Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003873 (rheumatoid arthritis)
 53,068 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 34 years old white male patient suffering from a seropositive "probable" rheumatoid arthritis developed a severe hypocomplementemic mesangiocapillary glomerulnophritis. Rheumatoid factor-Latextest and Waaler-Rose-Titers and IgM have been found highly elevated in the serum. The third component of complement (C3) was markedly depressed, while the fourth component (C4) was within the normal range. The rapid progression of both diseases forced us to start an immunosuppressive drug therapy using azathioprine and steroids, 18 months after the beginning of the treatment the patient is well, has only slight proteinuria, normal levels of complement and no joint pain. The possible connections between rheumatoid arthritis and mesangiocapillary glomerulonephritis in this case as well as the therapeutic approaches are discussed.
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PMID:[Mesangiocapillary glomerulonephritis and rheumatoid arthritis. A case with diagnostic and therapeutic questions (author's transl)]. 6 Nov 63

In simultaneous conditions of inflammatory changes in peripheral joints and in sacroiliac joints, a differential diagnosis, amongst others, of rheumatoid arthritis with involvement of the sacro-iliac joints and also ankylosing spondylitis with peripheral joint involvement should be considered. It seems that in rare cases both diseases occur together. We describe one female patient with coexistence of rheumatoid arthritis and ankylosing spondylitis. The X-rays showed sacro-iliitis, syndesmophytes and inflammatory changes of the finger and toes, which are typical for rheumatoid arthritis. Rheumatoid factor was detected in serum and in synovial fluid. HLA B27 was negative. The results of 13 patients with coexistence of rheumatoid arthritis and ankylosing spondylitis reported in the literature since 1975, are compared with the above described patient.
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PMID:[Case report of a patient with coexistent rheumatoid arthritis and ankylosing spondylitis]. 9 68

Forty-four subjects with classic or definite rheumatoid arthritis who were on individualized chrysotherapy were observed for changes in serum protein electrophoresis, immunoglobulins, and circulating lymphocyte counts. By paired variate analysis, significant declines from pretreatment values were recorded for the following--electrophoretic protein fractions: gamma, alpha-1, alpha-2, (P less than 0.05); immunoglobulins: IgM--53% (P less than 0.001), IgG--37% (P less than 0.01), IgA--34% (P less than 0.001). Rheumatoid factor decreased in 29 of 39 subjects, 15 becoming seronegative (P less than 0.001); circulating lymphocytes decreased by 27% (P less than 0.001). The maximal suppressive effect on IgG and IgM was not achieved until the third and fourth years of therapy by sustained weekly administration of gold sodium thiomalate (one year cumulative dosage, mean 2106 mg, range 1065-2,885; greater than or equal to 4 year cumulative dosage, mean 8747 mg, range 5,385-15,160 mg). An immunosuppressive effect is suggested by these results.
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PMID:Chrysotherapy. Suppression of immunoglobulin synthesis. 10 Jan 21

Thirty-nine subjects with classical or definite rheumatoid arthritis received weekly intramuscular gold sodium thiomalate (GST) to sustain gold blood levels of more than 320 microgram/dl. Statistical analysis revealed significant declines from pre-treatment values for IgM, IgG, and IaA. Rheumatoid factor titer decreased in 29 of 39 subjects, 15 becoming seronegative. Circulating lymphocytes decreased by 27%. The maximal suppressive effect on IgM was not achieved until the 3rd and 4th years of GST administration. Auranofin (AF) 6 mg/day was administered to 15 patients for an average interval of 45 weeks. In vitro and in vivo suppression of lymphocyte mitogen response with AF was more rapid in onset and significantly greater than with GST. Suppression of dinitrochlorobenzene skin sensitization was observed in AF patients. The clinical response in GST treated subjects correlated with suppression of immunoglobulins, rheumatoid factor titer, and circulating lymphocytes. A significant decline in these variables was not achieved for a corresponding interval with AF treatment. It is suggested that chrysotherapy may be applied more widely to immunologically-mediated disorders and perhaps be used to affect selectively B versus T mediated dysfunction.
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PMID:Effect of chrysotherapy on parameters of immune response. 11 52

Rheumatoid synovitis is characterized by the simultaneous occurrence of two major types of immunologically-induced inflammation. These usually occur concurrently in the same joint. A cellular immune response is present in the sublining layer of the synovial membrane and an immune complex-induced acute inflammatory reaction is present in the synovial effusion phase of the disease. The two reactions are closely related and mutually interdependent. The cellular immune response is reduced in rheumatoid arthritis, but the chronic inflammatory cells of the synovium are active in the synthesis of IgG and probably considerable amounts of IgG rheumatoid factor. Rheumatoid factor complexes, particularly IgG-RF complexes, appear to be responsible for the exudative, immune complex-induced inflammatory phase of the disease.
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PMID:General mechanisms of inflammation in rheumatoid arthritis. 16 Nov 78

