Low molecular weight IgM in rheumatoid arthritis and other rheumatic diseases

Low molecular weight (LMW) IgM was measured in the serum and synovial fluid of patients with rheumatoid arthritis (RA) and other rheumatic diseases. High levels were seen in RA, particularly in rheumatoid vasculitis and Felty's syndrome, and significant correlations occurred between LMW IgM and the rheumatoid factor (RF) level and other indices that reflected active or severe disease. LMW IgM-RF, measured by radio-immunoassay in those column fractions containing LMW IgM, correlated significantly with LMW IgM (P < 0.005); preliminary experiments suggested that in some sera, a considerable proportion of the LMW IgM consisted of LMW IgM-RF. We conclude that LMW IgM and LMW IgM-RF may have important implications in the immunopathogenesis of RA and other rheumatic diseases.     

In-vitro reactions of lymphocytes in rheumatoid arthritis and other rheumatic diseases.

Various lymphocyte functions and the percentage of different subpopulations have been measured in groups of patients with seropositive rheumatoid arthritis, seronegative ankylosing spondylitis, and psoriatic arthritis, Sjögren''s syndrome, sicca complex, and in normal controls. Several abnormal results were found--in the responses to mitogens, in the antibody-dependent cytotoxic test, and in the percentages of EA rosettes (antibody sensitised chick red cells test) and surface immunoglobulin-bearing cells. In the light of these findings cytotoxicity and lymphocyte subpopulations were measured in further groups of rheumatoid arthritis patients in whom the disease was at different stages. The results showed that the changes in cytotoxic potential occurred in patients with active arthritis. Correlation tests showed significant positive associations between the percentage of SE rosette-forming cells (sheep red cells test) and the mitogenic responses to phytohaemagglutinin and concanavalin A, and between the percentage of EA rosette-forming cells and the levels of antibody-dependent cytotoxicity. The results are discussed in the light of our understanding of cellular subpopulations in the immune system.     

Quantitation of human synovial mast cells in rheumatoid arthritis and other rheumatic diseases

We examined sections of synovial membranes from 14 patients with rheumatoid arthritis (RA), 7 with other rheumatic diseases, and 10 with no apparent joint disease. Patients with RA and other rheumatic diseases had significantly more synovial mast cells/vessel than patients with no joint disease (0.49 and 0.20, respectively, versus 0.03). They also had significantly more total mast cells/10 fields than patients with no joint disease (9.9 and 5.0, respectively, versus 0.4). Within the rheumatoid group, patients with active disease had more total mast cells/10 fields than patients clinically considered to have end-stage disease (P < 0.05). Synovial basophils were not identified in any patient. Synovial vascularity was similar for all groups (2.3 vessels/field). The role of the synovial mast cell in RA and other rheumatic diseases remains to be determined.     

Cell-mediated immunity to collagen and collagen α chains in rheumatoid arthritis and other rheumatic diseases

Peripheral blood mononuclear cells from patients with rheumatoid arthritis, gout, ankylosing spondylitis and degenerative joint disease were cultured in the presence of native types I, II and III collagens and α chains from each of these types of collagen. The culture supernatant fluids were harvested and assayed for lymphocyte-derived chemotactic factor for monocytes. Reactions to one or more of the native collagens was found in 50 per cent (10 of 20) of the patients with rheumatoid arthritis, 20 per cent (two of 10) of the patients with gout and ankylosing spondylitis but in none of the 10 patients with degenerative joint disease or in normal subjects. Reaction to one or more α chains was found in 90 per cent (18 of 20) of the patients with rheumatoid arthritis, 60 per cent (six of 10) of the patients with gout, 50 per cent (five of 10) of the patients with ankylosing spondylitis, 30 per cent (three of 10) of the patients with degenerative joint disease and in 10 per cent of the normal subjects (one of 10). All the reactions were quantitatively stronger in patients with rheumatoid arthritis. These results indicate that patients with rheumatoid arthritis have cell-mediated immunity to homologous native and denatured collagens but that the reaction is not specific for rheumatoid arthritis. Some patients with gout, ankylosing spondylitis and degenerative joint disease also have low levels of immunity.     

