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)

Twenty-five patients with juvenile chronic arthritis (JCA) were typed for HLA-A,-G,-C and -DR antigens to establish significant differences between normal controls and patients with adult rheumatoid arthritis (RA). HLA-DR antigens were correlated with subgroups of disease, and with several clinical features and immunological parameters of JCA. The frequency of DRW8 antigen was significantly higher in JCA than in normal adult controls or patients with RA. This significance was even higher in the persistent pauciarticular subgroup. Connections were found between DR antigens and clinical, immunological parameters, and some of them proved to be statistically significant. Results are presented and discussed in detail.
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PMID:HLA-DR antigens in juvenile chronic arthritis. 695 35

A total of 48 patients with juvenile chronic arthritis (JCA) were typed for HLA-A, -B, -C, -D and -DR antigens and 36 patients were also typed for HLA-D/DR associated "DR"-antigens with the primed lymphocyte typing technique. In the total group of patients, we found increased frequencies of HLA-B27, HLA-Dw/DP5 and HLA-Dw/DP8, and decreased frequencies of HLA-Dw/-DR/DP2. The increased frequencies of HLA-Dw/DP8 and the decreased frequencies of HLA-Dw/-DR/DP2 were primarily found among patients with persistent pauciarticular arthritis. The frequencies of HLA-Dw/-DR/DP4 were increased in patients with polyarticular arthritis. The frequencies of HLA-B27 and -Dw/DP5 were increased in both pauciarticular and polyarticular arthritis. The results indicate (i) that genetic factors controlled by HLA confer susceptibility and/or resistance to JCA, and (ii) that the clinical subdivision of JCA into pauciarticular and polyarticular JCA can be supported by the presence of different genetic markers (HLA-antigens) in the two groups of JCA-patients. If these data can be confirmed HLA-D, -DR or DP typing may be of value in the prognostic evaluation of patients with pauciarticular onset JCA.
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PMID:HLA-A, B, C, D, DR antigens and primed lymphocyte typing (PLT) defined DP-antigens in juvenile chronic arthritis. 703 4

Sixty-three Japanese patients with rheumatoid arthritis (RA) were typed for HLA-A, -B, and -DR locus specificities. A significant association was found only with increased frequency of HLA-DR4 in the patients (71.4%) compared with controls (41.8%) (corrected P = 0.007, relative risk = 3.5). No association was found with HLA-A9 or HLA-Bw54, which are in linkage disequilibrium with HLA-DR4 in the Japanese. The association between HLA-DR4 and RA observed in these Japanese patients has also been demonstrated in the white population.
Arthritis Rheum 1981 May
PMID:HLA and rheumatoid arthritis in the Japanese. 723 27

Linkage analysis of HLA haplotypes, HLA-B27 subtypes, and a 9.2-kb PvuII B7 restriction fragment length polymorphism (RFLP) (shown previously to be associated with peripheral arthritis in ankylosing spondylitis [AS]) in 115 relatives from 12 multiplex spondyloarthropathy (SNSA) and 2 B27-positive control families showed AS to be linked to HLA-B27 haplotypes. The RFLP segregated with HLA-A3- and HLA-A9-bearing haplotypes (lod score, 10.98; odds in favor of linkage, 9.2 x 10(10):1), although its linkage to AS or other SNSA per se was not seen. The association of HLA-A3/A9 with the RFLP was also seen in 52 AS patients and 92 controls, although no HLA-A, -B, -C, or -DR allele (other than HLA-B27) was significantly increased in frequency. The HLA-B27 subtype seen on all but one of the haplotypes studied was B*2705, the sole exception being HLA-B*2702. Although not ruling out a second HLA-A-linked gene influencing the clinical expression of AS, these data fail to support the role of a second MHC-associated gene in the pathogenesis of AS per se.
Semin Arthritis Rheum 1994 Apr
PMID:HLA in ankylosing spondylitis: is HLA-B27 the only MHC gene involved in disease pathogenesis? 791 56

