Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of Reiter's syndrome occurring in an 11-year-old, pre-pubertal boy is described. The boy was a heterozygote for the histocompatibility antigen B27 and other arthritic members of his family included his mother with colitic arthritis and an aunt with ankylosing spondylitis. His HLA-B27 negative sibs have remained well. Shigella Salmonella and Yersinia organisms have been previously incriminated as precipitating factors in some patients with Reiter's syndrome but no evidence of recent infection with any of these agents was found in this patient. The case is reported because of the rarity of the condition at this age.
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PMID:Juvenile Reiter's syndrome. 28 65

Two patients with acute gastroenteritis in whom polyarthritis subsequently developed were found to have positive serologic results for Yersinia pseudotuberculosis. With resolution of the arthropathy the antibody titres decreased. While the patient without the histocompatibility antigen HLA-B27 had an acute, self-limited arthritis, the patient with this antigen had a more chronic arthritis. Serologic typing and stool culture for Y. pseudotuberculosis should be done in cases of postdysenteric arthritis.
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PMID:Postdiarrheal arthropathy of Yersinia pseudotuberculosis. 34 3

Among the rheumatic diseases, non so clearly illustrates the relations between host and environmental factors as the seronegative spondyloarthropathy group of disorders. The strongest association is with the histocompatibility antigen HLA-B27, which accounts for a striking susceptibility to these diseases and is present in over 90% of individuals with idiopathic ankylosing spondylitis. Next in importance appears to be a difference in sex penetrance with males predominating in all categories. The most dramatic sex relationship is with postvenereal Reiter's syndrome which has a male-to-female ratio of nearly 50:1. Another potent host factor is age, with increased predisposition to onset at puberty and young adulthood in HLA-B27-positive patients. Environmental or possibly infectious agent influence are most apparent in Reiter's syndrome, where the antecedent circumstances of venereal contact and bacillary dysentery are frequent precipitating events. Secondary forms of peripheral arthritis, radiographic sacroiliitis, and ankylosing spondylitis frequently occur in psoriasis and inflammatory bowel disease; in the case of peripheral arthritis, there is no or a significantly reduced association with HLA-B27 compared to AS or RS. Secondary factor seem to be contributing to spondyloarthropathy in these disorders. These iterrelations emphasize the powerful effects of host characteristics on the type of rheumatic disease syndrome acquired and provide superb opportunities for more precise understanding of disease pathogenesis and ultimate control through the integration of epidemiologic, clinical, and laboratory research.
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PMID:A new look at the epidemiology of ankylosing spondylitis and related syndromes. 38 16

Vertebral ankylosing hyperostosis is a common skeletal disorder among Pima Indians. Prevalence rates of approximately 50% have been reported in Pima Indian males aged 44 or older. The HLA-B27 antigen is also found more commonly in Pima Indians than in Caucasians (18% versus 6%). Because of the increased prevalence of both vertebral ankylosing hyperostosis and HLA-B27 in Pima Indians, a possible association between the two was thought to exist. Therefore, histocompatibility testing was done on 44 adult male Pima Indians age 55 or older with classic vertebral ankylosing hyperostosis and 33 age-matched controls. No significant association between any histocompatibility antigen phenotype or haplotype and vertebral ankylosing hyperostosis was found. This disease, therefore, connot be classified with the HLA-B27 associated spondylarthropathies.
Arthritis Rheum 1978 May
PMID:Vertebral ankylosing hyperostosis (Forestier's disease) and HLA antigens in Pima Indians. 65 61

A study of 74 yersinia arthritis patients implied that the clinical picture of the disease may be modified by genetic background associated with the histocompatibility antigen B27 (HLA-B27). Sixty-six percent of patients were B27 positive. Joint symptoms were somewhat more severe in B27+ patients. Iritis, conjunctivitis, carditis, signs of urologic inflammation, and complete Reiter's triad occurred only in the B27 + group, whereas erythema nodosum was more common in B27 - group. Several B27 + patients also had "B27 + rheumatic diseases," such as ankylosing spondylitis or Reiter's disease, in their history.
Arthritis Rheum 1977 Jun
PMID:Relation between HLA-B27 and clinical features in patients with yersinia arthritis. 86 58

Seventy-one of 78 patients presenting to routine rheumatology clinics with seronegative arthritis were found to possess the histocompatibility antigen HL-A 27. Four principal components to their arthritis emerged, namely: spondylitis, sacroiliitis, peripheral polyarthritis, oligoarthritis (involvement of one or two large joints). It is suggested that each of these may be influenced by separate genetic determinants. The various combinations in which these occur warrant a unified nomenclature. A small subgroup of patients with HL-A 27-associated arthritis is described in whom the diseases may be especially benign.
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PMID:HL-A 27-associated arthritis. 93 38

