21 October 2009

Reactive Arthritis

Reactive arthritis (ReA) is a non‑purulent joint inflammation that usually follows bacterial gastrointenstinal or urogenital infections. The classic presentation of ReA is characterized by an asymmetric arthritis usually in the lower limbs associated with urethritis, conjunctivitis and occurrence of other articular or extra‑articular manifestations. ReA is classified as a type of seronegative spondyloarthopathy.
ReA not only affects the joints, but is also a systemic disease with extra‑articular symptoms. The clinical picture is dominated by syndromes of enthesitis (enthesopaties), peripheral arthritis (acute or subacute oligoarthritis mainly of the lower limb joints), pelvic and axial syndromes (spinal involvement with sacroilitis) and extramusculoskeletal syndromes.

Approximately 65–85% of patients with ReA are HLA‑B27 positive. Regardless of the preceding infection, the clinical picture is similar, but management can differ according to the triggering infection. Treatment of Chlamydia‑induced ReA should be started with antibiotics because of several mechanisms by which Chlamydia can cause persistent infection. The disease may have an acute or self‑limited course, however some patients develop chronic arthritis.

Etiology and pathophysiology of Reactive Arthritis:
Several factors contribute to the development of ReA, including:
1- The presence of bacteria or bacterial products in the joint and the local immune response directed against these bacteria
2- The effect of the arthritogenic peptides derived from ReA – triggering bacteria (Salmonella and Yersinia), which epitopes are presented by phagocytes to cytotoxic T lymphocytes in synovial membrane
3- Recognition of bacterial antigens outside
the cells, and forming complexes with class I human leukocyte antigens (HLA) and class II histocompatibility antigen (MHC II) presented on CD4 + and CD8 + T cells in Chlamydia infection
4- Tendency to persistent bacterial infections
and imbalance between tumor necrosis factor α (TNF‑α), interferon‑γ, IL‑12, IL‑10 activity (increased IL‑10 levels in the intestines, urogenital and respiratory system in patients with persistent infections).
5-Genetic factors also play an important role
in the etiology of ReA. The HLA‑B27 antigen is found in 65–80% of patients with ReA.

Extra‑articular manifestations of Reactive Arthritis:

Enthesopatic syndrome:

Heel pain, Achilles tendonitis, pain at the tibial tubercle
Pelvic and axial syndrome:
Sacroiliitis, spondylitis
Eye:
Conjunctivitis, iritis, keratitis, episcleritis
Genitourinary:
Urethritis, prostatitis, hemorrhagic cystitis, cervicitis
Gastrointestinal:
Diarrhea
Skin:
Keratoderma blennorhagica, circinate balanitis, oral ulcers, hyperkeratotis nails, erythema nodosum
Cardiovascular system:
Aortic disease, EKG conduction abnormalities
Renal:
Proteinuria, microhematuria, aseptic pyuria

3 comments:

  1. you stated that approximately 65–85% of patients with ReA are HLA‑B27 positive. what exactly is the B27 and what are the other 15% or so? Are they HLA-?? something else?

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  2. HLA-27 is a gene that when it is present it makes people to develop diseases such as ReA and Ankylosing Spondylitis, although these diseases could happen without the presence of this gene.

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  3. Is there an HLA class II gene that is associated with high risk for this disease?

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