Tumour necrosis factor in serum and synovial fluid of patients with active and severe rheumatoid arthritis

Article Abstract:

Rheumatoid arthritis (RA) is a chronic, inflammatory disease of the joints, and is characterized by: inflammation of the synovium, or lining, of the joint; deterioration of the cartilage tissue; bone injury; and immobility of the joints due to development of fiber-like tissue. The severity and progression of the disease process is related to the release of inflammatory factors called lymphokines and cytokines by lymphocytes and macrophages, which are cells involved in the natural defense mechanisms of the body. Lymphokines and cytokines also control the growth, development, and activity of other cells involved in the inflammatory and immune reactions. Tumor necrosis factor (TNF) is a lymphokine produced by macrophages when these cells are activated by toxic products of bacteria called endotoxins. TNF was shown to be toxic against tumor cells and may be useful in the treatment of cancer. One study reported the presence of TNF-alpha in the synovial fluid and blood of patients with RA. Furthermore, patients with TNF had higher erythrocyte sedimentation rates and white blood cell counts, which indicate increased disease activity, than RA patients without TNF. TNF is capable of activating the production of factors that enhance the inflammatory response. The levels of TNF were assessed in 15 blood samples and 29 synovial fluid samples of patients with RA. High levels of TNF were detected in the blood samples of patients with severe RA. In addition, TNF was also detected in 16 of 29 synovial fluid samples, with the highest levels of TNF being found in fluids with the most leukocytes, or white blood cells, per liter. Normal subjects and patients with osteoarthritis, another type of joint disease, did not have detectable levels of TNF. These findings suggest that an inflammatory factor such as TNF may contribute to the severity of RA. (Consumer Summary produced by Reliance Medical Information, Inc.)

Measurement, Physiological aspects, Tumor necrosis factor

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Urinary and synovial pyridinium crosslink concentrations in patients with rheumatoid arthritis and osteoarthritis

Article Abstract:

The effect of joint disease on collagen breakdown is reflected by the excretion of certain breakdown products. Hydroxylysylpyridinoline (HP) is a breakdown product of the connective tissue found in bone and lysylpyridinoline (LP) is a breakdown product of the connective tissue found in cartilage. Both are released into the blood and excreted. Urine, blood, and joint fluid samples were analyzed from 20 patients with active rheumatoid arthritis (RA) of the knee and 20 patients with osteoarthritic (OA) knees. Urinary concentrations of HP and LP were elevated in RA patients compared with OA patients. Only small amounts of HP were found in joint fluid from patients with either disease and LP was not detected at all. HP concentrations in joint fluid and urine were related in RA patients but not in OA patients. HP concentration in urine also were related to the number of swollen joints in RA patients.

Analysis, Osteoarthritis, Synovial fluid, Urine, Urinalysis

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Synovial hyaluronate in rheumatoid arthritis binds C1q and covalently bound to antibodies: a model for chronicity

Article Abstract:

The substance, hyaluronate, found in the synovium of joints, may play a role in the chronic inflammation leading to arthritis by binding to another substance known as C1q. Synovium is the membrane lining the cavity of a joint. Researchers analyzed the synovial fluid from rheumatoid arthritis patients for the presence of immune complexes which are known to bind to C1q. They found hyaluronate immune complexes in areas of C1q binding activity. Previous research has determined that hyaluronate binds to proteins in diseased joint fluid. An immune response to the joining of hyaluronate to immunoglobulin G and their bond to C1q may initiate inflammation. Inflammation may, on the other hand, cause hyaluronate to bind to immune complexes and create chronic inflammation.

Models, Joints, Joints (Anatomy), Inflammation

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