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)

The therapeutical effect of levamisole in ankylosing spondylitis as well as the effect of this therapy on the immunologic parameters were to be examined. Since the sample consisted of 10 patients only, statistically relevant results were not to be expected. Only male patients with positive HLA-B 27 have been examined. The therapeutical effect after treatment of 3 months has been observed as good to very good. The immunologic parameters reacted in a mode which had formerly been described as immunomodulating.
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PMID:[Therapy of spondylitis ankylopoetica with levamisole. Behavior of clinical and immunological parameters]. 685 56

The prevalence of serum leukocyte-reactive antinuclear antibody (LR-ANA) was determined in 31 patients with ankylosing spondylitis (AS), their age-and gender-matched normal controls, and two tribes of 340 West Coast Canadian Indians (Bella Coolas and Haidas). At a serum dilution of 1 : 10, the prevalence of LR-ANA in AS and controls was 45% and 7%, respectively. At 1 : 20 dilution, the prevalence was 23% in AS, 0% in controls, 29% in Bella Coolas and 27% in Haidas. No concordance was found among LR-ANA, HLA-B27 and CREG-B7, and nine HLA-A and seven HLA-B antigens in the Indian tribes. These studies confirm an increased prevalence of LR-ANA in AS and AS kindreds, but the latter association appears to be independent of HLA antigens.
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PMID:Population studies of leukocyte-reactive antinuclear antibody and HLA antigens. 698 Nov 81

The association between acute iridocyclitis (a.i.) and sacroiliitis/ankylosing spondylitis is well known. Since bone scintigraphy is a sensitive method of detecting sacroiliitis before radiologic evidence of this condition appears, we examined the role of scintiscanning in the investigation of sacroiliitis in patients with a.i. The sacroiliac-joint/sacrum ratio was determined in 30 control subjects and in 21 patients with a.i., who showed no radiologic signs of sacroiliitis. No discrimination between patients with a.i. and control subjects was obtained by scintigraphy, neither did we find any difference in the mean sacroiliac-joint/sacrum ratios between HLA-B-27-positive and HLA-B-27-negative individuals with a.i. This study does not support the claim that patients with a.i. often suffer from clinically and radiologically silent sacroiliitis which would be detected only by scintigraphy. According to our results, regular scintigraphic examinations of the sacroiliac joint in all patients with a.i. are not indicated.
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PMID:[Diagnostic value of sacroiliac-joint scintigraphy in acute iridocyclitis]. 698 55

The studies of histocompatibility (HLA) antigens have contributed to the understanding of the pathogenesis of uveitis. Acute anterior uveitis is associated with rheumatic disorders such as ankylosing spondylitis. HLA-B 27 antigen is present in 98% of these cases. There are genetic and environmental factors influencing the activity of the disease. HLA-B 27 was found to be associated with 43% of cases of acute anterior uveitis without systemic disease. In juvenile chronic polyarthritis with acute anterior uveitis HLA-B 27 helps in differentiating between ankylosing spondylitis and Still's disease. Specific HLA antigens were also found in other forms of uveitis such as Reiter's disease (HLA-B 27), Behcet's syndrome (HLA-B 5), VKH syndrome (HLA-Bw 22J) and ocular histoplasmosis (HLA-B 7). Despite these new findings, there are still many obscure factors and further studies are required to elucidate the pathogenesis of uveitis and to achieve its prevention.
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PMID:Histocompatibility antigens (HLA) and uveitis. 698 62

In addition to HLA-B27, other genetic factors are thought to be involved in the pathogenesis of ankylosing spondylitis (AS). Because of the localization, in the proximity of the HLA-B locus, and the biological activities of TNF-alpha, we investigated the association between AS and a single base polymorphism located at position -308 of the TNF-alpha gene. An allele-specific polymerase chain reaction was developed to monitor this polymorphism. The frequency of the TNF-alpha alleles was determined in 66 AS patients and 37 healthy controls. The TNF-alpha allele frequency was not significantly different between AS patients and controls.
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PMID:Polymorphism of tumour necrosis factor-alpha (TNF-alpha) at position -308 in relation to ankylosing spondylitis. 803 19

The NcoI polymorphism of the HSP70-Hom gene was investigated in the Finnish population and in two HLA-B27-associated autoimmune diseases. The two HSP70-Hom alleles were shown to be strongly associated to some specific HLA-B/DR haplotypes in random Finnish population and the segregation of the alleles as a part of these haplotypes was confirmed in 18 families. In addition, the HSP70-Hom alleles of 31 patients with ankylosing spondylitis (AS) and 38 with reactive arthritis (ReA) were compared with each other and with 56 unrelated healthy HLA-B27 positive individuals. The results indicated that the HSP70-Hom polymorphic variation is not connected independently to the different pathogenesis of AS and ReA, as no statistically significant differences between the patient groups and/or controls could be found. The HSP70-Hom status was investigated also in 28 homozygous HLA typing cells and when compared with previously published results of HSP70-l and HSP70-2 polymorphisms, it appeared that these three MHC Class-III linked HSP70 genes segregated in fixed allelic combinations.
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PMID:HSP70-Hom NcoI polymorphism and HLA-associations in the Finnish population and in patients with ankylosing spondylitis or reactive arthritis. 909 22

