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)

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

The occurrence of IgM, IgG and IgA class Yersinia antibodies was studied at the beginning of an inflammatory joint disease and one year later in 354 adult patients using an ELISA technique. The control groups consisted of age and sex matched healthy persons living in the same geographical area as the patients, and of 64 patients with chronic rheumatoid arthritis. Yersinia antibodies of any Ig class were found in 9.0% of all the patients at the beginning of the disease, in 4.0% of the healthy controls and in 1.6% of the patients with chronic rheumatoid arthritis. Patients with ankylosing spondylitis, Reiter's disease or other reactive arthritis showed the highest prevalence (19.4%) of Yersinia antibodies, but in the whole material one half of the patients with Yersinia antibodies were clinically classified as rheumatoid or nonspecific arthritis. The elevated prevalence of Yersinia antibodies in patients with probable rheumatoid or nonspecific arthritis may indicate a reactive etiopathogenesis of arthritis also in some cases without previous evidence of gastrointestinal infection. Quantitation of IgG and IgA antibodies to Yersinia is important in the diagnosis of Yersinia arthritis. These antibodies may not be detected by the generally used agglutination test.
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PMID:Yersinia antibodies in inflammatory joint diseases. 633 56

The objective of the study was to investigate potential triggering events for the onset of ankylosing spondylitis (AS). A large retrospective population survey of 1,080 AS patients was carried out by multi-faceted questionnaire. A nested case-control study compared the cohort to 102 patients with lumbar disc prolapse. Participants with AS had a mean age of 49.8 years, mean age of disease onset was 25.2 years and 63% of the cohort were male. Seventy-nine per cent knew they were human leucocyte antigen (HLA)-B27-positive, and a further 12.5% were unaware of their HLA-B27 status. Infections were relatively common in the 3 months leading to the first symptoms, 4.6% reporting gastrointestinal infection, 2.5% reporting urinary tract infection and 2.6% respiratory infection. Five per cent reported heavy physical activity in the 3 months prior to the onset of symptoms, 4.2% emotional stressors and 3.1% work stressors. Injury and surgery were less commonly reported (1.7 and 0.7%, respectively). Pregnancy was reported by 7.4% of the female participants. When the 12 months leading up to the first symptoms was compared to the 12 months previous to that, work stressors (OR 1.5), and pregnancy (OR 2.5) infection (OR 1.5 to 1.8) were significantly more common closer to disease onset. Infection and work stressors are potential triggers for the onset of AS; however, low rates suggest they are only a small part of the environmental milieu that combines with a genetic predisposition to cause the development of this chronic inflammatory disease.
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PMID:Infection and work stress are potential triggers of ankylosing spondylitis. 1663 12

This retrospective study analyzed the HLA-B 27 alleles in a group of 20 consecutive patients with the diagnosis of Reiter syndrome (RS) followed in a tertiary referral university hospital in Brazil, during the period 1990-2006, and compared the data with that observed in other patients with spondyloarthropathies followed at the same institution. Eight cases were associated to gastrointestinal infection, eight cases to previous urethritis, and four cases presented no established preceding infection. HLA-B 27 alleles were typed by polymerase chain reaction-amplified DNA hybridized with sequence-specific oligonucleotide probes (HLA-B 2,701 to HLA-B 2,721). They were compared to a group of 108 patients with ankylosing spondylitis (AS), 40 with undifferentiated spondyloarthropathy (uSpA) and 111 healthy controls. Among the 20 patients, 17 were HLA-B 27 positive (85%). Two HLA-B 27 alleles were observed: HLA-B 2,705 (65%) and HLA-B 2,702 (35%). In the other spondyloarthropathies, the observed alleles were HLA-B 2,705 (90% in AS and 92.5% in uSpA), HLA-B 2,702 (8% in AS and 5% in uSpA), HLA-B 2,704 (1% in AS and 2.5% in uSpA) and HLA-B 2,713 (1% in AS). Among the 111 healthy controls, 80% presented HLA-B 2,705, followed by HLA-B 2,702 in 10%, HLA-B 2,703 in 6%, HLA-B 2,707 in 3% and HLA-B 2,713 in 1%. Concluding, in the HLA-B 27 positive patients with RS in this study there was predominance of HLA-B 2,705 allele, in a lower frequency than that observed in patients with other spondyloarthropathies and healthy controls.
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PMID:Frequency of HLA-B27 and its alleles in patients with Reiter syndrome: comparison with the frequency in other spondyloarthropathies and a healthy control population. 1771 70

The purpose of the present study is to investigate the frequency of HLA-B27 and its alleles in reactive arthritis (ReA) and in ankylosing spondylitis (AS) in Tunisia. HLA-B27 alleles were typed by PCR amplification with sequence-specific primers. We studied 17 patients with ReA associated with urethritis or with gastrointestinal infection; 42 HLA-B27-positive patients with AS and 100 healthy controls. Eleven ReA patients (67.7%) were HLA-B27 positive. There was an increased frequencies of HLA-B27 (P = 7.76 x 10(-12), OR = 59.30) and a moderate increase of HLA-B51 (P = 0.015; OR = 4.91) alleles in ReA patients when compared with healthy controls. Four B27 subtypes were identified: B*2702, 05, 09 and B*2712. The distribution of these alleles in the ReA patients was 37.5% for B*2702 and B*2705. Only these two subtypes were detected in 18 (42.8%) and 24 (57.1%), respectively, of the AS patients. B*2709 and B*2712 were relatively rare in ReA patients and were identified in one case each. Our results showed a restricted number of HLA-B27 subtypes associated with ReA and AS. B*2702 and 2705 were common in ReA and AS patients.
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PMID:Distribution of HLA-B27 and its alleles in patients with reactive arthritis and with ankylosing spondylitis in Tunisia. 1915 94

Reactive arthritis (ReA) is a member of seronegative spondyloarthropathy (SSA), which involves an acute/subacute onset of asymmetrical lower limb joint inflammation weeks after a genitourinary/gastrointestinal infection. The diagnosis is clinical because it is difficult to culture the microbes from synovial fluid. Arthritis patients with a similar clinical picture but lapsed history of an immediate preceding infection that do not fulfill the diagnostic criteria of other members of SSA, such as ankylosing spondylitis, psoriatic arthritis, and arthritis associated with inflammatory bowel disease, are labeled as peripheral undifferentiated spondyloarthropathy (uSpA). Both ReA and uSpA patients show a strong association with class I major histocompatibility complex allele, HLA-B27, and a clear association with an infectious trigger; however, the disease mechanism is far from clear. Because the clinical picture is largely dominated by rheumatoid-arthritis (RA)-like features including elevated levels of inflammatory markers (such as ESR, CRP, etc.), these overlapping symptoms often confound the clinical diagnosis and represent a clinical dilemma, making treatment choice more generalized. Therefore, there is a compelling need to identify biomarkers that can support the diagnosis of ReA/uSpA. In the present study, we performed NMR-based serum metabolomics analysis and demonstrated that ReA/uSpA patients are clearly distinguishable from controls and further that these patients can also be distinguished from the RA patients based on the metabolic profiles, with high sensitivity and specificity. The discriminatory metabolites were further subjected to area under receiver operating characteristic curve analysis, which led to the identification of four metabolic entities (i.e., valine, leucine, arginine/lysine, and phenylalanine) that could differentiate ReA/uSpA from RA.
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PMID:NMR-Based Serum Metabolomics Revealed Distinctive Metabolic Patterns in Reactive Arthritis Compared with Rheumatoid Arthritis. 3037 45