Ultrasonographic evaluation of enthesitis in patients with ankylosing spondylitis.
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ABSTRACT:
SUBMITTER: Zhang H
PROVIDER: S-EPMC5445219 | biostudies-other | 2017 Jan
REPOSITORIES: biostudies-other
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Project description:ObjectivesThe aim of this study was to investigate the activities of serum paraoxonase and arylesterase in patients with ankylosing spondylitis with respect to those of healthy controls, to assess whether these enzyme levels are related to disease activity and functional capacity.MethodsThe study included 32 patients with ankylosing spondylitis whose diagnoses were made according to the modified New York criteria as well as 25 healthy controls matched for age and sex. The Bath Ankylosing Spondylitis Disease Activity Index and the Bath Ankylosing Spondylitis Functional Index were applied to the ankylosing spondylitis patients. As laboratory parameters, the erythrocyte sedimentation rate and serum C-reactive protein level were measured in patients and control subjects. Paraoxonase and arylesterase enzyme activities were measured using appropriate methods.ResultsNo statistically significant differences (p>0.05) were found between the ankylosing spondylitis patients and controls in terms of serum paraoxonase or arylesterase levels. Furthermore, there was no correlation between clinical and laboratory parameters in patients with ankylosing spondylitis.ConclusionSerum paraoxonase and arylesterase levels in ankylosing spondylitis patients may not differ from those of healthy controls, and there is no significant correlation between antioxidant parameters and the Bath Ankylosing Spondylitis Disease Activity Index or Bath Ankylosing Spondylitis Functional Index scores in ankylosing spondylitis patients. Further research is needed to provide deeper understanding of this disease.
| S-EPMC2827704 | biostudies-literature
Project description:BackgroundAnkylosing spondylitis (AS) is a chronic inflammatory disease mainly affecting the spine and sacroiliac joints. Macrophage migration inhibitory (MIF) factor is a regulatory cytokine that inhibits random immune cell migration. MIF gene promoter polymorphisms play a role in the progression of several inflammatory disorders.AimsTo investigate the relationship between the MIF gene -173 G/C single-nucleotide polymorphism (SNP) and AS.Study designCross-sectional study.MethodsIn this study, a total of 161 AS and 194 normal controls were recruited. The MIF gene -173 G/C SNP was analyzed by polymerase chain reaction using the restriction fragment length polymorphism method.ResultsThere was no significant difference between groups in terms of genotype distribution (p>0.05). When wild-type G/G and G/C+C/C genotypes are compared in terms of clinical characteristics, there is a significant difference between the average age and the duration of disease in AS patients (p<0.05).ConclusionNo significant relationship between AS disease and MIF -173 G/C polymorphism was found. MIF -173 G/C polymorphism (C allele) may affect the time of onset and the duration of disease in AS patients.
| S-EPMC5156461 | biostudies-literature
Project description:Ankylosing spondylitis is the most common form of the chronic inflammatory disease group known as spondyloarthritides. Recent discoveries of the CD4+ Th17 cells and IL-23/IL-17 axis have changed the paradigms in many autoimmune diseases. In this study, we aimed to evaluate the importance of IL-23/IL-17 pathway and IL-23 receptor polymorphism in the pathogenesis of ankylosing spondylitis. Blood samples for this study were obtained from 109 ankylosing spondylitis patients and 40 healthy control subjects. Serum levels of TNF-α, IL-6, IL-17, and IL-23 were measured by the ELISA method. The IL-23R gene polymorphisms rs11209026 (Arg381Gln) and rs4131362 (Val362Ile) were performed by the Sanger Sequence method. IL-6 levels were higher in the active and inactive ankylosing spondylitis groups than in the control group. However, levels of IL-17 and IL-23 were lower in the patient group. The frequency of IL-23R gene rs11209026 and rs4131362 polymorphism were 3.7% and 8.3% in the patient, respectively. As a result, dysregulation of the IL-23 / IL-17 pathway, which is caused by reduced levels of IL-17 and IL-23 in systemic circulation in patients with ankylosing spondylitis, may contribute to the pathogenesis of the disease by systemically producing chronic autoimmune inflammation.
