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)

Light microscopic studies on synovium obtained from seven knees and three hips of patients with ankylosing spondylitis and peripheral arthritis showed surface fibrin, proliferation of synovial lining cells, moderate infiltration with lymphocytes, and sometimes striking numbers of plasma cells. There was some vascular congestion and obliteration, occasional bone and cartilage debris, and a tendency toward increased fibrous tissue. Although the intensity of some findings varies from those in rheumatoid arthritis, there were no consistent distinguishing features. Electron microscopy of eight synovial tissue specimens showed increased type B or synthetic lining cells. Structures that could possibly have been organisms were seen among synovial cells in two patients. Immune complex-like deposits were not seen in vessel walls, although there were other vascular alterations. Synovial fluid studies showed 2,200 to 16,500 white blood cells/mm3 (mean, 8,236), 29% to 93% polymorphonuclear leukocytes (mean, 66%), and 0.5 to 32% lymphocytes (mean, 18%). The presence of at least some activated lymphocytes (lymphoblasts) in seven of nine patients in addition to the above findings in synovium suggest an immunological component to the driven process. No more than 32% lymphocytes was found in any synovial fluid despite the use of nonsteroidal antiinflammatory drugs. Thus no support for synovial fluid lymphocytosis, such as has been described in rheumatoid arthritis patients treated with nonsteroidal antiinflammatory drugs alone, is provided.
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PMID:Light and electron microscopic observations on the synovitis of ankylosing spondylitis. 141 82

Restrictive ventilatory dysfunction, lowered diffusing capacity, and apical fibrosis have been reported in ankylosing spondylitis. To investigate the pathogenesis of these abnormalities, we studied distal airspace cytology by performing bronchoalveolar lavage in 34 spondyloarthropathy patients (ankylosing spondylitis, n = 16; reactive arthritis, n = 4; axial psoriatic arthritis, n = 2; and undifferentiated spondyloarthropathy with HLA B27-positivity in every case but one, n = 12). Mean age was 32.4 +/- 13.7 years. None of the study patients had apical fibrosis, lower respiratory tract infection, or exposure to airborne pollutants other than tobacco smoke. The control group was composed of nine subjects who had no lung or inflammatory diseases and were not using medications. Significantly higher proportions of lymphocytes were found in bronchoalveolar lavage specimens from patients, as compared with controls. This difference was not influenced by smoking or medication use (non steroidal antiinflammatory drugs, sulfasalazopyridine). Alveolar lymphocytosis was not correlated with laboratory tests for disease activity (erythrocyte sedimentation rate, serum IgA levels) or with the presence of restrictive ventilatory dysfunction. Increases in the proportion of lymphocytes were of similar magnitude in patients with ankylosing spondylitis and in those with other spondyloarthropathies. Absolute total cell counts and relative neutrophil counts were similar in patients and controls. However, among the patients with spondyloarthropathies, those with a disease duration of more than five years had a significantly higher proportion of neutrophils than those with a disease duration of less than five years. These findings demonstrate that spondyloarthropathy patients have subclinical lymphocyte alveolitis. Although of unclear significance, this alveolitis may be related to the development of apical fibrosis in some patients with ankylosing spondylitis.
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PMID:[Demonstration of subclinical pulmonary alveolitis in spondylarthropathies]. 781 84

The objective is to report a case of atypical acute infectious mononucleosis in a juvenile ankylosing spondylitis patient who was treated with infliximab. A 20-year-old man was hospitalized for the evaluation of lymphadenopathy and systemic symptoms. His symptoms developed at the eighth week of the infliximab treatment and he required hospitalization. Lymph node biopsy was performed and he was diagnosed as atypical infectious mononucleosis (absence of fever, pharyngitis, lymphocytosis and negative atypical lymphocytosis on blood smear). Infections have become major concerns in patients treated with TNF-blocking agents. In theoretical base, it is not surprising as TNF-alpha has a crucial role in the body's defense against both bacterial and viral invasion. Blocking the action of TNF may also change the course of the disease and could lead to a delay in the diagnosis. TNF-alpha-blocking treatment may mask the typical symptoms of infectious mononucleosis and atypical cases should be included in the differential diagnosis of lymphadenopathy in patients receiving anti-TNF-alpha agents.
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PMID:Atypical infectious mononucleosis in a patient receiving tumor necrosis factor alpha inhibitory treatment. 1903 55