In order to address the possibility that the MICA gene located 47 kb upstream from HLA-B is involved in the pathogenesis of ankylosing spondylitis (AS), we have investigated microsatellite polymorphism in the transmembrane region of MICA in Caucasian patients with AS. The microsatellite allele consisting of 4 repetitions of GCT/AGC was present at significantly higher frequency in the patient group (Pc<0.0000001) than in the ethnically matched control group. However, the frequency of the (GCT/AGC)4 allele was significantly low in the B27-positive patients than in the B27-positive healthy controls (Pc=0.0145). These observations suggest that B27 itself remains the primary genetic marker for AS, although the significantly dissimilar phenotype frequency of the (GCT/AGC)4 allele in B27-positive patients and healthy individuals may reflect the existence of other genetic factor(s) in the HLA-B27 haplotype involved in the development of AS.
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PMID:MICA gene and ankylosing spondylitis: linkage analysis via a transmembrane-encoded triplet repeat polymorphism. 917 44

The system was designed with emphasis on the identification HLA-B alleles and genotypes associated or potentially associated with seronegative arthritides. By using a combination of multiplex SSP and PCR-RFLPs, the assays can be economically performed on a large range of sample sizes in diagnosis and epidemiology. 24 HLA-B alleles and subtypes can be discriminated, including options for PCR-RFLP or sequence specific amplification of the allele groups B27 and B60 (B*4001 and B*4007). In addition, the internal control carries central MHC polymorphisms, which can help to identify HLA extended halplotypes. False negatives, caused by preferential amplification of the internal control under suboptimal PCR conditions, were prevented by employing new, optimized PCR buffer. Four of the HLA-B primers were pooled into a multiplex reaction whose products were subtyped by digestion with seven restriction endonucleases. Specificity and sensitivity were verified in a panel of 68 homozygous cell lines and 200 heterozygous samples. An HLA-B*27-B*40 hybrid allele was observed in 3 out of 95 B*27-positive individuals from Berlin, Germany. Such an allele could be mistyped by some published assays as a B*27/B*40 heterozygote, a genotype reported to confer an increased risk for ankylosing spondylitis.
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PMID:An integrated multiplex-PCR and PCR-RFLP typing system for markers associated with seronegative arthritides. 953 35

Despite the strength of the association of ankylosing spondylitis (AS) with HLA-B27, other genetic elements could play a possible role in the pathophysiology of AS. Because of the localization, in the proximity of the HLA-B locus, and the involvement of heat shock proteins (HSP) in the immune response, we analyzed the influence of HSP70 gene polymorphism on the susceptibility to AS. HSP70-1, HSP70-2 and HSP70-hom genotypes were analyzed by PCR-RFLP in patients with AS and in healthy controls. The results obtained in the present study showed that there are not significant differences in the distribution of HSP70-hom genotypes, whereas significant differences in HSP70-1 and HSP70-2 genotypes between AS patients and random controls were found. However, when the distribution of these genotypes were compared in B*27-matched AS patients and controls, the differences disappeared. These data suggest that the polymorphism of HSP70 genes was not independently associated with AS, and that the differences in HSP70-1 and HSP70-2 genotypes among AS patients and controls appears to be due to the linkage disequilibrium between HSP70 alleles and HLA-B*27.
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PMID:HSP70 gene polymorphisms in ankylosing spondylitis. 958 10

Despite the strength of the association of ankylosing spondylitis (AS) with HLA-B27, other genetic elements could play a possible role in the pathophysiology of AS. In view of its gene location, in the proximity of the HLA-B locus, and biological effects, tumor necrosis factor (TNF) genes are potential candidates for additive susceptibility factors to AS. TNFalpha and TNFbeta genotypes were analyzed by PCR-RFLP in 57 patients with AS, 102 random controls and 30 HLA-B*27-positive controls. No significant differences of TNFalpha promoter variations at position -308 and -238 were found in AS patients in comparison with controls. The -244 polymorphism was not detected in our population. The TNFbeta genotype frequency was significantly different between AS patients and random controls. However, when the distribution of the TNFbeta genotype was compared in B*27-positive AS patients and controls, these differences disappeared. In addition, we demonstrated that the TNFbeta*1 was in strong linkage disequilibrium with the B*27 allele, which may explain the differences observed for the TNFbeta genotype among AS patients and random controls. Our data suggest that the polymorphisms of TNFalpha and TNFbeta genes do not have an independent effect on AS susceptibility.
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PMID:Tumor necrosis factor gene polymorphisms in ankylosing spondylitis. 958 11


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