Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using radial immunodiffusion in 7% agarose, 7S IgM was quantified in the sera of 45 normal individuals, 37 patients with rheumatoid arthritis (RA), 18 patients with psoriatic arthritis and 11 patients with ankylosing spondylitis. 7S IgM was only found in the sera of patients with RA, 43% of whom had detectable levels of 7S IgM (median 47.5 micrograms/ml). The patients with 7S IgM had significantly higher IgM rheumatoid factor (IgM RF) and C-reactive protein levels in their sera (p less than 0.005). There was a strong correlation between 7S IgM and IgM RF levels in the sera of these patients. These data demonstrate that patients with more active and severe disease have 7S IgM present in their sera but the absence of 7S IgM from the sera of some patients with high levels of IgM RF and CRP suggest that additional factors may influence the synthesis and secretion of 7S IgM by B cells in RA.
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PMID:7S IgM in the sera of patients with arthritis. 310 8

Serum IgG antibodies to native and denatured human type II collagen (Col II) were measured using an enzyme linked immunosorbent assay (ELISA). One hundred and thirty one patients with various forms of arthritis such as rheumatoid arthritis (RA), ankylosing spondylitis (AS), psoriatic arthritis (PSA). Reiter's Syndrome (RS), osteoarthritis (OA), and gout, 60 with autoimmune connective tissue disease, and 37 with the chronic inflammatory conditions--graft versus host disease and leprosy--were studied. With the exception of RS, PSA, OA, and gout, significant levels of Col II antibodies were detected in each disease group. Blocking studies with types I and II collagen on selected serum samples confirmed the specificity to native Col II, though some cross reactivity was apparent with denatured collagen. The patients with RA who were Col II antibody positive tended to fall into stage III of disease progression. There was, however, no correlation with rheumatoid factor, erythrocyte sedimentation rate, or disease duration and this, together with the finding that Col II antibodies are present in a wide array of diseases, makes their role in the pathogenesis of RA questionable. They may arise as a secondary disease perpetuating mechanism in some patients, or in turn may be an epiphenomenon secondary to generalised disturbed immunoregulation or B cell hyperreactivity, or both, that characterises these clinical conditions.
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PMID:Autoantibodies to type II collagen: occurrence in rheumatoid arthritis, other arthritides, autoimmune connective tissue diseases, and chronic inflammatory syndromes. 336 30

Since the second publication by some of the present authors in which 10 patients with coexisting rheumatoid arthritis (RA) and ankylosing spondylitis (AS) were described, 7 new cases have been found. For accuracy, all cases of the original study still available were reexamined. Of the total of 17 cases, 13 were male and 4 female. All had positive tests for rheumatoid factor and 6 had subcutaneous nodules. The male predominance and the frequency of nodules are consistent with other publications. In addition, our study demonstrates the strong association of each of these 2 diseases with its genetic marker: the antigen HLA-DR4 was present in 8 of 12 cases tested and the antigen HLA-B27 was present in 16 of the 17 cases. The coexistence of these 2 classical rheumatological entities in the same patient appears to occur by chance and is probably often overlooked.
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PMID:Coexisting rheumatoid arthritis and ankylosing spondylitis. 343 21

Intraperitoneal injection of human fetal cartilage proteoglycan (depleted of chondroitin sulfate) in Freund's complete or incomplete adjuvant induces a chronic erosive polyarthritis and spondylitis in all female BALB/c mice. This occurrence is strain-specific but not haplotype-specific, and it is sex-related. The development of the arthritis is associated with the natural presence of cellular immunity to the immunizing antigen and to chondroitinase ABC-treated mouse cartilage proteoglycan. In addition, relatively more antibody to the immunizing proteoglycan is elicited in arthritic mice, and antibodies are produced that cross-react with native mouse proteoglycan. This combination of immune responses is not observed in mice that do not develop arthritis. Associated with the arthritis is the development of cytotoxicity to mouse chondrocytes and, in some animals, of rheumatoid factor, immune deposits in joint tissues and kidneys, and the production of autoantibodies to mouse type II collagen. These observations might be related to our earlier demonstration that immunity to human cartilage proteoglycan is observed in some patients with ankylosing spondylitis.
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PMID:Immunity to cartilage proteoglycans in BALB/c mice with progressive polyarthritis and ankylosing spondylitis induced by injection of human cartilage proteoglycan. 356 22

