Tocilizumab in a patient with ankylosing spondylitis and Crohn's disease refractory to TNF antagonists

2010 ◽  
Vol 77 (6) ◽  
pp. 625-626 ◽  
Author(s):  
Laure Brulhart ◽  
Michael J. Nissen ◽  
Paola Chevallier ◽  
Cem Gabay
1989 ◽  
Vol 118 (1) ◽  
pp. 174-176 ◽  
Author(s):  
Steve Burdick ◽  
Donald D. Tresch ◽  
Richard A. Komokowski

2006 ◽  
Vol 26 (3) ◽  
pp. 289-297 ◽  
Author(s):  
Alan Ebringer ◽  
Taha Rashid ◽  
Harmale Tiwana ◽  
Clyde Wilson

1997 ◽  
Vol 17 (1) ◽  
pp. 11-16 ◽  
Author(s):  
H. Tiwana ◽  
C. Wilson ◽  
R. S. Walmsley ◽  
A. J. Wakefield ◽  
M. S. N. Smith ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Taha Rashid ◽  
Clyde Wilson ◽  
Alan Ebringer

Both ankylosing spondylitis (AS) and Crohn’s disease (CD) are chronic and potentially disabling interrelated conditions, which have been included under the group of spondyloarthropathies. The results of a large number of studies support the idea that an enteropathic pathogen,Klebsiella pneumoniae, is the most likely triggering factor involved in the initiation and development of these diseases. Increased starch consumptions by genetically susceptible individuals such as those possessing HLA-B27 allelotypes could trigger the disease in both AS and CD by enhancing the growth and perpetuation of theKlebsiellamicrobes in the bowel. Exposure to increased levels of these microbes will lead to the production of elevated levels of anti-Klebsiellaantibodies as well as autoantibodies against cross-reactive self-antigens with resultant pathological lesions in the bowel and joints. Hence, a decrease of starch-containing products in the daily dietary intake could have a beneficial therapeutic effect on the disease especially when used in conjunction with the currently available medical therapies in the treatment of patients with AS and CD.


2011 ◽  
Vol 38 (9) ◽  
pp. 1953-1956 ◽  
Author(s):  
NAI LEE LUI ◽  
ADELE CARTY ◽  
NIGIL HAROON ◽  
HUA SHEN ◽  
RICHARD J. COOK ◽  
...  

Objective.To determine the association between urolithiasis and syndesmophyte formation and the effect of urolithiasis on ankylosing spondylitis (AS) disease activity.Methods.In a longitudinal cohort of 504 patients with AS, we conducted an analysis of all patients with AS who have a history of urolithiasis. All patients met the modified New York criteria for AS. Demographics, clinical characteristics, extraarticular features, and comorbidities are systematically recorded in the database. We compared disease activity, functional indices, medical therapy and radiographic damage between AS patients with (Uro+) and without urolithiasis (Uro–) using the modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS).Results.Thirty-eight patients with AS (7.5%) had a history of urolithiasis in our cohort. Seventy-six patients with AS who did not have urolithiasis, matched for age, sex, and ethnicity, were selected as controls. Patients who were Uro+ were more likely to have more functional disability, based on the Bath AS Functional Index (BASFI; mean 5.3 vs 3.6 in control group, p = 0.003). Trends were noted in the Uro+ group toward higher Bath AS Disease Activity Index (BASDAI; mean 4.9 vs 4.0, p = 0.09), more peripheral joint involvement (p = 0.075), and higher frequency of biologic therapy (p = 0.09). No significant difference was detected in mSASSS or the Bath AS Metrology Index (BASMI). Significant association with diabetes mellitus (DM; p = 0.016) and Crohn’s disease (p = 0.006) was noted in the Uro+ group.Conclusion.Although there is no acceleration of syndesmophyte formation or spinal mobility restriction, more functional disability was detected in the urolithiasis group. The higher risk with concomitant DM or Crohn’s disease should alert clinicians to these comorbidities in Uro+ patients with AS.


PLoS ONE ◽  
2010 ◽  
Vol 5 (11) ◽  
pp. e13795 ◽  
Author(s):  
Debby Laukens ◽  
Michel Georges ◽  
Cécile Libioulle ◽  
Cynthia Sandor ◽  
Myriam Mni ◽  
...  

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5088
Author(s):  
Rebecca L. Roberts ◽  
Mary C. Wallace ◽  
Andrew A. Harrison ◽  
Douglas White ◽  
Nicola Dalbeth ◽  
...  

Background Genome-wide association studies have identified a plethora of risk genes for both Crohn’s disease (CD) and ankylosing spondylitis (AS). A subset of genes found to be risk factors for CD have also been found to be risk factors for AS. The objective of our study was to assess whether CD risk genes were associated with non-invasive clinical markers of gut inflammation in patients with AS, indicating a potential subset of patients with clinical as well as genetic overlap. Methods A total of 308 Caucasian patients who fulfilled the modified New York Criteria for AS, were assessed for bowel symptoms using the Dudley Inflammatory Bowel Symptom Questionnaire (DISQ). Of these patients, 157 also had faecal calprotectin measured. All AS patients and 568 healthy controls were genotyped for 10 CD risk loci using predesigned single nucleotide polymorphism (SNP) genotyping assays. Chi-square analysis was used to test for association between genotype and DISQ score and faecal calprotectin level. Results The minor allele of two SNPs, one in chromosome region 1q32 SNP (rs11584383), and one in the gene coding for IL23R (rs11209026) conferred protection against AS. Only the association of 1q32 remained significant after Bonferroni correction for multiple testing. Stratification by DISQ score and faecal calprotectin did not influence the association of 1q32 with AS. Conclusion In patients with AS, the association of the CD 1q32 SNP was independent of non-invasive markers of bowel inflammation. Other CD related SNPs were not found have a significant association with AS.


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