Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred and sixty-six patients with different forms of rheumatic diseases were tissue typed for 26 antigens of the A and B locus of the HLA system, using a modified KN cytotoxicity test. Among 25 patients with confirmed ankylosing spondylitis, 23 had HLA B27 (92 per cent), compared to 2.5 per cent in the normal controls. This confirms the strong association of HLA B27 with ankylosing spondylitis. Eight patients had doubtful AS, five of whom were positive for B27. In 21 patients with mechanical disorders of the spine no B27 was found. Thirty-six patients with osteoarthrosis of the knee joints did not show any significant relationship with any HLA antigens. Twenty-one patients with systemic lupus erythematosus showed an increase of HLA B13 and B17.
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PMID:Histocompatibility antigens (HLA) in rheumatic diseases in Iran. 30 Nov 91

100 consecutive Chinese patients with SLE were recruited for study of HLA-A, B and DR antigen. Clinical and serological parameters were analysed with respect to the HLA antigens. B5 was associated with presence of other autoimmune diseases (thyrotoxicosis, myasthenia gravis, diabetes mellitus, corrected p less than 0.025); absence of malar rash (corrected p less than 0.025); B35, with male sex (corrected p less than 0.025); DR2 with anti-Ro (anti-SSA) antibody (p less than 0.05). Previous study of association with B13, B17 was not present in our cohort. Except for malar rash, subclassification of disease status with respect to HLA antigen did not reveal significant association.
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PMID:Immunogenetics in Chinese patients with SLE. 203 Nov 54

The expression of HLA class I was assessed on erythrocytes by haemagglutination with monoclonal antibodies to monomorphic epitopes on the heavy and light (beta 2-microglobulin) chains. Previously, enhancement of HLA class I expression was observed on erythrocytes of many patients with systemic lupus erythematosus (SLE) and chronic lymphatic leukaemia (CLL), and we have now tested erythrocytes from patients (and 130 normal controls) with other auto-immune diseases and renal and haematological disorders. The striking enhancement in patients with SLE and CLL was confirmed. A significant increase in expression was also observed in aplastic anaemia patients following bone marrow transplantation and in renal patients with primary glomerulonephritis who had received a transplant. No class I was expressed by erythrocytes from many patients with inherited haemoglobinopathies and high reticulocyte counts, which suggests that the enhancement in SLE patients cannot be accounted for by immature or young erythrocyte populations. The distribution of HLA-A and -B types in the patients with enhanced class I expression did not relate to those antigens previously detected more frequently on erythrocytes, B7(Bga), B17(Bgb), A28(Bgc), B8 or A10, and the enhancement was not associated with any particular HLA types.
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PMID:Erythroid HLA class I expression in 300 patients with haematological, renal and rheumatological disorders. 239 73

In a study of 32 white patients with systemic lupus erythematosus from 28 families, 60 unique chromosome 6 haplotypes were defined. The MHC extended haplotype HLA-B8, -DR3, SC01, GL02 was strongly disease-associated (0.09 patients, 0.02 controls, RR = 4.5, C.I. = 1.6-12.4, P less than 0.05), while the corresponding haplotype with the GL01 specificity was not increased in frequency (0.05 in both patients and controls). In the present data, the increase in the haplotype bearing GL02 accounted entirely for the association between HLA-DR3 and SLE. Furthermore, the phenotype of complete C4A deficiency was also strongly disease-associated (patients 0.14, controls 0.02, RR = 8.5, C.I. = 1.8-37.0, P less than 0.05). The only other MHC association in these patients was an increased occurrence of the HLA-B17, -DR7, SC61 haplotype (patients 0.07, controls 0.01, RR = 6.0, C.I. = 1.8-20.6, P corr. less than 0.05). The relationship between MHC markers and autoimmune disease appears to be a result of an association with MHC extended haplotypes and complete complement component deficiencies rather than with individual alleles. It is important that future studies include family members so that such haplotypes can be defined.
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PMID:Major histocompatibility complex extended haplotypes in systemic lupus erythematosus. 326 26

