is needed for targeted CPPD therapies.