Monocyte activation in early onset rheumatoid arthritis

Article Abstract:

Rheumatoid arthritis (RA) is a joint disease characterized by the inflammation of the joints, swelling, overgrowth of cartilage tissue, and pain. To see if a specific marker for early stages of RA can be identified, 44 RA patients and 16 normal controls were evaluated. In the RA patients, monocytes, a type of white blood cell from the peripheral circulation and synovial or joint fluids, produced greater amounts of certain factors involved in inflammation. These included prostaglandin E2 (PGE2), a biologically active fatty acid; interleukin-1-beta, a factor involved in activating processes leading to tissue damage; and leucotriene B4, an inflammatory factor. Peripheral monocytes from RA patients produced greater amounts of PGE2 than those from normal subjects when activated by lipopolysaccharides (lipid and carbohydrate compounds). The amounts of PGE2 released from peripheral monocytes were greater in RA patients than healthy subjects, regardless of disease stage or extent of joint abnormalities. The release of the enzymes superoxide and N-acetyl-beta-D-glucosaminidase, which break down proteins, was similar in both normal subjects and patients. The release of N-acetyl-beta-D-glucosaminidase from peripheral monocytes of RA patients was related to decreased duration of disease and was greater among patients with RA of less than one year duration. No relationship was found between type of treatment and amounts of PGE2, LTB4, IL-1-beta or N-acetyl-beta-D-glucosaminidase released by peripheral monocytes. The results suggest that in RA, monocytes produce large amounts of factors that may be involved in inflammatory processes leading to tissue damage. (Consumer Summary produced by Reliance Medical Information, Inc.)

Monocytes

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Chain breaking antioxidant status in rheumatoid arthritis: clinical and laboratory correlates

Article Abstract:

Rheumatoid arthritis (RA) is a disease that causes inflammation of the joints. During the process of inflammation, oxygen radicals (highly reactive atoms with unpaired electrons) are generated within the joint tissue. When samples of joint tissue are grown in culture and oxygen radicals are added, the radicals damage (oxidize) and destroy the joint tissue. In this way, oxygen radicals are thought to be involved in RA. Under normal circumstances, the body makes its own proteins, called antioxidants, that inactivate oxygen radicals and prevent them from causing tissue damage. These antioxidants include specific enzymes and vitamins E and C (ascorbic acid). In order to investigate the relationship between oxygen radicals and RA, blood samples from 20 patients with RA and 20 healthy volunteers were tested for the presence of antioxidants. The levels of antioxidants (vitamin E, ascorbic acid and urate) present in the blood samples were determined by measuring the amount of protein damage that occurred following the addition of oxygen radicals to the blood. The patients with RA had lower blood levels of antioxidants than those without RA. Lower blood levels of antioxidants appeared to be related to morning joint stiffness, pain and grip strength. Also, the blood samples that contained high levels of urate were less susceptible to damage by oxygen radicals. These findings indicate that patients with RA are more susceptible to tissue damage caused by oxygen radicals than people who do not have RA. (Consumer Summary produced by Reliance Medical Information, Inc.)

Measurement, Antioxidants, Antioxidants (Nutrients), Active oxygen, Active oxygen in the body

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Serum osteocalcin concentrations in patients with rheumatoid arthritis

Article Abstract:

Rheumatoid arthritis (RA) is an inflammatory joint disease, characterized by stiffness, swelling and pain. RA is associated with generalized decalcification or loss of mineral from bone and teeth. Decalcification may result from inactivity, the use of corticosteroid drugs, or the disease process itself. In addition, an increase in bone resorption or dissolution and a decrease in bone formation may also cause the loss of bone tissue. The blood levels of osteocalcin, a bone protein produced by bone-forming osteoblast cells, provides a measure of bone formation. The blood levels of osteocalcin and other factors involved in calcium metabolism, including 25-hydroxyvitamin D, parathyroid hormone, and calcitonin, were measured in 29 patients with RA and 30 normal subjects. Osteocalcin, parathyroid hormone, and calcitonin levels were similar in the two subject groups. The steroid hormone 25-hydroxyvitamin D, which increases calcium absorption from the gut and kidney, was reduced in patients with RA as compared with normal subjects. The findings suggest that osteocalcin levels, and hence the rate of bone formation, are normal in patients with RA. (Consumer Summary produced by Reliance Medical Information, Inc.)

Research, Bones, Growth, Calcium metabolism, Bone development

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