| S-EPMC7050057 | biostudies-literature
Project description:BackgroundPreference-based measures of health-related quality of life (HRQoL), such as the EQ-5D or the SF-6D, are essential for health economic evaluation. However, they are rarely included in clinical trials of ankylosing spondylitis (AS). This study aims to develop mapping algorithms to predict EQ-5D-3L and EQ-5D-5L health utility scores from the Bath Ankylosing Disease Activity Index (BASDAI) and the Bath Ankylosing Spondylitis Functional Index (BASFI).MethodsPatients with AS were recruited from the largest tertiary hospital in Shandong province, China, between December 2019 and October 2020. Patients were selected by convenience sampling method according to the following criteria: (1) diagnosed with AS according to the New York criteria; (2) aged 18 years and above; and (3) without mental disorders; (4) able to understand the questionnaires; (5) without serious complications. There were 243 patients who completed the face-to-face questionnaire survey, and 5 cases with missing values in key variables were excluded. Ordinary least squares, censored least absolute deviations, Tobit, adjusted limited dependent variable mixture model and beta-mixture model (BM) in the direct approach and ordered logit and multinomial logit (Mlogit) model in the response approach were used to develop mapping algorithms. Mean absolute error, root mean square error, Spearman's correlation coefficient and concordance correlation coefficient were used to access predictive performance.ResultsThe 238 patients with AS had a mean age of 35.19 (SD = 9.59) years, and the majority (74.47%) were male. The observed EQ-5D-3L and EQ-5D-5L health utility values were 0.88 (SD = 0.12) and 0.74 (SD = 0.27), respectively. The EQ-5D-5L had higher conceptual overlap with the BASDAI and BASFI than the EQ-5D-3L did. The Mlogit was the best-performing model for the EQ-5D-3L, and the BM showed better performance in predicting EQ-5D-5L than other direct and indirect mapping models did.ConclusionThis study demonstrates that the EQ-5D-5L, rather than EQ-5D-3L, should be selected as the target outcome measure of HRQoL in patients with AS in China, and the BM mapping algorithm could be used to predict EQ-5D-5L values from BASDAI and BASFI for health economic evaluation.
| S-EPMC11304938 | biostudies-literature
Project description:Introduction: A number of genetic-association studies have identified genes contributing to AS susceptibility but such approaches provide little information as to the gene activity changes occurring during the disease process. Transcriptional profiling generates a “snapshot” of the sampled cells activity and thus can provide insights into the molecular processes driving the disease process. We undertook a whole-genome microarray approach to identify candidate genes associated with AS and validated these gene-expression changes in a larger sample cohort. Methods: 18 active AS patients, classified according to the New York criteria. and 18 gender-and age-matched controls were profiled using Illumina HT-12 Whole-Genome Expression BeadChips which carry cDNAs for 48000 genes and transcripts. Class comparison analysis identified a number of differentially expressed candidate genes. These candidate genes were then validated in a larger cohort using qPCR-based TaqMan Low Density Arrays (TLDAs). Results: 239 probes corresponding to 221 genes were identified as being significantly different between patients and controls with a p-value <0.0005 (80% confidence level of false discovery rate). Forty seven genes were then selected for validation studies, using the TLDAs. Thirteen of these genes were validated in the second patient cohort with 12 down-regulated 1.3-2-fold and only 1 upregulated (1.6-fold). Among a number of identified genes with well-documented inflammatory roles we also validated genes that might be of great interest to the understanding of AS progression such as SPOCK2 (osteonectin) and EP300 which modulate cartilage and bone metabolism. Conclusion: We have validated a gene expression signature for AS from whole blood and identified strong candidate genes that may play roles in both the inflammatory and joint destruction aspects of the disease. RNA was extracted from whole blood using PAXGene tubes. 16 AS patients with active disease and 16 gender- and age-matched controls were analysed.
2010-11-04 | E-GEOD-25101 | biostudies-arrayexpress
Project description:We have compared synovial biopsies from ankylosing spondylitis and undifferentiated spondylitis patients with healthy controls and osteoarthritis patients Objective: In spondylarthropies, whole-genome gene expression profiling studies have been limited to peripheral blood to date. By undertaking a study in knee synovial biopsies from spondylarthropy (SpA) and ankylosing spondylitis (AS) patients we aimed to identified joint-specific candidate genes and pathways. These pathways may mediate systemic inflammation driven joint damaging processes and more specifically, the osteoproliferation that is characteristic of these conditions. Methods: RNA was extracted from six seronegative SpA, two AS, three osteoarthritis (OA) and four normal control knee synovial biopsies. Whole genome expression profiling was undertaken using the Illumina DASL system, which assays 24000 cDNA probes. Differentially expressed candidate genes were then validated using quantitative PCR and immunohistochemistry. Results: 416 differentially expressed genes were identified that clearly delineated between AS/SpA and control groups. Pathway analysis showed altered gene-expression in oxidoreductase activity, osteoblast activity, B-cell associated, matrix catabolic, and metabolic pathways. The inflammatory mediator, MMP3, was strongly upregulated in AS/SpA samples and the Wnt pathway inhibitors DKK3 and Kremen1 were downregulated. Conclusion: Pathways mediating both systemic inflammation as well as local tissue changes were identified. This suggests initial systemic inflammation in spondylarthropies transfers to and persists in the local joint environment, subsequently mediating changes in genes directly involved in the destructive tissue remodelling. Fifteen knee synovial biopsy tissue samples consisting of six seronegative spondyloarthropy (SpA), two ankylosing spondylitis (AS), three osteoarthritis (OA) and four normal control biopsies were obtained from the Synovial Tissue Bank at the Repatriation General Hospital in Adelaide, South Australia with the appropriate ethical approval (Supplementary Table 1). All patients provided informed written consent.