When rheumatoid factor in rheumatoid arthritis and multiple sclerosis sera was titrated by the fluorescent antibody method on measles virus-infected cells, there was a marked and variable drop in titer on acetone-fixed cells as compared with unfixed cells. This was accounted for by the failure of measles virus hemolysin-inhibiting (HLI) antibody of the immunoglobulin G class to bind to acetone-fixed infected cells. It was shown by staining unfixed and acetone-fixed measles virus-infected cells that rheumatoid factor in most rheumatoid arthritis sera combined with measles virus-specific hemagglutinin-inhibiting and HLI antibodies, whereas rheumatoid factor in multiple sclerosis sera combined only with HLI antibody. Rheumatoid factor of similar specificity was also observed in normal sera and occasionally in rheumatoid arthritis sera. Both rheumatoid arthritis and multiple sclerosis sera showed almost identical increases in average titer above normal of measles virus-specific fluorescent staining immunoglobulin G and HLI antibodies.
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PMID:Measles virus-specific antibodies and immunoglobulin M antiglobulin in sera from multiple sclerosis and rheumatoid arthritis patients. 31 21

Cells producing rheumatoid factor (RF) were readily detected in vitro by means of a haemolytic plaque assay system employing sheep erythrocytes (SRBC) sensitized with reduced and alkylated rabbit IgG anti-SRBC antibody as target cells. Rheumatoid factor-producing, plaque-forming cells (RF-PFC) were observed in all of the synovial tissue cell preparations from seropositive rheumatoid arthritis patients studied. The numbers of RF-PFC varied considerably without any direct correlation with serum titres of RF antibody activity. However, high numbers of RF-PFC were never found in patients with low rheumatoid factor titres whereas, high and low numbers of RF-PFC were found among the patients with high RF titres. Synovial tissue cell preparations from a group of seronegative patients, with only one exception, failed to exhibit RF-PFC.
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PMID:Rheumatoid factor plaque-forming cells in rheumatoid synovial tissue. 32 44

Part 1, which begins on page 64, discusses diagnosis of rheumatic disease by radiography. The most popular laboratory tests in rheumatic disease are nonspecific and include those based on the formation of autoantibodies. Rheumatoid factor assays actually are of little diagnostic help in rheumatoid arthritis, but antinuclear antibody tests have become mandatory for identification of systemic lupus erythematosus. Studies based on immune complexes and cell immunity are valuable in specific clinical situations.
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PMID:Diagnosis of rheumatic disease. 2. Laboratory tests. 36 40

A serological and clinical study was performed to find the common features of 130 patients without antibodies against 11 or more different antigens in the complement fixation (CF) test. These patients (=1.6%) were discovered during hte screening of 8,021 adult patients. Rheumatoid factor(s) (RF) were found in the sera of 113 of the patients. In the remaining 17 patients no common serological or clinical markers were found. Myeloma M-components were found in three cases. The lack of measurable CF antibodies in RF positive cases was apparently due to the inhibitory effect of RF(s) in the CF test. This was indicated by a positive reaction in CF after centrifugal separation of IgM and IgG fractions and also by the detection of antibodies using immunodiffusion method. Possible immune complexes were sought using the platelet aggregation test, which was positive for the sera of 47 (=37%) of the patients. The clinical diagnosis of the 130 CF-nonreactors was rheumatoid arthritis (RA) (ARA criteria) in 23 cases and pulmonary diseases in 65 cases. In a comparison group of equal size there were only 3 RA patients and 15 with pulmonary disease. RA was thus found in 20% of the RF positive CF-nonreacting patients. In the comparison group of 52 RA patients 8 CF-nonreactors were found (=15%). This suggests that the effect of RF(s) from RA patients in CF reaction varies greatly.
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PMID:Lack of measurable complement fixing antibodies against viral antigens. 40 40

Thirty-six women from a Northwest Indian population known to have an increased prevalence of rheumatoid arthritis were studied. The course of the clinical disease was that of erosive rheumatoid arthritis with characteristic involvement of metacarpophalangeal and wrist joints. Rheumatoid factor and antinuclear antibody tests were frequently positive, and reactions to gold therapy were more frequent than in other rheumatoid populations. Viral antibodies were similar in the rheumatoid and the control groups. HL-A W24 and HL-A BW40 were increased in both the diseased and the control Indian populations.
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PMID:Studies of rheumatoid arthritis among a tribe of Northwest Indians. 81 80


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