scholarly journals SAT0007 Ankylosing spondylitis initiated as a reactive arthritis

Author(s):  
ZA Curcic
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.


1985 ◽  
Vol 4 (4) ◽  
pp. 487-487 ◽  
Author(s):  
J. Roudier ◽  
H. De Montclos ◽  
D. Thouvenot ◽  
J. J. Chomel ◽  
F. N. Guillermet ◽  
...  

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

Author(s):  
Murray Longmore ◽  
Ian B. Wilkinson ◽  
Andrew Baldwin ◽  
Elizabeth Wallin

The rheumatological historyAssessing the locomotor systemRheumatological investigationsBack painOsteoarthritis (oa)Septic arthritisRheumatoid arthritis (ra)Crystal arthropathies:Goutcppd arthropathySpondyloarthritides:Ankylosing spondylitis (as)Enteropathic, psoriatic and reactive arthritisAutoimmune connective tissue diseases:Mixed connective tissue disease...


2008 ◽  
Vol 35 (11) ◽  
pp. 2236-2240 ◽  
Author(s):  
ROBERTO DÍAZ-PEÑA ◽  
MIGUEL ANGEL BLANCO-GELAZ ◽  
PANGANANI NJOBVU ◽  
ANTONIO LÓPEZ-VAZQUEZ ◽  
BEATRIZ SUÁREZ-ÁLVAREZ ◽  
...  

ObjectiveTo analyze the distribution of HLA-B alleles and to investigate their contribution in the susceptibility to spondyloarthropathies (SpA) in a sample population from Zambia, in order to determine a relationship between some HLA-B alleles and development of ankylosing spondylitis (AS), reactive arthritis (ReA), or undifferentiated SpA (uSpA).MethodsWe selected 72 patients with SpA and found that 46 had uSpA, 23 ReA, and 3AS.We also selected 92 matched controls; 55 of these had human immunodeficiency virus type I (HIV-I) infection.ResultsWe found a significant increase in the rate of uSpA and ReA with features of Reiter’s syndrome (RS) in HIV-positive individuals who carried the HLA-B*5703 allele (pc < 0.0001 and pc < 0.001, respectively). Among the significant new findings identified were the presence of B*1403 in 2 of the 3 AS patients (pc < 0.05, OR 47), confirming previous data in the Togolese population.ConclusionThe presence of B*5703 and HIV infection may not affect susceptibility to AS and ReA, but they do show an important influence in uSpA and RS. Our findings confirm that HLA-B* 1403 is the only factor to increase the risk of AS in a sub-Saharan African population, whereas HLA-B27 was virtually absent in patients with AS.


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