A case control study of 50 rheumatoid factor positive (RA+) and 50 rheumatoid factor negative (RA-) patients with rheumatoid arthritis has been carried out. As expected, the RA+ group has significantly more nodules and vasculitis. In terms of clinical joint involvement, the RA- had large-joint involvement. Radiologically, seropositive disease was characterized by more severe involvement of the metacarpophalangeal joints of the thumb and index fingers and in all the metatarsophalangeal joints of the feet. There was no difference either clinically or radiologically between the two groups in terms of symmetry of joint disease or wrist involvement. Of special interest was the finding that the prevalence of HLA-DR4 was elevated to the same degree in both groups but that genetic markers for ankylosing spondylitis and for psoriasis (HLA-B27 and Cw6 respectively) were similar in both groups and not increased above control population levels. It is concluded that the entity defined as RA includes patients with and without rheumatoid factor (RF) in their serum and that this determines differences in disease expression. Whether these differences are the consequences or the cause of RF cannot be concluded on the basis of this study.
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PMID:Seronegative and seropositive rheumatoid arthritis: similar diseases. 358 Jul 12

We tested the sera of 50 patients with Lyme disease for IgM-rheumatoid factor (IgM-RF) using a sensitive ELISA. Levels of IgM-RF greater than 3 SD above the mean of normal subjects were found in 2 of 15 patients with erythema chronicum migrans, 7 of 10 with neurologic abnormalities, and 7 of 25 with Lyme arthritis (p = 0.038). Only 2 of these sera were positive by latex agglutination. In contrast, none of the 23 control patients with osteoarthritis, ankylosing spondylitis, or Reiter's syndrome had positive tests. The levels of IgM-RF correlated with disease activity (p = 0.002), total serum IgM levels (p = 0.002), and specific IgM antibody titers to Borrelia burgdorferi (p = 0.006). IgM-RF reactivity was absorbed with heat aggregated IgG (HAGG), but the titer of specific IgM antibody was insignificantly affected by this procedure. Thus, small amounts of RF are produced at certain times in many patients with Lyme disease, and IgM-RF production appears to be linked to the specific IgM response.
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PMID:IgM rheumatoid factor in Lyme disease: correlation with disease activity, total serum IgM, and IgM antibody to Borrelia burgdorferi. 366 82

Ninety-two patients who satisfied the criteria proposed by Kellgren for the diagnosis of ankylosing spondylitis were re-evaluated by clinical, radiological and laboratory parameters after an average length of illness of 18.7 years. The following associated clinical lesions were studied: aortic insufficiency 8%, heart block 3%, iritis 11%, and other associated lesions. Long-term effects of x-ray therapy were evaluated by comparing irradiated and non-irradiated patients; no significant difference was noted in the clinical course of these two treatment groups. On serum protein electrophoresis no characteristic dysproteinemia was demonstrated; in no instance was there a marked hypergammaglobulinemia. Test results for rheumatoid factor, antinuclear factor and antithyroglobulin were all within the range expected for a normal population. In addition to bilateral sacroiliitis, several other characteristic radiological lesions, such as anterior spondylitis, were present in a high percentage of cases. It is suggested that the diagnostic criteria proposed by Kellgren, although useful, should be enlarged and refined.
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PMID:Ankylosing spondylitis: a late re-evaluation of 92 cases. 594 93

