Introduction

Reactive arthritis, formerly known as Reiter's syndrome, is a term used to refer to the appearance of rheumatologic disease following an infection (1). It is called "reactive" because the musculoskeletal complaints are triggered by an autoimmune reaction to the initial infection.

Anatomy

Reactive arthritis usually affects the large joints

Pathogeneis

GI infections like Yersinia, Camplobacter, Salmonella, Chlamydia and Shigella can produce an arthritic symptoms (3,4). In fact, the incidence of arthritis after an acute attack of dysentery is reported to be between 2 and 33 percent (5). The HLA-B27 phenotype in particular, seems to predispose to a reactive arthitis following a Yersinia infection; in fact, the HLA-B27 genotype has been reported in up to 90% of reactive arthritis due to a Yersinia infection (2) E. coli has also been noted to produce an arthritic picture, but no connection between HLA-B27 and the subsequent development of reactive arthritis has been found (6).

Natural History

Overall, reactive arthritis is an uncommon disease; with a prevalence estimated at 30-40 per 100,000 adults and an annual incidence of 5-28 per 100,000 (7). It is more prevalent in Scandinavian populations; in fact, most study's on reactive arthritis are conducted in Scandinavian populations. Most cases are sporadic, but there have been outbreaks reported with specific strains of each pathogen (7).
The peak age is the 3rd and 4th decades
The condition is more common in white, male patients

Patient History and Physical Findings

Typically, the arthritis will develop between 2 and 3 weeks following the GI infection. In reactive arthritis, the knee, ankle, wrist, and sacroiliac joints are commonly involved. The typical arthritis pattern is lower extremity dominant and is in an asymmetrical mono- or oligo joint pattern.
Enthesitis (insertional tendinopathy), conjuctivitis, anterior uveitis, urethritis and a skin or genital rash may all be seen.
Enthesitis can present as sausage like digits and swelling of the heels. The insertions of the Achilles tendon and the plantar fascia on the calcaneus are commonly involved. The urethritis may be sterile and can present with dysuria and increased frequency of urination.

Imaging and other Diagnostic Studies

Only 50% of patient's with reactive arthritis will be HLA-B27 positive, so the genotyping test is usually reserved in highly suspect circumstances.

Differential Diagnosis

Chlamydia or Gonnococal infection may cause urethritis
Analyzing synovial fluid for culture and crystal involvement is important to rule out other arthritites like septic arthritis and gout.

Treatment

Treat the underlying infection
Provide palliation for the reactive symptoms

Outcome

The prognosis for these patients is dependent on the strain of pathogen, genetic and environmental factors. Overall, the prognosis is good, with the arthritis remitting in less than 6 months. For example, only 4 to 10 percent of patients in one Finland study had reactive arthritis that lasted greater than one year. Their reactive arthritis was induced by strains of either Yersinia, Salmonella, Shigella or Chlamydia (7). Importantly, the presence of HLA-B27 does not seem to correlate with either the severity or the duration of the disease. It was noted that patients who develop a reactive arthritis following a GI infection are more likely to develop other auto-immune associated conditions like psoriasis, ankylosing spondylitis, and inflammatory bowel disease later in life (8).

Complications

Pearls and Pitfalls

The triad of "Can't see; can't pee; can't bend my knee" suggests reactive arthritis
Rule out Chlamydia or Gonnococal infection other causes of acute joint inflammation such as septic arthritis and gout

Miscellany

German physician Hans Reiter first described reactive arthritis and gives his name to the eponym for it.
Reactive arthritis is a so-called "seronegative spondylarthropathy" in that it appears similar to rheumatoid arthritis (ie, it's a "spondylarthropathy") but the rheumatoid factor blood test is negative (hence "seronegative")

Selected References

1. Panush, RS, Wallace, DJ, Dorff, RE, Engleman, EP. Retraction of the suggestion to use the term "Reiter's syndrome" sixty-five years later: the legacy of Reiter, a war criminal, should not be eponymic honor but rather condemnation. Arthritis Rheum 2007; 56:693.
2. Rudwaleit, M, Baeten, D. Ankylosing spondylitis and bowel disease. Best Pract Res Clin Rheumatol. 2006; 20:451.
3. De Keyser, F, Van Damme, N, De Vos, M, et al. Opportunities for immune modulation in the spondyloarthropathies with special reference to gut inflammation. Inflamm Res 2000; 49:47.
4. De Keyser, F, Baeten, D, Van den Bosch, F, et al. Gut inflammation and spondyloarthropathies. Curr Rheumatol Rep 2002; 4:525.
5. Inman, RD. Arthritis and enteritis--an interface of protean manifestations. J Rheumatol 1987; 14:406.
6. Schiellerup, P, Krogfelt, KA, Locht, H. A Comparison of Self-reported Joint Symptoms Following Infection with Different Enteric Pathogens: Effect of HLA-B27. J Rheumatol 2008; 35:480.
7. Leirisalo-Repo, M, Sieper, J. Reactive arthritis: epidemiology, clinical features, and treatment, in Ankylosing spondylitis and the spondyloarthropathies, M.H. Weisman, D. van der Heijde, and J.D. Reveille, Editors. 2006, Mosby Elsevier: Philadelphia. p. 53-64.
8. Kvien, TK, Gaston, JS, Bardin, T, et al. Three month treatment of reactive arthritis with azithromycin: a EULAR double blind, placebo controlled study. Ann Rheum Dis 2004; 63:1113.

Related topics

ankylosing spondylitis
Psoriatic arthritis
rheumatoid arthritis

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