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Query: UMLS:C0003873 (rheumatoid arthritis)
 53,068 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphological changes in the pulmonary artery and its major branches were studied histologically and histochemically on autopsy cases of polyarteritis nodosa (23), systemic lupus erythematosus (10), systemic scleroderma (12), and rheumatoid arthritis (5). The ages of the fatalities ranged from 9 months to 77 years. An identical type of lesions was revealed: disorders of the connective tissue, destruction of elastic fibers, alterations of vasa vasorum, with cellular reactions typical of each nosological form reflecting the peculiarities of the immunological processes. The initial stage in the genesis of lesions in the vascular walls of the major pulmonary arteries is the involvement of vasa vasorum as a regular disorder of the microcirculatory ways in all collagen diseases.
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PMID:[Changes in the pulmonary artery in collagen diseases]. 3 80

A passive hemagglutination assay was used to detect antibodies to native human collagens and to collagen chains in the sera of 110 rheumatoid patients and those of 75 normal controls. The incidence and titer of anticollagen antibodies in rheumatoid arthritis are high, but in controls they are low or in most instances absent. No correlation was found between the stage of RA, or titers of rheumatoid factor, or ANA and the incidence and/or titers of antibody to any given type of collagen.
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PMID:Antibodies to native and denatured collagens in sera of patients with rheumatoid arthritis. 5 2

To elucidate the mechanism of synovial damage in rheumatoid arthritis, we studied the activation of latent collagenases released from adherent rheumatoid synovial cells in culture. Latent enzyme was not complexed with alpha2 macroglobulin, the prinicpal proteinase inhibitor in serum, and could be activated by trypsin in the presence of alpha2 macroglobulin if sufficient proteinase was added to saturate inhibitor. Latent collagenase bound half as effectively to collagen fibrils as active enzyme. Plasmin was a threefold better activator of latent enzyme than trypsin and could be generated by addition of plasminogen to synovial-cell cultures. Production of both collagenase and plasminogen activator was inhibited by dexamethasone (10(-9) M). These studies emphasize in importance of control of activation in regulation collagenase activity, It is likely that rheumatoid synovium produces both latent collagenase and plasminogen activator; plasmin is activated from its zymogen, plasminogen, present in inflamed tissues, and in turn activates collagenase.
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PMID:Endogenous activation of latent collagenase by rheumatoid synovial cells. Evidence for a role of plasminogen activator. 6 27

Articular cartilage from thirteen patients with rheumatoid arthritis was studied by both light and electron microscopy using recently developed staining techniques for proteoglycan. Normally proteoglycan is concentrated about active chondrocytes, but in the cartilage from these patients it was found to be diminished about most of the chondrocytes while it was increased around a few. Fragmentation of collagen and phagocytosis of the fragments by chondrocytes were also noted. This dissolution of collagen was associated with loss of proteoglycan in the matrix. These findings are consistent with the variable nature of the rheumatoid destructive process and appear to be morphological reflections of biochemical changes which formerly were thought to occur in this disease only at the cartilage-pannus junction.
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PMID:Changes in proteoglycan and collagen in cartilage in rheumatoid arthritis. 7 75

This paper examines the extent to which understanding of six of the principle disorders of connective tissue: the glycosaminoglycan storage diseases, ankylosing spondylitis, rheumatoid arthritis, systemic lupus erythematosus, chondrocalcinosis, and osteoarthrosis, has progressed during the past ten years. The paper recalls the pioneer observations of PAUL KLEMPERER on the systemic diseases of collagen, and introduces a series of reviews in which advances in present understanding of some of the connective tissue diseases will be examined in greater detail.
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PMID:New knowledge of the connective tissue diseases I. 12 Mar 50

