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Search Results for : Ankylosing Spondylitis
Merck Online Lab
Diagnosis Therapy Rehabilitation Imaging Clinical Laboratory
Autoimmune disease classification by inverse association with SNP alleles.
Author(s): Sirota, M; Schaub, MA; Batzoglou, S; Robinson, WH; Butte, AJ
Journal: PLoS Genet 2010 Mar 23; Vol. 5, Issue 12; Page(s) e1000792
[Medline ID - 20041220]

With multiple genome-wide association studies (GWAS) performed across autoimmune diseases, there is a great opportunity to study the homogeneity of genetic architectures across autoimmune disease. Previous approaches have been limited in the scope of their analysis and have failed to properly incorporate the direction of allele-specific disease associations for SNPs. In this work, we refine the notion of a genetic variation profile for a given disease to capture strength of association with multiple SNPs in an allele-specific fashion. We apply this method to compare genetic variation profiles of six autoimmune diseases: multiple sclerosis (MS), ankylosing spondylitis (AS), autoimmune thyroid disease (ATD), rheumatoid arthritis (RA), Crohn's disease (CD), and type 1 diabete s (T1D), as well as five non-autoimmune diseases. We quantify pair-wise relationships between these diseases and find two broad clusters of autoimmune disease where SNPs that make an individual susceptible to one class of autoimmune disease also protect from diseases in the other autoimmune class. We find that RA and AS form one such class, and MS and ATD another. We identify specific SNPs and genes with opposite risk profiles for these two classes. We furthermore explore individual SNPs that play an important role in defining similarities and differences between disease pairs. We present a novel, systematic, cross-platform approach to identify allele-specific relationships between disease pairs based on genetic variation as well as the individual SNPs which drive the relationships. While recognizing similarities between diseases might lead to identifying novel treatment options, detecting differences between diseases previously thought to be similar may point to key novel disease-specific genes and pathways.

Monitoring Achilles enthesitis in ankylosing spondylitis during TNF-alpha antagonist therapy: an ultrasound study.
Author(s): Aydin, SZ; Karadag, O; Filippucci, E; Atagunduz, P; Akdogan, A; Kalyoncu, U; Grassi, W; Direskeneli, H
Journal: Rheumatology (Oxford) 2009 Dec 31; Vol. 49, Issue 3; Page(s) 578-82
[Medline ID - 20360034]

OBJECTIVE: Enthesitis is considered as the primary anatomical lesion in ankylosing spondylitis (AS). Therapeutic effects of TNF-alpha antagonist treatments for enthesitis on imaging changes are still limited to case reports or small sample-sized trials. We aimed to investigate the potential of ultrasonography (US) to detect early changes after TNF-alpha antagonist therapy of Achilles enthesis of AS patients. METHODS: Forty-three AS patients with active disease, requiring TNF-alpha antagonist therapy, were included. Physical examination was performed to detect Achilles enthesitis and/or retrocalcaneal bursitis. US of the Achilles tendon was performed bilaterally. Grey-scale (GS) and power Doppler (PD) scores on a 0-2 semi-quantitative scale and total additive scores (TS) were calculated. Follow-up US examinations were performed 2 months after the initiation of therapy. RESULTS: At baseline, 11 patients (26.2%) were symptomatic in physical examination for either Achilles enthesitis or retrocalcaneal bursitis, whereas 36 (83%) had GS US pathological findings and 10 (23.3%) had PD signal. GS score and TS decreased significantly [3.6 (3.0) vs 2.3 (2.2), P < 0.001 and 4.7 (4.9) vs 2.7 (3.3), P < 0.001, respectively], whereas the decrease in PD score was not significant after 2 months of follow-up. The Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), ESR and CRP levels also showed significant improvements. CONCLUSIONS: Subclinical Achilles enthesitis, detected only with GS US, is present in a subset of AS patients and a significant improvement can be demonstrated after 2 months of TNF-alpha antagonist therapy. In addition to standard outcome measures, US might be an additional useful tool to monitor therapy in SpA patients with Achilles enthesitis.

