Abstract
Inflammation and hyperuricemia drive the gout cascade. Understanding of the role of inflammation, including involvement of the innate immune system, helps to improve the diagnosis and therapeutic course of the disease. Treatment of acute and chronic gouty inflammation is of utmost importance in preventing long-term disability. In this chapter, we discuss the clinical presentation of gout and its diagnosis, immunopathogenesis, and treatment. The anti-inflammatory therapies used to combat gouty inflammation are highlighted.
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Abbreviations
- ACP:
-
American College of Physicians
- ACR:
-
American College of Rheumatology
- ACTH:
-
Adrenocorticotropic hormone
- DAMP:
-
Damage-associated molecular patterns
- DECT:
-
Dual-energy computed tomography
- EULAR:
-
European League Against Rheumatism
- FDA:
-
Food and Drug Administration
- IL:
-
Interleukin
- MSU:
-
Monosodium urate
- MTP:
-
Metatarsophalangeal
- NLRP3:
-
NACHT, LRR and PYD domains-containing protein 3
- NSAID:
-
Non-steroidal anti-inflammatory drugs
- SU:
-
Serum urate
- TA:
-
Triamcinolone acetonide
- TLR:
-
Toll-like receptor
- TNF:
-
Tumor necrosis factor
- URL:
-
Urate lowering therapy
- US:
-
Ultrasound
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Schlesinger, N., Kay, J.C. (2019). Gouty Inflammation. In: Hashkes, P., Laxer, R., Simon, A. (eds) Textbook of Autoinflammation. Springer, Cham. https://doi.org/10.1007/978-3-319-98605-0_34
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DOI: https://doi.org/10.1007/978-3-319-98605-0_34
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