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)

A cohort analytic study was performed to investigate serum IgA-class antibodies against Chlamydia in 24 patients with chlamydial-induced arthritis (CIA). IgA-class antibodies against chlamydial antigens were positive (titre greater than or equal to 1:16) in 23 of the 24 IgG-positive CIA-patients (96%) in contrast to 16 of 40 patients (40%) with other rheumatic diseases (ankylosing spondylitis n = 6; undifferentiated arthritis n = 11; rheumatoid arthritis n = 12; degenerative joint disease n = 11), also positive for IgG-class chlamydial antibodies. Both the presence of specific IgA-antibodies and their geometric mean titre (1:28 vs. 1:4) differed significantly (p less than 0.001) between the two groups.
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PMID:Specific serum IgA-antibodies in chlamydial-induced arthritis. 273 57

A study of 95 serum samples from 61 patients with ankylosing spondylitis (AS) showed that 21 patients (34%) had raised levels of IgA-alpha 1 antitrypsin complexes. These were associated with active disease as measured by a clinical index and also with erythrocyte sedimentation rate, C reactive protein, and serum IgA. In particular, an association was noted between 'extraspinal' manifestations of AS such as synovitis, uveitis, and active inflammatory properties of these complexes. It is suggested that these complexes may have a role in the pathogenesis of such clinical manifestations.
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PMID:IgA-alpha 1 antitrypsin complexes in ankylosing spondylitis. 278 5

Multiple myeloma has rarely been reported in patients with ankylosing spondylitis. We observed a patient with a 20-year history of ankylosing spondylitis, who subsequently developed IgA myeloma. This association may not be simply coincidental. It has been proposed that the protracted stimulation of immunocytes by inflammatory lesions on the mucosal surfaces of the gastrointestinal, respiratory, and biliary tracts, where lymphocytes are already committed to IgA production, may be implicated in the pathogenesis of IgA myeloma in some patients. Ankylosing spondylitis is a chronic inflammatory disease, probably resulting from the interaction of a genetic predisposition involving HLA-B27 with an environmental event such as enteric bacterial infection. We propose that ankylosing spondylitis and IgA myeloma occurring concomitantly in our patient implies a possible pathogenetic relationship. In ankylosing spondylitis, persistent reticuloendothelial stimulation, due to chronic subclinical gastrointestinal infection, may lead to IgA-producing plasma cell activation and proliferation, and subsequent IgA myeloma development.
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PMID:Association of ankylosing spondylitis with IgA-multiple myeloma: report of a case and pathogenetic considerations. 280 65

Although testing for circulating immune complexes (CIC) is regarded as a useful, complementary, laboratory parameter in the differential diagnosis and management of immune complex-induced vasculitis syndromes, there is still an uncertainty with regard to assay systems used for the demonstrated of soluble immune complexes. This is partly due to difficulties in the reproducibility, handling and principle limitations of available test systems for the assessment of soluble immune complexes in body fluids. In the present communication a modification of the anti-C3 test for the determination of CIC was developed using nitrocellulose as a solid phase matrix. IgG-, IgA- and IgM-containing CIC were determined and quantified using standard immune complex preparations. When 39 sera of SLE patients, 12 sera of patients with vasculitis syndromes, 10 sera of rheumatoid arthritis patients and 11 sera of patients with ankylosing spondylitis were tested, predominantly IgG-containing CIC could be demonstrated. Only in SLE patients was a significant amount of other immunoglobulin isotypes detected in CIC. In these patients a significant difference of IgG-containing CIC levels was found with regard to patients with high and low disease activity (P less than 0.0001). A significant correlation was also established between IgG-containing CIC and anti-dsDNA antibodies (P less than 0.001). In a longitudinal study the isotypes in the isolated CIC were found to be constant.
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PMID:C3-containing serum immune complexes in patients with systemic lupus erythematosus: correlation to disease activity and comparison with other rheumatic diseases. 281 9

Eighty-five patients with active ankylosing spondylitis (AS) were randomized to receive either sulfasalazine (less than or equal to 3 gm/day, mean 2.5) or placebo for 26 weeks. There was a statistically significant improvement, compared with baseline, in most of the clinical variables in patients receiving the active drug. Laboratory parameters (erythrocyte sedimentation rate, C-reactive protein, IgG, IgM, and IgA) also improved during the active treatment, suggesting a beneficial effect of sulfasalazine on AS. At the end of the treatment, significant differences between the sulfasalazine and placebo groups were observed in morning stiffness, chest expansion, erythrocyte sedimentation rate, and in all immunoglobulin classes. Two patients in each treatment group discontinued the trial because of side effects. Enteric-coated sulfasalazine seemed to be effective and well tolerated in patients with active AS.
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PMID:Sulfasalazine in the treatment of ankylosing spondylitis. A twenty-six-week, placebo-controlled clinical trial. 290 39

Cutaneous immunofluorescence studies were carried out in 21 patients with ankylosing spondylitis (AS) and the results compared with those for 18 healthy subjects. The most prominent finding was the presence of IgA in dermal vessels of patients with AS (71% compared with 17% of the control group). IgG and IgM cutaneous deposits were also observed in patients with AS, but these results did not differ from those of the control group. A renal biopsy was performed in three of the patients presenting with unexplained microscopic haematuria. One of them had an IgA nephropathy, but no correlation was found between kidney and skin deposits of IgA. These findings suggest that IgA cutaneous deposits in AS are not a marker of IgA nephropathy but stress the role of immunoglobulin A in the pathogenesis of this disease.
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PMID:Immunoglobulin A in the skin of patients with ankylosing spondylitis. 306 67