Functional autoantibodies against serpin E2 in rheumatoid arthritis.
Author(s): Maciejewska-Rodrigues, H; Al-Shamisi, M; Hemmatazad, H; Ospelt, C; Bouton, MC; J; äger, D; Cope, AP; Charles, P; Plant, D; Distler, JH; Gay, RE; Michel, BA; Knuth, A; Neidhart, M; Gay, S; J; üngel, A
Journal: Arthritis Rheum 2010 Mar 12; Vol. 62, Issue 1; Page(s) 93-104
[Medline ID - 20039430]

OBJECTIVE: To search for novel autoantibodies in patients with rheumatoid arthritis (RA) in an effort to better understand the processes of joint destruction in this disease. METHODS: Using a modified SEREX technique and complementary DNA derived from RA synovium, serpin E2 was identified as a novel autoantigen and was analyzed by immunohistochemistry. Levels of anti-serpin E2 autoantibodies in serum and synovial fluid from patients with RA, osteoarthritis (OA), psoriatic arthritis, and ankylosing spondylitis, and/or from healthy individuals were assessed by enzyme-linked immunosorbent assay. Since serpin E2 is an inhibitor of serine proteases, we studied the inhibitory activity of serpin E2 toward its target, urokinase plasminogen activator (uPA), in vitro in the presence of isolated anti-serpin E2 autoantibodies and in vivo using the uPA activity assay. R ESULTS: We identified autoantibodies against serpin E2 by the SEREX technique. Serpin E2 was overexpressed in RA synovial tissues as compared with OA synovial tissues. Significantly higher levels of anti-serpin E2 autoantibodies were present in samples of synovial fluid (28%) and serum (22%) from RA patients as compared with OA patients (0 and 6%, respectively) or with healthy individuals (6% of sera). Most importantly, anti-serpin E2 autoantibodies isolated from RA sera reversed the inhibitory activity of serpin E2 by 70%. Furthermore, the levels of anti-serpin E2 autoantibodies correlated with the uPA activity in vivo. CONCLUSION: This study characterizes a functional property of a novel autoantibody in RA. Since anti-serpin E2 autoantibodies interfere with the inhibitory activity of serpin E2 toward serine proteases, they might facilitate the joint destruction in RA.

Evidence that Dkk-1 is dysfunctional in ankylosing spondylitis.
Author(s): Daoussis, D; Liossis, SN; Solomou, EE; Tsanaktsi, A; Bounia, K; Karampetsou, M; Yiannopoulos, G; Andonopoulos, AP
Journal: Arthritis Rheum 2010 Mar 12; Vol. 62, Issue 1; Page(s) 150-8
[Medline ID - 20039407]

OBJECTIVE: Dkk-1 is an inhibitory molecule that regulates the Wnt pathway, which controls osteoblastogenesis. This study was undertaken to explore the potential role of Dkk-1 in ankylosing spondylitis (AS), a prototypical bone-forming disease. METHODS: Serum Dkk-1 levels were measured in 45 patients with AS, 45 patients with rheumatoid arthritis (RA), 15 patients with psoriatic arthritis (PsA), and 50 healthy subjects by sandwich enzyme-linked immunosorbent assay (ELISA). A functional ELISA was used to assess the binding of Dkk-1 to its receptor (low-density lipoprotein receptor-related protein 6). Furthermore, we studied the effect of sera from patients with AS and healthy subjects on the activity of the Wnt pathway in the Jurkat T cell model, with and without a neutralizing anti-Dkk-1 monoclonal antibody, by Western immunoblotting. RESULTS: Serum Dkk-1 levels were significantly increased in patients with AS (mean +/- SEM 2,730 +/- 135.1 pg/ml) as compared with normal subjects (P = 0.040), patients with RA (P = 0.020), and patients with PsA (P = 0.049). Patients with AS receiving anti-tumor necrosis factor alpha (anti-TNFalpha) treatment had significantly higher serum Dkk-1 levels than patients with AS not receiving such treatment (P = 0.007). Patients with AS studied serially prior to and following anti-TNFalpha administration exhibited a significant increase in serum Dkk-1 levels (P = 0.020), in contrast to patients with RA, who exhibited a dramatic decrease (P < 0.001). Jurkat cells treated with serum from AS patients exhibited increased Wnt signaling compared with cells treated with control serum. In that system, Dkk-1 blockade significantly enhanced Wnt signaling in control serum-treated, but not AS serum-treated, Jurkat T cells. CONCLUSION: Our findings indicate that in patients with AS, circulating bone formation-promoting factors functionally prevail. This can be at least partially attributed to decreased Dkk-1-mediated inhibition.