Serum antibody levels against T mycoplasmas (Ureaplasma urealyticum) were determined by the metabolic inhibition method in several populations. A higher prevalence of antibody was found in Haida Indians and Bella Coola Indians than in blood donors, patients with rheumatoid arthritis, and patients attending a VD clinic. Antibody levels did not correlate with the presence of spodylitis or the histocompatibility antigen HLA-B27, although both these Indian populations have a high prevalence of spondylitis and HLA-B27.
Arthritis Rheum
PMID:Serum antibody levels against T mycoplasmas in two North American Indian populations predisposed to spondylitis. 99 41

The histocompatibility antigen W27 has been found to have a high incidence in ankylosing spondylitis (96%), Reiter syndrome (74%), and other forms of arthritis that may involve the axial skeleton. In patients with Reiter syndrome, there was no correlation between the presence of W27 antigen and the extent or duration of the symptoms. Sacroiliitis was predominantly found in those patients with W27 antigen in all the axial arthropathies. Tissue-typing techniques may be of value in detecting early or atypical disease.
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PMID:HL-A antigens and sacroiliitis. 117 31

Immunological responses to bacterial heat shock proteins have been implicated in the pathogenesis of arthritis in animals and humans. The predicted amino acid sequence of dnaJ, a heat shock protein from Escherichia coli, contains an 11-amino acid segment that is homologous to the third hypervariable region of the human histocompatibility antigen (HLA) DRB10401 (formerly known as HLA Dw4), the part of the molecule that carries susceptibility to rheumatoid arthritis. To test the biological significance of this finding, we expressed and purified recombinant dnaJ (rdnaJ), and determined its immunologic cross-reactivity with HLA DRB10401. A rabbit antipeptide antiserum raised against the sequence of the third hypervariable region of HLA DRB10401 specifically bound to 'dnaJ, thus confirming that a similar sequence is expressed on the bacterial protein. Of greater consequence, an antiserum to the 'dnaJ protein recognized not only a peptide from the third hypervariable region of HLA DRB10401, but also the intact HLA DRB10401 polypeptide. Furthermore, the antibody to 'dnaJ reacted with HLA DRB10401 homozygous B lymphoblasts, but not with HLA DRB11501, DRB10101, DRB10301, and DRB10701 (formerly known as HLA Dw2, DR 1, DR 3, and DR 7, in the same order) homozygous cells. These results demonstrate that exposure to a bacterial heat shock protein can elicit antibodies against the rheumatoid arthritis susceptibility sequence in the third hypervariable region of HLA DRB10401.
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PMID:The susceptibility sequence to rheumatoid arthritis is a cross-reactive B cell epitope shared by the Escherichia coli heat shock protein dnaJ and the histocompatibility leukocyte antigen DRB10401 molecule. 137 Mar

Ankylosing spondylitis (AS) is closely associated with the histocompatibility antigen HLA-B27. Pathogenesis of AS is thought to involve interactions between B27 and certain enterobacterial antigens. However, this is uncertain and contested by some. The present paper argues that the presence of statistically raised specific serum IgA to a common enterobacterial heat modifiable major outer membrane protein (h-momp; Mr 35,000) in active AS (N = 25; IgA = 1485 +/- 20) in comparison to controls, most notably hospital patients without known arthropathies or gastrointestinal disease (N = 12; IgA = 548 +/- 59), supports an inductive contribution of enterobacterial antigens to the pathogenesis of secondary AS. Serum IgG and IgM did not statistically differ. Raised specific serum IgA to h-momp might indicate enterobacterial antigenic stimulation from the gastrointestinal tract. It does not necessarily imply direct involvement in the pathogenesis of primary AS. H-momp appears to be a convenient tool for serological studies of AS and at present is likely to be more suitable than other bacterial antigens, notably those with B27-like epitopes. Namely, the confirmed presence in AS of enterobacteria with freely accessible B27-like antigenic epitopes on their cell surface might induce unusual tolerance to these organisms in B27 positive hosts, thus causing chronic inflammation, initially sacroiliitis (and spondylitis) due to the proximity of presacral and para-aortic colon draining lymph nodes, later becoming more generalized (for reasons unclear) to include other lesions (e.g. peripheral arthritis, uveitis, enthesopathies). Thus, antibodies to B27-like antigenic epitopes need not be detectable or may be absent. Also, cellular immune responsiveness to these antigens might be involved.
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PMID:Enterobacterial involvement in the pathogenesis of secondary ankylosing spondylitis. 245 14


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