Joint inflammation

Sergejeva S, Ivanov S, Lotvall J, Linden A Interleukin-17 as a recruitment and survival factor for airway macrophages in allergic airway inflammation. Am J Respir Cell Mol Biol 2005 33 248-253. 96 Bush KA, Farmer KM, Walker JS, Kirkham BW Reduction of joint inflammation and bone erosion in rat adjuvant arthritis by treatment with interleukin-17 receptor IgGl Fc fusion protein. Arthritis Rheum 2002 46 802-805. 

Signs of joint inflammation are present (tenderness, warmth, swelling, and erythema). 

Choy EH, Panayi GS. Cytokine pathways and joint inflammation in rheumatoid arthritis. N Engl J Med 2001 344( 12) 907—916. Cronstein BN. Low-dose methotrexate A mainstay in the treatment of rheumatoid arthritis. Pharmcol Rev 2005 57(2) 163—172. 

NSAIDs are a reasonable alternative when acetaminophen fails to provide an acceptable analgesic response. Some authorities recommend NSAIDs over acetaminophen for patients presenting with severe pain or signs and symptoms of inflammation, but this is a matter of much contention. The rationale for this recommendation is that acetaminophen s central mechanism of action renders it ineffective against peripheral joint inflammation, and therefore, less effective.18 Consensus guidelines support the use of NSAIDs as an alternative to acetaminophen if clinical features of peripheral inflammation or severe pain are detected.11,12 Unfortunately there is no validated mechanism to identify patients who are more likely to respond to NSAIDs than acetaminophen. 

Ellingsen T, Buus A, Stengaard-Pedersen K. Plasma monocyte chemoattractant protein 1 is a marker for joint inflammation in rheumatoid arthritis. J Rheumatol... 

Matthys P, Hatse S, Vermeire K, et al. AMD3100, a potent and specific antagonist of the stromal cell-derived factor-1 chemokine receptor CXCR4, inhibits autoimmune joint inflammation in IFN-gamma receptor-deficient mice. J Immunol 2001 167(8) 4686-4692. 

Rheumatoid arthritis (RA) is an inflammatory disease of the synovium which results in erosion, deformity and finally the destruction of joints. Inflammation of the joints is associated with a villous hypertrophy of the synovial membrane, which on microscopy shows proliferation of the lining layer with an inflammatory infiltrate. There is extensive expression of HLA-... 

This disorder is characterized by hyperuricemia with recurrent attacks of acute arthritic joint inflammation, caused by deposition of uric acid crystals. 

Matsuda Y, Yamanaka H, Higami K, Kashiwazaki S (1998) Time lag between active joint inflammation and radiological progression in patients with early rheumatoid arthritis. J Rheumatol 25(3) 427—432... 

Choy EH, Pnaayi GS. 2001. Cytokine pathways and joint inflammation in rheumatoid arthritis. NEJM. 344 907-916. 

Mechanism of Action. Leflunomide acts primarily by inhibiting the synthesis of RNA precursors in lymphocytes.65,70 When stimulated, lymphocytes must radically increase their RNA synthesis to proliferate and become activated during the inflammatory response. Leflunomide blocks a key enzyme responsible for RNA synthesis, so that these lymphocytes cannot progress to a more activated state and cannot cause as much joint inflammation.58,107... 

Yagnik DR, Hillyer P, Marshall D, Smythe CDW, Krausz T, Haskard DO, Landis RC. Noninflammatory phagocytosis of monosodium urate monohydrate crystals by mouse macrophages. Implications for the control of joint inflammation in gout. Arthritis and Rheumatism 2000, 43, 1779-1789. 

In the study of SLE patients, we and other authors have found that there is a correlation between SLE disease activity index (SLEDAI) and the production of IL-16 (L7) and IL-18 (W19). It was suggested that IL-16 and IL-18 may be a useful indicator of disease activity of SLE. Plasma MCP-1 concentration has also been proposed as a marker for monitoring joint inflammation in rheumatoid arthritis (El). 

Van den Berg, W. B. (1998). Joint inflammation and cartilage destruction may occur uncoupled. Springer Semin. Immunopathol. 20, 149—164. 

Reduces joint inflammation and erosion in murine collagen-induced arthritis [169]... 

A histogram of the above data (Figure 2.4) shows the difficulty we are going to have. Most of the patients have shown reduced joint inflammation, but there are two distinct sub-populations so far as side effects are concerned. Slightly under half the patients are relatively free of side effects, so their quality of life improves markedly, but for the remainder, side effects are of such severity that their lives are actually made considerably worse overall. 

Kim HY, Kim S, Chung DH. FcgammaRIII engagement provides activating signals to NKT cells in antibody-induced joint inflammation. J Clin Invest 2006 116 2484-92. 

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