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)

Serologic evidence of Yersinia enterocolitica infection was sought by agglutination testing in serum samples from several populations, including Haida Indians, Red Cross blood donors, and Caucasian patients with rheumatoid arthritis, ankylosing spondylitis, and Reiter's syndrome. No evidence was found to indicate that yersinial infection was etiologically related to Haida spondylitis or Reiter's syndrome. Four of 28 patients with acute arthritis were diagnosed from serologic evidence as having Yersinia-related arthritis.
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PMID:Yersinia-related arthritis in the Pacific Northwest. 90 97

Sera from 156 patients with ulcerative colitis and Crohn's disease were tested for the presence of immune complexes, by the detection of anti-complementary activity and 125I-labelled Clq precipitation. Using aggregated IgG, a comparison between the two tests indicated that the anti-complementary test was most sensitive to aggregates of 11S in size, while the 125I-labelled Clq test detected aggregates over 20S in size. Excess anti-complementary activity was common in patients with active bowel disease, and in those with extra-intestinal manifestations, particularly acute arthritis, ankylosing spondylitis and liver disease. Large complexes were only common in patients with liver disease. Immune complexes in the gut mucosa may play a role in the pathogenesis of these diseases, and the deposition of circulatory immune complexes may explain at least some of the extra-intestinal manifestations.
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PMID:Immune complexes in ulcerative colitis and Crohn's disease. 90 71

Murine progressive ankylosis (MPA) is an heritable disorder which produces acute arthritis and ankylosis of peripheral and axial joints similar to ankylosing spondylitis. Because indomethacin inhibits heterotopic bone formation in vivo, we studied its effects on MPA. Indomethacin was administered for 6 weeks beginning at weaning to litters from heterozygote breeder pairs. Progression curves for peripheral, spinal and thoracic joint ankylosis in treated and untreated ank/ank animals wer compared. There was no delay in ankylosis of peripheral or spinal joint ankylosis in MPA animals treated with indomethacin. interestingly, transient delay of thoracic ankylosis occurred in indomethacin treated MPA animals.
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PMID:Transient inhibition of murine progressive ankylosis by indomethacin. 179 41

This study has identified a group of patients with inflammatory chronic, or relapsing acute arthritis who even in the absence of gastrointestinal symptoms have histological evidence of ileocolitis. At colonoscopy simultaneous biopsies of the terminal ileum and colon were taken from 108 patients with reactive arthritis (n = 55) or ankylosing spondylitis (n = 53), 47 patients with other rheumatic diseases and 19 control patients suffering from colonic polyps, adenocarcinoma, or chronic constipation. All control patients and all but one patient with rheumatoid arthritis, juvenile chronic arthritis, systemic lupus erythematosus, lumbar back ache, and psoriatic arthritis did not have histological evidence of acute or chronic inflammatory bowel disease. In contrast, in 30 of 35 (56.6%) patients with ankylosing spondylitis, and in 37 of 55 (67%) patients with reactive arthritis, regardless of HLA B27 phenotype, there was histological evidence of inflammatory bowel disease with features either of acute enterocolitis, or early Crohn's disease. Only 18 of 67 (27%) of the patients with histological gut inflammation, however, had intestinal symptoms.
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PMID:Histopathology of intestinal inflammation related to reactive arthritis. 349 71

Antibodies specific for glucose-6-phosphate isomerase (G6PI) from T-cell receptor transgenic K/BxN mice are known to induce arthritis in mice, and immunization of DBA/1 mice with G6PI led to acute arthritis without permanent deformation of their joints. Because rheumatoid arthritis is a chronic disease, we set out to identify the capacity of G6PI to induce chronic arthritis in mice. Immunization with recombinant human G6PI induced a chronically active arthritis in mice with a C3H genomic background, whereas the DBA/1 background allowed only acute arthritis and the C57BL/10 background permitted no or very mild arthritis. The disease was associated with the major histocompatibility region sharing an allelic association similar to that of collagen-induced arthritis (i.e. q > p > r). All strains developed a strong antibody response to G6PI that correlated only in the C3H.NB strain with arthritis severity. Similarly, a weak response to type II collagen in a few mice was observed, which was associated with arthritis in C3H.NB mice. Mice on the C3H background also developed ankylosing spondylitis in the vertebrae of the tail. Both C3H.Q and B10.Q mice deficient for B cells were resistant to arthritis. We conclude that G6PI has the ability to induce a chronic arthritis, which is MHC associated and B-cell dependent. Thus, there are striking similarities between this and the collagen-induced arthritis model.
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PMID:Induction of a B-cell-dependent chronic arthritis with glucose-6-phosphate isomerase. 1627 85

Some authors sustained that the pessimistic thought of the Italian writer and philosopher Giacomo Leopardi (1798-1837) may be attributed to his unhappy life, characterized by several health problems. His philosophical theories appear as the result of depressive and melancholic state, related to his precarious health conditions, so limiting their intrinsic values. Several authors formulated various hypotheses on the diseases that Leopardi suffered from and postulated different theories on the cause of his early death. This article assumed that Leopardi may have been affected by juvenile ankylosing spondylitis, conditioning spinal deformities, relapsing-remitting uveitis, urinary tract and bowel tract problems, and acute arthritis. Chest deformity, as a complication of juvenile ankylosing spondylitis, may have caused progressive cardiorespiratory failure, worsened by recurrent bronchial and pulmonary complications, until his death caused by acute right ventricular heart failure. The acknowledgment of a physical cause of Leopardi's disease contributes to reevaluate his "cosmic pessimism" as an original expression of his thought, so leading a general revaluation of the figure of one of the most important European thinkers of the 19th century.
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PMID:The Disease of the Italian Poet Giacomo Leopardi (1798-1837): A Case of Juvenile Ankylosing Spondylitis in the 19th Century? 2848 25