HLA-B27 and Clinical Characteristics of Reactive Arthritis

AbstractReactive arthritis (ReA) is a form of sterile arthritis that occurs secondary to an extra-articular infection in genetically predisposed individuals. The extra-articular infection is typically an infection of the gastrointestinal tract or genitourinary tract. Infection-related arthritis is a sterile arthritis associated with streptococcal tonsillitis, extra-articular tuberculosis, or intravesical instillation of bacillus Calmette–Guérin (iBCG) therapy for bladder cancer. These infection-related arthritis diagnoses are often grouped with ReA based on the pathogenic mechanism. However, the unique characteristics of these entities may be masked by a group classification. Therefore, we reviewed the clinical characteristics of classic ReA, poststreptococcal ReA, Poncet’s disease, and iBCG-induced ReA. Considering the diversity in triggering microbes, infection sites, and frequency of HLA-B27, these are different disorders. However, the clinical symptoms and intracellular parasitism pathogenic mechanism among classic ReA and infection-related arthritis entities are similar. Therefore, poststreptococcal ReA, Poncet’s disease, and iBCG-induced ReA could be included in the expanding spectrum of ReA, especially based on the pathogenic mechanism.

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FRI0445 HLA-B27 IN POSTSTREPTOCOCCAL REACTIVE ARTHRITIS WITH ENTHESITIS

Annals of the Rheumatic Diseases ◽

10.1136/annrheumdis-2020-eular.2546 ◽

2020 ◽

Vol 79 (Suppl 1) ◽

pp. 820.1-820

Author(s):

I. Naishtetik ◽

L. Khimion ◽

O. Yashchenko ◽

P. Dolinskiy

Keyword(s):

Rheumatic Fever ◽

Reactive Arthritis ◽

Streptococcal Infection ◽

Joint Involvement ◽

Hla B27 ◽

Aseptic Inflammation ◽

Beta Hemolytic Streptococcus ◽

Common Diagnosis ◽

Poststreptococcal Reactive Arthritis ◽

Rheumatology Practice

Background:Poststreptococcal reactive arthritis (PSRA) is a very common diagnosis in rheumatology practice, which develops after recent pharyngeal streptococcal infection and characterized by aseptic inflammation in one or more joints and periarticular involvement. Now no diagnostic criteria have been agreed [2,4]; association of the expression of HLA-B27 and PSRA is not clear [1,3].Objectives:In our study we analyzed the features of PSRA in presence of HLA-B27.Methods:88 patients (48 female and 40 male) aged between 18-55 years with complains of pain, tender and swollen joints developed after recent pharyngeal streptococcal infection underwent standard physical and laboratory rheumatological examinations. Acute rheumatic fever and other inflammatory arthritis were excluded.Results:60 patients (68,2%) had oligo-polyarthralgia, 10 patients (11,4%) - monoarthritis, 24 patients (27,3%) had asymmetrical olygoarthritis, 4 patients (4,5%) had polyarthritis, enthesitis was found in 4 (4,5%) patients, tenosynovitis of the palmar flexor tendons in 10 cases (11,4%) and the peroneal tendons of the ankles in 5 patients (5,7%), one-sided sacroiliitis (confirmed by MRI) in 5 patients (5,7%).The mean level of ASL-O was 542 U/ml, CRP -15 mg/L, ESR - 34 mm/H; HLA-B27 was present in 24 (30,7%) patients. HLA-B27 positivity was connected to enthesitis, sacroiliitis, more joint involvement with higher levels of ESR and CRP.Conclusion:30% of patients with poststreptococcal reactive arthritis are HLA-B27 positive, the presence of HLA-B27 leads to more frequent development of enthesitis, polyarthritis and sacroiliitis with higher level of inflammatory activity which dictate the need for longer supervision of such patients for possible triggering of ankylosing spondylitis development.References:[1]Ahmed S, Ayoub EM, ScorniK JC, Wang C-Y, She J-X. Poststreptococcal reactive arthritis. Clinical characteristics and association with YLA-DR alleles. Arthritis Rheum 1998; 41:1096-102.9[[2]Gibofsky A, Khanna A, Suh E, et al. The genetics of rheumatic fever: Relationship to streptococcal infection and autoimmune disease. J Rheumatol Suppl. 1991;30:1–5. [PubMed] [Google Scholar][3]Leitch DN, Holland CD/ Reactive arthritis, beta-hemolytic Streptococcus and Staphylococcus aureus. Br J Rheumatol 1996;35:912.[4]Mackie SL, Keat A. Poststreptococcal reactive arthritis: what is it and how do we know? Rheumatology (Oxford) 2004;43:949–54. 10.1093/rheumatology/keh225 [PubMed].Disclosure of Interests:None declared

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Arthritis and Foodborne Bacteria

Journal of Food Protection ◽

10.4315/0362-028x-57.10.935 ◽

1994 ◽

Vol 57 (10) ◽

pp. 935-941 ◽

Cited By ~ 11

Author(s):

JAMES L. SMITH

Keyword(s):

T Cells ◽

Ankylosing Spondylitis ◽

Reactive Arthritis ◽

Molecular Mimicry ◽

Food Poisoning ◽

Cell Subset ◽

Bacterial Cells ◽

Hla B27 ◽

Reiter's Syndrome ◽

Reiter’S Syndrome

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.