2012-12-01 | E-GEOD-41038 | biostudies-arrayexpress
Project description:Recent advances in knowledge of the biology of Ankylosing Spondylitis (AS) using innovative genetic and biomarker approaches offer the opportunity to address current challenges in AS diagnosis and management. Altered expression of microRNAs (miRNAs) may contribute to immune dysregulation and play a significant role in the onset and persistence of inflammation in AS. The capacity of exosomes to transport miRNAs between cells, thereby inducing phenotypic alterations in recipient cells has been the subject of considerable attention in recent years. This study reports the first comprehensive miRNA profiling of plasma-derived exosomes utilizing Gene Ontology (GO) annotation and pathway analysis.
2022-12-08 | GSE220130 | GEO
Project description:Introduction: A number of genetic-association studies have identified genes contributing to AS susceptibility but such approaches provide little information as to the gene activity changes occurring during the disease process. Transcriptional profiling generates a “snapshot” of the sampled cells activity and thus can provide insights into the molecular processes driving the disease process. We undertook a whole-genome microarray approach to identify candidate genes associated with AS and validated these gene-expression changes in a larger sample cohort. Methods: 18 active AS patients, classified according to the New York criteria. and 18 gender-and age-matched controls were profiled using Illumina HT-12 Whole-Genome Expression BeadChips which carry cDNAs for 48000 genes and transcripts. Class comparison analysis identified a number of differentially expressed candidate genes. These candidate genes were then validated in a larger cohort using qPCR-based TaqMan Low Density Arrays (TLDAs). Results: 239 probes corresponding to 221 genes were identified as being significantly different between patients and controls with a p-value <0.0005 (80% confidence level of false discovery rate). Forty seven genes were then selected for validation studies, using the TLDAs. Thirteen of these genes were validated in the second patient cohort with 12 down-regulated 1.3-2-fold and only 1 upregulated (1.6-fold). Among a number of identified genes with well-documented inflammatory roles we also validated genes that might be of great interest to the understanding of AS progression such as SPOCK2 (osteonectin) and EP300 which modulate cartilage and bone metabolism. Conclusion: We have validated a gene expression signature for AS from whole blood and identified strong candidate genes that may play roles in both the inflammatory and joint destruction aspects of the disease.
2010-11-04 | GSE25101 | GEO
Project description:Whole blood RNA-sequencing data from 5 AS patients who met 1984 AS criteria and 3 healthy human were obtained to gain insight into the potential mechanism of ankylosing spondylitis.
2021-11-10 | GSE181364 | GEO
Project description:We have compared synovial biopsies from ankylosing spondylitis and undifferentiated spondylitis patients with healthy controls and osteoarthritis patients Objective: In spondylarthropies, whole-genome gene expression profiling studies have been limited to peripheral blood to date. By undertaking a study in knee synovial biopsies from spondylarthropy (SpA) and ankylosing spondylitis (AS) patients we aimed to identified joint-specific candidate genes and pathways. These pathways may mediate systemic inflammation driven joint damaging processes and more specifically, the osteoproliferation that is characteristic of these conditions. Methods: RNA was extracted from six seronegative SpA, two AS, three osteoarthritis (OA) and four normal control knee synovial biopsies. Whole genome expression profiling was undertaken using the Illumina DASL system, which assays 24000 cDNA probes. Differentially expressed candidate genes were then validated using quantitative PCR and immunohistochemistry. Results: 416 differentially expressed genes were identified that clearly delineated between AS/SpA and control groups. Pathway analysis showed altered gene-expression in oxidoreductase activity, osteoblast activity, B-cell associated, matrix catabolic, and metabolic pathways. The inflammatory mediator, MMP3, was strongly upregulated in AS/SpA samples and the Wnt pathway inhibitors DKK3 and Kremen1 were downregulated. Conclusion: Pathways mediating both systemic inflammation as well as local tissue changes were identified. This suggests initial systemic inflammation in spondylarthropies transfers to and persists in the local joint environment, subsequently mediating changes in genes directly involved in the destructive tissue remodelling.
2012-12-01 | GSE41038 | GEO