Antibodies to beta 2 microglobulin are found in systemic lupus erythematosus patients and are important in the lymphocytotoxic reactions of sera from such patients. In this study, beta 2 microglobulin antibodies were measured with the use of an enzyme-linked immunosorbent assay with purified beta 2 microglobulin antigen and peroxidase-labeled anti-human IgG or IgM. IgG antibodies to beta 2 microglobulin were found in 68% of 22 patients with ankylosing spondylitis. This incidence was higher than the 5% in 80 controls (P less than 0.01) and similar to the 71% incidence found in 35 patients with systemic lupus erythematosus. Eleven (27%) of 41 patients with rheumatoid arthritis had elevated levels of antibodies to beta 2 microglobulin (P less than 0.01). The mean antibody levels expressed in enzyme units were 0.125 for patients with ankylosing spondylitis, 0.157 for those with systemic lupus erythematosus, 0.101 for those with rheumatoid arthritis, and 0.067 for controls. IgM anti-beta 2 microglobulin was not significantly different from controls. A competitive binding assay with enzyme-labeled beta 2 microglobulin was used to determine serum beta 2 microglobulin. These values were also found to be elevated in 48% of patients in all 3 disease categories (P less than 0.01). Beta 2 microglobulin antibodies and serum beta 2 microglobulin did not correlate with each other, renal diseases or antinuclear antibodies in patients with systemic lupus erythematosus, with rheumatoid factor or severity of articular disease in patients with rheumatoid arthritis, or with peripheral arthritis or iritis in those with ankylosing spondylitis. Although antibodies to beta 2 microglobulin might reflect a general disturbance of immune regulation in patients with systemic lupus erythematosus, their presence in those with ankylosing spondylitis, a disease closely associated with a specific HLA allotype and not usually associated with formation of autoantibody, suggests that they might play a role in the pathogenesis of the latter disease.
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PMID:Antibodies to and elevations of beta 2 microglobulin in the serum of ankylosing spondylitis patients. 617 46

Spondyloarthritis (Sp) is newly defined as arthritis that is clinically, pathologically, and genetically related to and predisposed to ankylosing spondylitis (AS) and Reiter's syndrome (RS) rather than to rheumatoid arthritis (RA). A diagnosis of Sp does not necessarily imply arthritis of the spine and does not depend on the demonstration of roentgenographic sacroiliitis that, in this conceptualization, is recognized not as the essential hallmark, but rather merely as a diagnostic "way station" on a continuum of disease, which may (but need not necessarily) begin with RS or be complicated during its course by AS or RS. Spondyloarthritis is distinctively characterized morphologically and clinically by disproportionate inflammation at the entheses, the sites of attachment of tendons and ligaments to bone. Family history or presence of enthesopathic pain, psoriasis, inflammatory bowel disease, uveitis, recurrent urethritis, prostatitis or cervicitis, keratoderma blennorrhagicum, HLA-B27, and asymmetric pauciarticular lower lower extremity arthritis without rheumatoid factor or rheumatoid nodules suggests a diagnosis of Sp rather than RA.
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PMID:Spondyloarthritis and enthesopathy. Current concepts in rheumatology. 621 89

An ELISA has been developed for serum antibodies to streptococcal cell wall peptidoglycan-polysaccharide polymers (PG-GSP). A significantly increased prevalence of serum anti-PG-GSP antibody was found in juvenile chronic arthritis and both seropositive and seronegative rheumatoid arthritis (RA), compared with ankylosing spondylitis, systemic lupus erythematosus, myeloma and healthy controls. Anti-PG-GSP antibody was always of the IgG class and there was no correlation of anti-PG-GSP levels with C reactive protein, rheumatoid factor (RF) or anti-streptolysin O titres. There was no direct cross-reaction of RF with PG-GSP, nor did the presence of IgM-RF significantly interfere with the assay. Examination of paired serum and synovial fluid samples offered no evidence for local production of anti-PG-GSP antibody in synovial tissue. These data are compatible with an increased systemic immunization by bacterial fragments in RA.
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PMID:Antibody to streptococcal cell wall peptidoglycan-polysaccharide polymers in seropositive and seronegative rheumatic disease. 636 31


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