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Absence of cross-reaction between HLA B27 and yersinia enterocolitica or chlamydia trachomatis in reactive arthritis and ankylosing spondylitis

Clinical Rheumatology ◽

10.1007/bf02031909 ◽

1985 ◽

Vol 4 (4) ◽

pp. 487-487 ◽

Cited By ~ 3

Author(s):

J. Roudier ◽

H. De Montclos ◽

D. Thouvenot ◽

J. J. Chomel ◽

F. N. Guillermet ◽

...

Keyword(s):

Ankylosing Spondylitis ◽

Chlamydia Trachomatis ◽

Yersinia Enterocolitica ◽

Reactive Arthritis ◽

Cross Reaction ◽

Hla B27

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A comparative study of HLA genes in HLA–B27 positive ankylosing spondylitis and HLA–B27 positive peripheral reactive arthritis

Arthritis & Rheumatism ◽

10.1002/art.1780390611 ◽

1996 ◽

Vol 39 (6) ◽

pp. 943-949 ◽

Cited By ~ 9

Author(s):

Pia Westman ◽

Marjatta Leirisalo-Repo ◽

Jukka Partanen ◽

Saija Koskimies

Keyword(s):

Ankylosing Spondylitis ◽

Comparative Study ◽

Reactive Arthritis ◽

Hla B27 ◽

Hla Genes

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HLA-B27-Associated Reactive Arthritis: Pathogenetic and Clinical Considerations

Clinical Microbiology Reviews ◽

10.1128/cmr.17.2.348-369.2004 ◽

2004 ◽

Vol 17 (2) ◽

pp. 348-369 ◽

Cited By ~ 97

Author(s):

Inés Colmegna ◽

Raquel Cuchacovich ◽

Luis R. Espinoza

Keyword(s):

Reactive Arthritis ◽

Bacterial Infections ◽

The Body ◽

Current Evidence ◽

Intracellular Bacteria ◽

Molecular Pathways ◽

Hla B27 ◽

Immune Mediated ◽

Clinical Considerations ◽

Active Bacteria

SUMMARY Current evidence supports the concept that reactive arthritis (ReA) is an immune-mediated synovitis resulting from slow bacterial infections and showing intra-articular persistence of viable, nonculturable bacteria and/or immunogenetic bacterial antigens synthesized by metabolically active bacteria residing in the joint and/or elsewhere in the body. The mechanisms that lead to the development of ReA are complex and basically involve an interaction between an arthritogenic agent and a predisposed host. The way in which a host accommodates to invasive facultative intracellular bacteria is the key to the development of ReA. The details of the molecular pathways that explain the articular and extra-articular manifestations of the disease are still under investigation. Several studies have been done to gain a better understanding of the pathogenesis of ReA; these constitute the basis for a more rational therapeutic approach to this disease.

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Lower level of synovial fluid interferon- in HLA-B27-positive than in HLA-B27-negative patients with Chlamydia trachomatis reactive arthritis

Rheumatology ◽

10.1093/rheumatology/keg440 ◽

2003 ◽

Vol 43 (2) ◽

pp. 249-250 ◽

Cited By ~ 1

Author(s):

R. Cuchacovich

Keyword(s):

Chlamydia Trachomatis ◽

Synovial Fluid ◽

Reactive Arthritis ◽

Hla B27

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Reactive arthritis due to Chlamydia psittaci associated with HLA‐B27 genotype

The Medical Journal of Australia ◽

10.5694/j.1326-5377.2009.tb02600.x ◽

2009 ◽

Vol 190 (11) ◽

pp. 649-650 ◽

Cited By ~ 1

Author(s):

Peter N Gonski ◽

Bobby Chan

Keyword(s):

Reactive Arthritis ◽

Chlamydia Psittaci ◽

Hla B27

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Reactive arthritis and enteropathic arthropathy

10.1093/med/9780199642489.003.0115_update_002 ◽

2016 ◽

Author(s):

J. S. Hill Gaston

Keyword(s):

Inflammatory Bowel Disease ◽

Back Pain ◽

Immune Responses ◽

Reactive Arthritis ◽

Inflammatory Back Pain ◽

Hla B27 ◽

Genetic Studies ◽

Inflammatory Bowel ◽

Disease Modifying ◽

Crystal Induced Arthritis

Reactive arthritis (ReA), and enteropathic arthritis secondary to inflammatory bowel disease, are forms of spondyloarthritis, all of which share an association with HLA B27 and can involve both axial and peripheral joints. Genetic studies strongly implicate the cytokines IL-17 and IL-23 in their pathogenesis, and evidence for autoimmunity is lacking. ReA is triggered by particular bacteria, mainly affecting the gut and genitourinary tract, though infections are sometimes asymptomatic. Classically an acute oligo- or monoarthritis with enthesitis occurs, often with inflammatory back pain, though mild polyarthritis can also occur. Septic and crystal-induced arthritis are the principal differential diagnoses. Extra-articular features may aid diagnosis, which otherwise requires laboratory evidence of preceding infection. Bacterial components traffic to the joint (which is nevertheless sterile), and elicit local pro-inflammatory immune responses. Most ReA is self-limiting, but persistent cases may require disease-modifying anti-rheumatic drugs or even biologics.

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