scholarly journals Further observations upon HLA-B27, Yersinia enterocolitica, and ankylosing spondylitis.

1986 ◽  
Vol 45 (6) ◽  
pp. 526-528 ◽  
Author(s):  
P E Pease ◽  
S E Balmer ◽  
J E Tallack ◽  
H Chahal ◽  
J Ibbotson ◽  
...  
1985 ◽  
Vol 4 (4) ◽  
pp. 487-487 ◽  
Author(s):  
J. Roudier ◽  
H. De Montclos ◽  
D. Thouvenot ◽  
J. J. Chomel ◽  
F. N. Guillermet ◽  
...  

1980 ◽  
Vol 39 (4) ◽  
pp. 415-416 ◽  
Author(s):  
P Pease ◽  
J England ◽  
R Tyler ◽  
P Mackintosh

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 429.2-429
Author(s):  
L. Hu ◽  
X. Ji ◽  
F. Huang

Background:Obesity population are rising rapidly and have become a major health issue. Studies have shown that obesity is a low-grade inflammatory status characterized by increase in proinflammatory cytokines.Objectives:To examine the impact of overweight or obesity on disease activity and treatment responses to biologics in patients with ankylosing spondylitis (AS) in a real-world setting.Methods:Body mass index (BMI) is available in 1013 patients from the Chinese Ankylosing Spondylitis Imaging Cohort (CASPIC). Differences in clinical outcomes (such as BASDAI, ASDAS, BASFI, and ASAS HI) and treatment responses to biologics (ΔBASDAI and ΔASDAS) over 3, 6, 9, and 12 months are assessed between BMI categories (normal weight BMI <24 kg/m2; overweight BMI=24-28 kg/m2; obesity BMI ≥28 kg/m2) using Kruskal-Wallis test. The association between BMI and clinical characteristics and treatment responses to biologics was determined, and multivariate median regression analyses were conducted to adjust for confounders (such as age, gender, smoke, and HLA-B27).Results:Among 1013 patients with AS, overweight accounts for 33%, while obesity for 12.4%. There were significant differences between patients who were obese or overweight and those with a normal weight regarding clinical outcomes (BASDAI: 2.90/2.56 vs 2.21; ASDAS-CRP: 2.20/1.99 vs 1.81; BASFI: 2.13/1.69 vs 1.38; ASAS HI: 6.87/5.29 vs 5.12 and BASMI: 2.35/1.76 vs 1.62; all P<0.05). After adjusting for age, gender, smoke, and HLA-B27, obesity remained associated with higher disease activity (BASDAI: β=0.55, P=0.005; ASDAS-CRP: β=0.40, P<0.001), poorer functional capacity (BASFI: β=0.58, P=0.001), worse health index (ASAS HI: β=1.92, P<0.001) and metrology index (BASMI: β=0.71, P=0.013). For TNFi users, BMI was found to be negatively correlated with changes in disease activity (ΔBASDAI and ΔASDAS) in the multivariate regression model (all P<0.05), and overweight and obese patients showed an unsatisfactory reduction in disease activity during 3-month, 6-month, 9-month, and 12-month follow-up period, compared to normal weight patients (all P<0.05).Conclusion:Overweight or obesity impacts greatly on clinical outcomes and treatment responses to biologics in patients with ankylosing spondylitis, which argues strongly for obesity management to become central to prevention and treatment strategies in patients with AS.References:[1]Maachi M, Pieroni L, Bruckert E, et al. Systemic low-grade inflammation is related to both circulating and adipose tissue TNFalpha, leptin and IL-6 levels in obese women. Int J Obes Relat Metab Disord 2004;28:993–7.Figure 1.Changes of disease activity for TNFi users during 3-, 6-, 9- and 12-month follow-up according to BMI categories. a: vs. normal weight, P<0.05 in 3 months; b: vs. normal weight, P<0.05 in 6 months; c: vs. normal weight, P<0.05 in 9 months; d: vs. normal weight, P<0.05 in 12 months.Acknowledgments:We appreciate the contribution of the present or former members of the CASPIC study group.Disclosure of Interests:None declared


1994 ◽  
Vol 57 (10) ◽  
pp. 935-941 ◽  
Author(s):  
JAMES L. SMITH

Diarrheic episodes caused by the foodborne pathogens Campylobacter, Salmonella, Shigella or Yersinia may lead to a sterile arthritis such as reactive arthritis, Reiter's syndrome or ankylosing spondylitis. Reiter's syndrome and reactive arthritis have been shown to be sequelae in a few well-studied bacterial food poisoning outbreaks. Reactive arthritis, Reiter's syndrome and ankylosing spondylitis show strong familial association related to the gene for HLA-B27 (HLA = human leucocyte antigen) antigen. Why HLA-B27-positive individuals are more susceptible to arthritis is not known, but molecular mimicry between the HLA-B27 antigen and antigens of triggering bacteria has been demonstrated and this mimicry has been proposed as a mechanism involved in etiology of the arthritides. Antigens from bacteria that triggered the arthritis are present in arthritic joints but bacterial cells are not found. Antibodies and T-cells specific for the triggering bacteria have been demonstrated in arthritic patients. T-cells present in synovial joints respond specifically to the particular arthritic triggering pathogen. The cells that respond to bacterial antigens belong to the T-cell subset TH1 that secrete a limited number of cytokines but it is not known if cytokines are involved in arthritis. A few studies have demonstrated that T-cells from the joints of arthritic patients respond to both bacterial and human heat shock proteins indicating that autoimmunity may be involved in causation of arthritis. While only about 2% of a population exposed to a triggering infection will acquire arthritis, these individuals undergo pain and suffering as well as economic hardships as a result of their disease.


1990 ◽  
Vol 28 (4) ◽  
pp. 382-396 ◽  
Author(s):  
Cheryl L Nickerson ◽  
Harvinder S Luthra ◽  
Suresh Savarirayan ◽  
Chella S David

1996 ◽  
Vol 39 (6) ◽  
pp. 943-949 ◽  
Author(s):  
Pia Westman ◽  
Marjatta Leirisalo-Repo ◽  
Jukka Partanen ◽  
Saija Koskimies

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