Tumor necrosis factor-alpha antagonists improve aortic stiffness in patients with inflammatory arthropathies: a controlled study.
Author(s): Angel, K; Provan, SA; Gulseth, HL; Mowinckel, P; Kvien, TK; Atar, D
Journal: Hypertension 2010 Feb 23; Vol. 55, Issue 2; Page(s) 333-8
[Medline ID - 20038753]

The chronic inflammatory state of rheumatoid arthritis and other inflammatory arthropathies, such as ankylosing spondylitis and psoriatic arthritis, contributes to the accelerated atherosclerosis associated with these conditions. This study evaluates the effect of treatment with tumor necrosis factor (TNF)-alpha antagonists on arterial stiffness in patients with inflammatory arthropathies. A total of 60 patients with rheumatoid arthritis, ankylosing spondylitis, or psoriatic arthritis and clinical indication for anti-TNF-alpha therapy were included. Thirty-five patients started with anti-TNF-alpha therapy and were compared with a nontreatment group of 25 patients. Aortic stiffness (aortic pulse wave velocity), augmentation index, and disease activity were assessed at baseline and after 3 months. Aortic pulse wave velocity (mean+/-SD) was reduced in the treatment group but not in the control group (-0.50+/-0.78 m/s versus 0.05+/-0.54 m/s, respectively; P=0.002). Concomitantly, C-reactive protein and the disease activity score were reduced in the treatment group (-9.3+/-20.2 mg/L [P < 0.001] and -0.74+/-0.91 [P=0.004]). Augmentation index remained unchanged in both groups (0.1+/-7.1% versus -1.0+/-5.8%, respectively; P=0.53). In a multivariate linear regression model, only treatment with TNF-alpha antagonist and change in mean arterial pressure predicted alterations in aortic pulse wave velocity. In summary, anti-TNF-alpha therapy improved aortic stiffness in patients with inflammatory arthropathies. These findings support the idea that anti-inflammatory treatment has a favorable effect on cardiovascular risk in patients with inflammatory arthropathies.

[Ankylosing spondylitis]
Author(s): Braun, J
Journal: MMW Fortschr Med 2010 Feb 2; Vol. 151, Issue 47; Page(s) 79-83; quiz 84
[Medline ID - 20037984]

ABSTRACT NOT AVAILABLE

Application of Biostatistics and Bioinformatics Tools to Identify Putative Transcription Factor-Gene Regulatory Network of Ankylosing Spondylitis and Sarcoidosis.
Author(s): Choi, D; Sharma, SM; Pasadhika, S; Kang, Z; Harrington, CA; Smith, JR; Planck, SR; Rosenbaum, JT
Journal: Commun Stat Theory Methods 2009 Dec 29; Vol. 38, Issue 18; Page(s) 3326-3338
[Medline ID - 20037664]

Transcription factors and corresponding cis-regulatory elements are considered key components in gene regulation. We combined biostatistics and bioinformatics tools to streamline identification of putative transcription factor-gene regulatory networks unique for two immune-mediated diseases, ankylosing spondylitis and sarcoidosis. After identifying differentially expressed genes from microarrays, we employed tightCluster to find tight clusters of potentially co-regulated genes. By subsequently applying bioinformatics tools to search for common cis-regulatory elements, putative transcription factor-gene regulatory networks were found. Recognition of these networks by applying this methodology could pave the way for new insights into disease pathogenesis.