The pathogenesis of ankylosing spondylitis (AS) remains unknown, although previous studies have strongly suggested that it may result from immunological aberration. To further explore the pathogenetic mechanisms, in vitro syntheses of immunoglobulins and interleukin-2 (IL-2) by peripheral blood mononuclear cells (MNC), and the serum level of the interleukin-2 receptor (IL-2R) were studied in 35 patients with definite AS and in 28 healthy controls. MNC were cultivated in the presence of pokeweed mitogen (PWM) for seven days. Immunoglobulins in the supernatants were measured by rate nephelometer (Immunochemistry System Analyser II, Beckman.) In vitro synthesis of IL-2 was carried out by cultivating MNC in medium only; in medium containing physiological concentration of the male sex hormone i.e., testosterone 500 ng/dl and estradiol 2 ng/dl; and in medium containing physiological concentration of female sex hormone, i.e., testosterone 50 ng/dl and estradiol 20 ng/dl. IL-2 was quantitated using an IL-2-dependent cytotoxic T lymphoid cell line (CTLL). Serum IL-2R was measured using an IL-2R test kit (CELLFREE, T Cell Sciences, Cambridge, MA). The results showed: In vitro synthesis of IgG, IgA and IgM was significantly higher in AS than in controls; In vitro synthesis of IL-2 was significantly enhanced by testosterone in normal control, but not in AS; and Serum IL-2R was significantly elevated in patients with AS. These findings, viewed in conjunction with previous results here, lead to postulation that an inflammatory process, elicited in HLA-B27-positive males and caused by an infectious agent invading via the mucosa may both cause immunological abnormalities and provoke various symptoms and signs of AS.
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PMID:Elevated serum interleukin-2 receptor; increased in vitro immunoglobulin synthesis and lack of response to testosterone-enhanced in vitro interleukin-2 production in ankylosing spondylitis. 310 49

Serum titres of IgA are raised in ankylosing spondylitis and increased titres of antibodies to klebsiella have also been reported. The humoral response was investigated in ankylosing spondylitis and other inflammatory disorders. IgA antibodies to klebsiella pneumoniae K43 were measured in patients with ankylosing spondylitis, Crohn's disease, ulcerative colitis, and rheumatoid arthritis and in controls. Significantly raised median titres of anti-klebsiella IgA, measured as optical density at 405 nm with an enzyme linked immunosorbent assay (ELISA), were seen among the patients with ankylosing spondylitis (0.7), Crohn's disease (0.8), rheumatoid arthritis (0.6), and ulcerative colitis (0.8) compared with controls (0.4). Activity of disease in ankylosing spondylitis and titres of anti-klebsiella IgA were not correlated. In contrast, titres of anti-klebsiella IgM were significantly lower in patients with ankylosing spondylitis and ulcerative colitis. The increase in the titres of anti-klebsiella IgA may be due to increased permeability of the gut to bacterial antigens, leading to an increased IgA response in the gut mucosa and permitting the release of IgA into the circulation. As the increased antibody titres were seen in Crohn's disease and rheumatoid arthritis as well as in ankylosing spondylitis the response may be nonspecific, occurring because of possible underlying inflammatory bowel disease in these conditions.
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PMID:Raised titres of anti-klebsiella IgA in ankylosing spondylitis, rheumatoid arthritis, and inflammatory bowel disease. 313 77

Because the etiology of IgA and IgG hyperimmunoglobulinemia in ankylosing spondylitis (AS) remains unknown, the cellular immune system has been further studied by measuring the lymphocyte and its subpopulations in peripheral bloods of 50 definite AS patients and 40 normal controls. The system's functions have also been assessed in terms of proliferative responses to phytomitogens (Con A, PHA and PWM) and autologous mixed lymphocyte reaction (AMLR). The following results were obtained: The number of lymphocytes, total T, active T, OKIa1, OKT3, OKT4 and OKT8 cells in peripheral bloods of AS patients decreased more significantly when compared to the normal controls. The ratio of OKT4/OKT8 also decreased. However, the number of OKT8 cells was normal in inactive stage. While the lymphocytes of AS responded hyperreactively to PWM (B-cell mitogen), the response to Con A (T-cell mitogen) was depressed significantly. AMLR was impaired in AS patients no matter whether monocytes or B cells were used as stimulators. The aforementioned changes were especially evident in the active stage and most of them returned to normal after the disease became quiescent. It is therefore concluded that the etiology of hyperreactivity of B-cells in AS may be caused by T-cell immune aberration as evidenced by depressed lymphoproliferative response to T-cell mitogen (Con A) and impaired AMLR and/or the hyperfunction of B-cells themselves.
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PMID:Lymphocyte aberrations in ankylosing spondylitis. 316 9

The occurrence of circulating immune complexes containing IgA (IgA-IC) was studied in groups of patients with ankylosing spondylitis (AS) selected for the presence or absence of hematuria. In studies done with 4 kinds of assays, IgA-IC were found more frequently and in higher titers in the 18 patients with AS with hematuria than in the 40 patients with AS without hematuria. Comparison of clinical indices of disease activity in these patient groups showed that the disease was more active in patients with AS with hematuria. Our findings confirm those made in a previous retrospective study on the relation between hematuria and circulating IgA-IC in AS and suggest that circulating IgA-IC play a role in the pathogenesis of hematuria in AS.
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PMID:IgA containing immune complexes and hematuria in ankylosing spondylitis. A prospective longitudinal study. 323


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