The HLA associations in skin diseases among the Chinese were reviewed. Tuberculoid leprosy was associated with B17 (RR = 4.1). This HLA association was reinforced in the finding of excess HLA haplotype sharing among affected siblings in multiple case families. In psoriasis the associations were with A1, AW30 and B13. The relative risk associated with AW30, B13 was 16.1. In SLE, mild patients were associated with B13 (RR = 3.7) and severe patients with B17.
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PMID:HLA and skin disease in the Chinese. 622 84

We present a case of retroperitoneal fibrosis associated with systemic lupus erythematosus (SLE) and review the etiology of retroperitoneal fibrosis. The HLA antigens found were A2, AW33, B8, B17, DR3, and DR6. The HLA antigens associated with retroperitoneal fibrosis and SLE are discussed.
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PMID:Retroperitoneal fibrosis associated with systemic lupus erythematosus: a case report and brief review. 673 76

Seventy-five unrelated Chinese SLE patients were HLA typed and subdivided into mild and severe disease. The HLA-B13 was associated with mild disease. Fourteen of 30 (46.7%) mild disease patients had B13 compared to 63/330 (19.1%) normal subjects (p less than 0.0005, corrected p less than 0.013, RR = 3.7). The HLA-B17 on the other hand was observed in 29% of 45 severe disease patients compared to 13.9% of 330 normal subjects (p less than 0.01, RR = 2.5). The frequency of HLA-B17 in 11 patients who died was even higher (45.5%).
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PMID:HLA and systemic lupus erythematosus in Chinese. 732 52

Although null alleles of complement C4 genes (C4A*Q0 and C4B*Q0) are frequent in the normal population, the occurrence of two null alleles on the same chromosome is very rare and therefore complete C4 deficiency is exceptional. We describe a 16-year-old North African boy who presented with systemic lupus erythematosus with renal involvement and persistent undetectable classical pathway activity and C4 protein and hemolytic activity in plasma, with normal C3 levels. Similar complement abnormalities were observed in his healthy 12-year-old brother. Complete C4 deficiency was documented in the two brothers by investigation of the family and the lack of C4A and C4B bands upon phenotyping of C4. Southern blot analysis of the C4/CYP21 gene organization in the family indicated that the deficiency resulted from a deletion of the C4B/CYP21A genes associated with nonexpression of a C4A gene. The double-null haplotype was found to be associated with homozygous A2 B17 C2C BFF C4 AQ0 BQ0 DR7 HLA haplotype. Thus, similar C4 deficiencies with HLA identity may lead to different clinical presentations.
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PMID:Complete inherited deficiency of the fourth complement component in a child with systemic lupus erythematosus and his disease-free brother in a north African family. 781 56

Male (NZW x BXSB)F1 (W/BF1) mice develop systemic autoimmunity involving autoantibodies, thrombocytopenia, lupus nephritis, and coronary vascular disease (CVD) with myocardial infarction. To determine whether this murine lupus-associated CVD can be prevented by the reduction of dietary calories, male W/BF1 mice were separated into five experimental groups and fed either ad libitum (designated group A, n = 50), fed 32% fewer calories of an otherwise comparable diet (designated group B6, n = 20), or initially fed ad libitum and then switched to reduced calorie intake (RCI) feeding at ages 14, 17, or 22 weeks (designated B14, n = 10; B17, n = 20; or B22, n = 20). Occlusive CVD was prevented by RCI. Life-span was significantly extended among the early onset RCI cohorts, B6 and B14 (P = 0.0001 and P = 0.005), compared to group A mice. Mean anti-cardiolipin autoantibody titers and mean levels of circulating immune complexes were also lowered in RCI mice when all RCI mice were compared to ad libitum fed group A mice. Histological grades of both coronary vascular and glomerular lesions were significantly less than those of group A mice (P < 0.001). Immunoprecipitates indicative of immunoglobulin deposition within coronary or glomerular vascular walls were also substantially less than those of group A mice. These findings indicate a possible causal role for anti-cardiolipin autoantibody in development of autoimmune CVD in W/BF1 mice and suggest that regulating dietary calories can influence the mechanism involved in pathogenesis of autoimmune-associated CVD development.
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PMID:Calorie restriction prevents the occlusive coronary vascular disease of autoimmune (NZW x BXSB)F1 mice. 818 20