Pulmonary manifestations of ankylosing spondylitis treated as pulmonary tuberculosis: a case report and review of literature.
Author(s): Ibinaiye, PO; Salawu, F
Journal: Niger Postgrad Med J 2010 Jun 16; Vol. 16, Issue 4; Page(s) 274-6
[Medline ID - 20037624]

A 45 year old trader presented with history of persistent productive cough, progressively increasing dyspnoea, malaise and fever of 6 months prior to presentations. He also complained of severe lower backache and stiffness that radiated to both legs of 5 years duration. Chest radiograph revealed left apical fibrosis, coarse, linear shadows with cavities. There was also super infection with aspergilloma in the left apical region. The sputum AAFB was negative. Despite the fact that the patient complained of lower backache and stiffness, the plain radiograph of the affected spine was not requested for by the attending physician. Rather, the patient was commenced on antituberculous therapy based on pulmonary changes on chest radiograph. But after completing the treatment (nine months regimen), there were no improvement in patient's clinical conditions and pulmonary changes on repeated chest radiograph. The plain radiographs of the lumbosacral spine, pelvis and both hips were suggested by the author (Radiologist) who reviewed the patient's chest radiographs. The radiographs of the lumbosacral spine, as well as pelvis and both hips showed features of ankylosing spondylitis with pulmonary complication. His treatment was later reviewed based on the above new findings. This report highlights the fact that pulmonary manifestation in ankylosing spondylitis, a rare entity in our environment can present the same pattern as pulmonary tuberculosis which is far more common in this environment. A high index of suspicion will enhance early proper diagnosis.

[Monoclonal antibodies in chronic autoimmune inflammatory diseases]
Author(s): Semerano, L; Boissier, MC
Journal: Med Sci (Paris) 2010 Jun 4; Vol. 25, Issue 12; Page(s) 1108-12
[Medline ID - 20035687]

Among chronic inflammatory diseases, rheumatoid arthritis is a common inflammatory and destructive arthropathy, characterized by the release of potent proinflammatory cytokines mostly TNFa and IL-1, which both mediate systemic effects and contribute to joint destruction. Many therapeutic agents have been proposed to antagonise these cytokines, among which monoclonal antibodies. Thus twenty years ago the anti-TNFa infliximab was the first monoclonal antibody to be proposed in a non-cancerous indication, rheumatoid arthritis. Since then, several other monoclonal antibodies and/or antagonists either targeting cytokines (IL-1, IL-6, RANKL), but also immune cellular effectors T and B cells, have been evaluated not only in rheumatoid arthritis, but also in systemic lupus, Crohn's disease, multiple sclerosis, or ankylosing spondylitis. Clinical benefit has been unambiguously demonstrated, but before these novel molecules enter routine clinical practice, several parameters will have to be accurately documented such as their safety, long term efficacy, and economical cost.

Vitamin D level: is it related to disease activity in inflammatory joint disease?
Author(s): Braun-Moscovici, Y; Toledano, K; Markovits, D; Rozin, A; Nahir, AM; Balbir-Gurman, A
Journal: Rheumatol Int 2009 Dec 25
[Medline ID - 20033415]

The objectives of this study are to assess the vitamin D status in patients (pts) with inflammatory joint diseases (IJD), and its correlation with disease activity. 121 consecutive pts (85 rheumatoid arthritis (RA), 22 psoriatic arthritis (PSA), 14 ankylosing spondylitis (AS)) underwent clinical and laboratory evaluation which included kidney and liver function tests, serum calcium and phosphor levels, 25(OH)D and parathyroid hormone (PTH). Disease activity was assessed by DAS 28 in RA and PSA pts and by BASDAI in AS pts, sedimentation rate (ESR) and CRP. According to activity indexes, pts were divided into subgroups with low (DAS28 < 3.2 and BASDAI < 4), and moderate-to-high disease activity (DAS28 > 3.2 and BASDAI > 4). Associations between serum levels of 25(OH)D and age, gender, ethnicity, type and disease duration, treatment, (anti-tumor necrosis factoralpha (TNFalpha) agents or DMARDs), seasonal variations, and disease activity were assessed. Vitamin D deficiency was found in 51 pts (42.1%). The incidence was higher among Arab pts (76.7%) compared to Jews (23%). The difference of 25(OH)D levels between Arabs (mean 9.4 +/- 4.2 ng/ml) and Jews (mean 17.8 +/- 8.4 ng/ml) was statistically significant (p < 0.0001). We did not find correlation between vitamin D levels and the other evaluated factors. A surprisingly high incidence of vitamin D deficiency was found in IJD patients in a sunny Mediterranean country. This finding justifies the inclusion of vitamin D in the routine lab work-up of pts with IJD. The only statistical significant correlation was found between vitamin D level and ethnic origin. Further studies are needed to look for genetic polymorphism of vitamin D receptors.
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