Reactive arthritis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
It is thought that reactive arthritis is the result of previous gastrointestinal or genitourinary infections, which results in an autoimmune condition. The most commonly associated organisms include Chlamydia, Yersinia, Salmonella, Shigella, and Campylobacter infection. | It is thought that reactive arthritis is the result of previous gastrointestinal or genitourinary infections, which results in an autoimmune condition. The most commonly associated organisms include Chlamydia, Yersinia, Salmonella, Shigella, and Campylobacter infection.<ref name="pmid16195157">{{cite journal |vauthors=Leirisalo-Repo M |title=Reactive arthritis |journal=Scand. J. Rheumatol. |volume=34 |issue=4 |pages=251–9 |date=2005 |pmid=16195157 |doi=10.1080/03009740500202540 |url=}}</ref> | ||
*Reactive arthritis is associated with HLA-B27 (MHC class I molecule). | *Reactive arthritis is associated with HLA-B27 (MHC class I molecule). | ||
*It is estimated around 75% patients of reactive arthritis are positive for HLA-B27. Other alleles associated with reactive arthritis include HLA-B51 and HLA-DRB1. | *It is estimated around 75% patients of reactive arthritis are positive for HLA-B27. Other alleles associated with reactive arthritis include HLA-B51 and HLA-DRB1. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
It is thought that reactive arthritis is the result of previous gastrointestinal or genitourinary infections, which results in an autoimmune condition. The most commonly associated organisms include Chlamydia, Yersinia, Salmonella, Shigella, and Campylobacter infection.[1]
- Reactive arthritis is associated with HLA-B27 (MHC class I molecule).
- It is estimated around 75% patients of reactive arthritis are positive for HLA-B27. Other alleles associated with reactive arthritis include HLA-B51 and HLA-DRB1.
- HLA B27 association with reactive arthritis can also be attributed to the fact that patients with family history of reactive arthritis tend to have a more severe form of disease.
- The exact mechanism by which infecting organism cause reactive arthritis is not fully understood. It is thought that microbial antigens are similar to certain body proteins (self proteins). When an immune response is mounted against the microbial proteins, the antibodies produced against microbial proteins also reacts with the self proteins of the body causing reactive arthritis.
- Antigen presenting cells (APCs) present microbial antigens to T helper cells which leads to their activation.
- T helper cells then differentiates into TH2 cells which leads to secretion of interleukins (IL-3, IL-4, IL-6),TGF-β and TH17 cells.
- Interleukins IL-3, IL-4, IL-6 leads to increased production of antibodies from plasma cells.
- The Th17 cells release IL-17 which is also a pro-inflammatory cytokine.
- Furthermore, studies have shown the presence of T cells and intra-articular antibodies on synovial fluid analysis .
Reactive Arthritis in HIV patients
- Patients with HIV who later on develop reactive arthritis tend to have a more serious presentation.
- These patients present with severe generalised rash resembling psoriasis (pink color and scaly), severe arthritis and other AIDS related symptoms.
References
- ↑ Leirisalo-Repo M (2005). "Reactive arthritis". Scand. J. Rheumatol. 34 (4): 251–9. doi:10.1080/03009740500202540. PMID 16195157.