Explants of articular cartilage from young pigs were maintained in organ culture for 10--16 days, and degradation of matrix was induced by retinol or complement-sufficient antiserum. The percentage breakdown of proteoglycan and collagen (as hydroxyproline release) was measured. The response of the cartilage depended on whether or not the explants were cut so as to include some of the invading marrow ('invasion zone'). In media containing retinol, cartilage lost up to three-quarters of its proteoglycan whether the invasion zone was present or not, but very little of its collagen unless this region was included. In the presence of complement-sufficient anti-serum, however, cartilage without the invasion zone was virtually unaffected, but both proteoglycan and hydroxyproline were released when invasion zone was included; here proteoglycan release began almost immediately, but there was a time-lag of 6--8 days before a substantial amount of hydroxyproline appeared in the medium. Histological examination of sample explants from the experiments supported the biochemical findings. The possible significance of the results in relation to rheumatoid arthritis is discussed.
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PMID:Breakdown of proteoglycan and collagen induced in pig articular cartilage in organ culture. 12 55

41 compounds, anti-inflammatory agents, acid mucopolysaccharides, and other substances were investigated in vitro for their ability to influence the formation of collagen fibrils. The acid anti-inflammatory agents accelerated the formation of collagen fibrils partially, acid mucopolysaccharides inhibited it. The results are discussed regarding the effects exhibited by anti-inflammatory agents and mucopolysaccharides in rheumatoid arthritis and osteo-arthrosis.
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PMID:[Influence of antiphlogistics, antireheumatics, and acid mucopolysaccharides on in-vitro collagen fibril formation]. 13 17

We sought to explore immunological factors in patients who died with rapidly fatal fibrosing lung diseases (Hamman-Rich syndrome). A retrospective review of cases of interstitial lung disease showed 12 recent deaths from Hamman-Rich syndrome. The mean age was 62, men outnumbering women 3 : 1. Five patients had proved collagen vascular disease (rheumatoid arthritis three, lupus two). Four others had a history of allergic disorders, syphilis, chronic eosinophilia, or hypersensitivity reactions. One patient showed disappearance of immunofluorescence as fibrosis advanced, which has not previously been reported. The study suggests a possible aetiological link between disorders of immunity and Hamman-Rich syndrome. The evidence also supports the notion that Hamman-Rich syndrome is an accelerated variant of the more indolent interstitial pneumonias.
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PMID:Rapidly fatal pulmonary fibrosis: the accelerated variant of interstitial pneumonitis. 16 92

As the proliferative lesion of rheumatoid arthritis becomes polarized and invasion of articular cartilage and subchondral bone begins, it is likely that many mesenchymal cells, including periosteal and perichondral cells, and perhaps even the chondrocytes and osteoblasts themselves can be activated to produce destructive enzymes. Early in the course of RA cartilage proteoglycans are depleted, leaving the remaining collagen more susceptible to mechanical breakdown as well as to enzymatic breakdown. Specific collagenases are released by synovial cells and, in addition, by polymorphonuclear leukocytes. The latter enzyme may account for free collagenase found in synovial fluid, a finding possibly related to saturation of inhibitory proteins by proteases with greater affinity for them, leaving collagenase active. At this time in the course of rheumatoid arthritis, a joint would be under double jeopardy from enzymes released by the invading pannus as well as by collagenase free and active in the synovial fluid. Rapid destruction could occur. Although cartilage collagen has an intrinsic resistance to collagenase conferred by its primary structure and by higher order structure (e.g. intermolecular cross-links), it seems wise to cool down hot joints because increased temperature may increase the rate of collagen degradation and, therefore, cartilage destruction. In addition, superimposed sepsis or acute flares of rheumatoid disease result in enough influx of polymorphonuclear leukocytes into the joints to result in free collagenolytic activity being present. This provides a rationale for frequent aspiration of any joint fluid, septic or otherwise, containing high polymorphonuclear leukocyte counts.
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PMID:Collagenolytic systems in rheumatoid arthritis. 16 97

The authors sought serum antinuclear antibodies by the indirect immunofluorescent method in 3,260 patients, and found these antibodies in 293 of them. 90 patients had a level equal or greater than 1/50. Among the latter, 54 had some form of collagen disease. The following facts are emphasized: -- antinuclear antibodies are always present in lupus erythematosus. Their levels fall under the influence of treatment when nephritis occurs; -- their frequency is greater (13 cases out of 16) during scleroderma, with often a hazy appearance; -- they are lower during rheumatoid arthritis (23% of cases had a significant level), and their presence is not a sign of worse prognosis; -- they were absent in other forms of collagen diseases.
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PMID:[Anti-nuclear antibodies in collagen diseases]. 16 88


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