The purpose of the present work was to find out whether there is an HLA type common to the patients who, in spite of being B27 negative, have developed reactive arthritis (ReA). We compared the HLA-antigens of 25 HLA-B27 negative ReA patients to those of healthy control persons. No statistically significant differences were observed in the HLA-A, B, C, DR and DQ antigen frequencies between the patients and the control group. The frequency of DR4 was slightly lower in the patients than in the controls, although this difference was not statistically significant. On the other hand, 18/25 (72%) of the B27-negative ReA patients experienced a chronic or prolonged course of the disease. These findings indicate that DR4 does not contribute to the chronicity of ReA in the same way that it is known to do in rheumatoid arthritis (RA) or Lyme arthritis. They do not support the hypothesis that some other HLA-antigen, in addition to HLA-B27, could have a predisposing or protective effect in ReA.
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PMID:HLA frequencies in HLA-B27 negative patients with reactive arthritis. 857 44

The major initial clinical manifestations of systemic lupus erythematousus (SLE) were skin and mucous membrane involvement (52%), fever and malaise (48%), arthritis and arthralgias (44%). Lupus nephritis was diagnosed in 74% of patients and diffuse proliferative nephritis was the commonest histologic picture encountered. Except for a higher prevalence of anti-SS-A (Ro) (63%), other autoantibodies were within the normal range reported from Western countries. There was no significant association between HLA-A, B or DR specificities in 51 Chinese patients, nor was there any differences seen in the polymorphism of tumour necrosis factor alpha gene (TNF-alpha). Arthritis was less commonly seen in males with SLE. Prevalences of leukopenia and antibodies to anti-SS-A (Ro) and anti-La (SS-B) antigens were lower in men. Late onset lupus patients (> 50 years of age) tended to have more insidious onset of disease, lower female predominance and less frequent complaints of fever, alopecia, arthritis and malar rash at presentation. The causes of death were often treatment related. Survival studies among 183 SLE patients during the period from 1970 to 1980 revealed a 5- and 10-year survival rate of 70% and 60%, respectively. Infections and active lupus disease were 2 major causes of death. Research into SLE is targeted at increasing our understanding of the disease process and improving outcome and prognosis.
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PMID:Systemic lupus erythematosus in Singapore. 958 73

Previous studies have shown that susceptibility to Pauciarticular Juvenile Arthritis is associated with HLA-A*0201. Recently, autoantibodies against the protein of the DEK oncogene have been found in sera of patients with this disease. If T cells are involved in the pathogenesis of joint lesions, it is possible that they target autoantigens presented by HLA-A*0201. Therefore, we investigated whether DEK-derived peptides can bind efficiently to HLA-A*0201. Nonameric peptides selected considering anchor positions 2 and 9, and preferred amino acids at other positions, were incubated either with the human TAP-deficient cell line 174CEM.T2 (T2) or with the homozygous B cell line JESTHOM (A*0201, B*2705, Cw1), previously depleted of endogenous peptides. Binding was measured as the increase of detection of fully assembled, HLA-A*0201 molecules by flow cytometry with the anti-HLA-A2 monoclonal antibody (mAb) BB7.2. Three out of ten selected DEK-derived peptides showed binding to HLA-A*0201, which was peptide concentration-dependent (1 microM to 100 microM). DEK155-163 (AMLKSICEV), which also has two preferred amino acid residues at positions 6 and 8, yielded the highest binding. DEK163-171 (VLDLERSGV) and DEK72-80 (SLQREPFTI), which also has one preferred amino acid residue at position 8, also were able to bind to HLA-A*0201. Furthermore, peptide-induced, fully assembled, HLA-A*0201 molecules were immunoprecipitated with the BB7.2 mAb from metabolically-labeled T2 cells incubated with DEK72-80, DEK155-163, and DEK163-171. A faint band was observed in the immunoprecipitates of cells incubated with DEK65-73 (it carries a preferred amino acid residue at position 6), suggesting that this peptide interacts weakly with HLA-A*0201. These results indicate that several nonameric peptides derived from the DEK protein can bind to HLA-A 0201 and suggest that the complexes formed may be able to stimulate CD8+ T cells in patients with Pauciarticular Juvenile Arthritis.
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PMID:Juvenile arthritis, HLA-A2 and binding of DEK oncogene-peptides. 968 94