The lifetime risk of adult‐onset rheumatoid arthritis and other inflammatory autoimmune rheumatic diseases

Objective

Understanding of the personal risks for rheumatoid arthritis (RA) and other rheumatic diseases remains poor, despite advances in knowledge with regard to their pathogenesis, therapeutics, and clinical impact, in part because the personal lifetime risk of developing these diseases is unknown. This study was undertaken to estimate the lifetime risk of RA, as well as other inflammatory autoimmune rheumatic diseases, including systemic lupus erythematosus, psoriatic arthritis, polymyalgia rheumatica (PMR), giant cell arteritis, ankylosing spondylitis, and Sjögren's syndrome, and to provide an overall estimate of the risk of developing inflammatory autoimmune rheumatic disease over a lifetime.

Methods

Using the incidence rates obtained from our population‐based studies of rheumatic diseases among residents of Olmsted County, Minnesota, and mortality rates from life tables for the general population, we estimated the sex‐specific lifetime risk of rheumatic disease.

Results

The lifetime risk of RA developing in US adults was 3.6% for women and 1.7% for men, and the lifetime risk of rheumatoid factor–positive RA was 2.4% for women and 1.1% for men. The second most common inflammatory autoimmune rheumatic disease was PMR, with a lifetime risk of 2.4% for women and 1.7% for men. The overall lifetime risk of inflammatory autoimmune rheumatic disease was 8.4% for women and 5.1% for men.

Conclusion

One in 12 women and 1 in 20 men will develop an inflammatory autoimmune rheumatic disease during their lifetime. These results can serve as useful guides in counseling patients regarding their lifetime risk of these conditions and have important implications regarding disease awareness campaigns.

     

Catastrophizing and pain in arthritis, fibromyalgia, and other rheumatic diseases

OBJECTIVE: Pain is among the most frequently reported, bothersome, and disabling symptoms described by patients with osteoarthritis, rheumatoid arthritis, fibromyalgia, and other musculoskeletal conditions. This review describes a growing body of literature relating catastrophizing, a set of cognitive and emotional processes encompassing magnification of pain-related stimuli, feelings of helplessness, and a generally pessimistic orientation, to the experience of pain and pain-related sequelae across several rheumatic diseases. METHODS: We reviewed published articles in which pain-related catastrophizing was assessed in the context of one or more rheumatic conditions. Because much of the available information on catastrophizing is derived from the more general chronic pain literature, seminal studies in other disease states were also considered. RESULTS: Catastrophizing is positively related, in both cross-sectional and prospective studies across different musculoskeletal conditions, to the reported severity of pain, affective distress, muscle and joint tenderness, pain-related disability, poor outcomes of pain treatment, and, potentially, to inflammatory disease activity. Moreover, these associations generally persist after controlling for symptoms of depression. There appear to be multiple mechanisms by which catastrophizing exerts its harmful effects, from maladaptive influences on the social environment to direct amplification of the central nervous system's processing of pain. CONCLUSION: Catastrophizing is a critically important variable in understanding the experience of pain in rheumatologic disorders as well as other chronic pain conditions. Pain-related catastrophizing may be an important target for both psychosocial and pharmacologic treatment of pain.     

Very late activation antigen on synovial fluid T cells from patients with rheumatoid arthritis and other rheumatic diseases

We used flow cytometry and immunoprecipitation techniques to study the expression of the activation molecules transferrin receptor, interleukin-2 receptor, HLA-DR, and very late activation antigen 1 (VLA-1) on purified T lymphocytes from peripheral blood and synovial fluid of 9 patients with rheumatoid arthritis and 7 patients with other rheumatic diseases. We found a T cell subset bearing VLA-1 in synovial fluid from 8 rheumatoid arthritis patients and 4 patients with other rheumatic diseases. VLA-1 was not found in peripheral blood T lymphocytes from either group.