Sydenham's chorea (SC) may occur in rheumatic fever (RF) patients without arthritis and carditis. In this study we typed HLA antigens and alleles in patients presenting with the distinct major clinical manifestations of RF, i.e., chorea, carditis, or arthritis, in population and family studies. We evaluated 91 patients with RF for HLA-A, HLA-B, and HLA-DR antigens; of these, 33 had pure chorea, 26 pure carditis, 16 pure arthritis, and 16 carditis plus arthritis. We also typed 24 SC patients and their unaffected siblings for HLA-DRB1 and HLA-DQB1 alleles using molecular methods. HLA-B49 and HLA-DR1 antigens were overrepresented in the total group of patients with RF and in all the subgroups studied, excluding the SC subgroup in which the frequency of HLA-DR1 antigen was not increased. The frequencies of the HLA-DRB1 and HLA-DQB1 alleles in patients with pure chorea were not significantly different from those observed in controls. Similarly, the frequencies of HLA class II alleles in SC patients did not differ significantly from those observed in unaffected siblings. These findings show that immunogenetic susceptibility to RF varies according to the major clinical manifestation presented by the patient.
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PMID:HLA class I and class II profiles of patients presenting with Sydenham's chorea. 1075 Nov 15

Psoriatic arthritis (PsA) is an inflammatory arthritis that may affect as many as 30% of patients with psoriasis (Ps). Genetic factors play an important role in the susceptibility to and the expression of PsA. The objective of this study was to identify whether haplotype sharing among affected sibling pairs of individuals with PsA is increased compared with unaffected sibling pairs. We collected 182 sibling pairs of probands affected with PsA. Extracted genomic DNA was amplified in polymerase chain reactions using locus specific primers homologous to nucleotide sequences for each of the HLA-A, -B, -C, -DR, and -DQ loci. Polymerase chain reaction amplicons were identified by reverse line blot assay using sequence-specific oligonucleotide probes. Evidence for excessive haplotype sharing was examined through Green and Woodrow's test. Results indicate that of the 182 sibling pairs, 46 were affected by PsA, 48 by Ps, and 88 were unaffected. The sharing of 2, 1, and 0 haplotypes for the PsA affected sibling pairs was 14, 27, and 5, respectively (p = 0.04); whereas the haplotype sharing for the Ps affected sibling pairs was 12, 26, and 10, respectively (p = 0.38). In conclusion, the human leukocyte antigen region on chromosome 6p is implicated as one of the candidate regions in PsA.
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PMID:HLA is a candidate region for psoriatic arthritis. evidence for excessive HLA sharing in sibling pairs. 1294 44

Juvenile idiopathic arthritis (JIA) is one of the most common forms of pediatric chronic arthritis. JIA is a clinically heterogeneous disease. Therefore, the genetic background of JIA may also be heterogeneous. The aim of this study was to investigate associations between human leukocyte antigen (HLA) and susceptibility to JIA and/or uveitis, which is one of the most devastating complications of JIA. A total of 106 Japanese articular JIA patients (67 with polyarthritis and 39 with oligoarthritis) and 678 healthy controls were genotyped for HLA-A, -B and -DRB1 by PCR-sequence-specific oligonucleotide probe methodology. HLA-A(*)02:06 was the risk factor for JIA accompanied by uveitis after adjustment for clinical factors (corrected P-value < 0.001, odds ratio (OR) 11.7, 95% confidence interval (CI) 3.2-43.0). On the other hand, HLA-DRB1(*)04:05 was associated with polyarticular JIA (corrected P-value < 0.001, OR 2.9, 95% CI 1.7-4.8). We found an association of HLA-A(*)02:06 with susceptibility to JIA accompanied by uveitis, which might be considered a separate clinical JIA entity. We also found an association between HLA-DRB1(*)04:05 and polyarticular JIA. Thus, clinical subtypes of JIA can be classified by the presence of the specific HLA alleles, HLA-A(*)02:06 and DRB1(*)04:05.
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PMID:Association of HLA-A*02:06 and HLA-DRB1*04:05 with clinical subtypes of juvenile idiopathic arthritis. 2117 6


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