3. Reactive Arthritis

Reactive Arthritis

This PatientPlus article is written for healthcare professionals so the language may be more technical than the condition leaflets. You may find the abbreviations list helpful.

Synonym: Reiter's syndrome

Reactive arthritis is an autoimmune condition that develops in response to an infection.

It was first described in 1916 by Hans Reiter who reported the triad of nongonococcal urethritis, conjunctivitis, and arthritis in a young German officer with bloody dysentery. In the same year, Fiessinger and Leroy described four patients with what they called oculo-urethro-synovial syndrome associated with shigella dysentery. The term Reiter's syndrome, used to describe the same clinical presentations, is used less often. This may be because of Reiter's experimentation on prisoners during World War II.

There appears to be a strong association with HLA B27 (~75%) and the seronegative arthropathies. The syndrome is sometimes subdivided into two subgroups:

  • Incidence 5.0/100,000 patients aged 18-60 years.[2]
  • Most patients are aged 20-40 and it is more common in Caucasians.
  • HLA-B27 is a risk factor.[3]
  • Reactive arthritis usually develops 2-4 weeks after a genitourinary or gastrointestinal infection. About 10% of patients do not have a preceding symptomatic infection.
  • The onset is most often acute, with malaise, fatigue, and fever.
  • An asymmetrical, predominately lower extremity, oligoarthritis (usually no more than six joints) is the major presenting symptom.
  • Low back pain occurs in 50% of patients.
  • Heel pain is common because of inflammation of the Achilles or plantar aponeurosis insertions on the calcaneus.
  • The complete Reiter's triad of urethritis, conjunctivitis, and arthritis may occur.
  • Skin (eg erythema nodosum, circinate balanitis), nails (dystrophic changes) and mucous membranes (mouth ulcers) may all be affected.
  • Other features include:
    • Eyes: uveitis, episcleritis, keratitis, and corneal ulcerations.
    • Gastrointestinal: some patients have intermittent bouts of abdominal pain and diarrhoea - and show lesions on colonoscopy, similar in appearance to inflammatory bowel disease.
    • Cardiovascular: aortitis with or without aortic regurgitation (2%), conduction defects.
  • ESR and CRP are usually very high.
  • FBC: normocytic normochromic anaemia, mild leukocytosis and thrombocytosis during the acute phase.
  • HLA-B27 is positive in 65-96% of cases. Rheumatoid factor and antinuclear antibodies are absent.
  • Joint aspiration may be required to rule out septic or crystalline arthritis. Synovial fluid analysis in patients with reactive arthritis shows a high white blood cell count (mostly polymorphonuclear leukocytes in acute phase).
  • Culture of stools, throat and urogenital tract samples in order to identify the causative organism.
  • Serology for detection of chlamydia (refer to an STD clinic for further genitourinary investigation in sexually active patients).
  • X-rays: normal in early stages of disease. In advanced or long-term disease, they may show periosteal reaction and proliferation at sites of tendon insertion, plantar spurs, marginal erosions with adjacent bone proliferation in the hands and feet and, less often, features of sacroiliitis and ankylosing spondylitis.[4]
  • ECG: in patients with prolonged disease to assess for conduction disturbances.
  • In the acute phase, rest affected joints, aspirate synovial effusions.
  • Physiotherapy.
  • Non-steroidal anti-inflammatory drugs (NSAIDs).
  • Corticosteroids:
    • These can be used as either intra-articular injections or systemic therapy. Joint injections can help avoid the use of other systemic therapy. Sacroiliac joints can be injected, usually under fluoroscopic guidance.
    • Systemic corticosteroids can be used (particularly in patients unresponsive to NSAIDs or who develop adverse effects).
  • Antibiotics to treat an identified causative organism. Antibiotic treatment does not change the course of reactive arthritis, even when an infective cause is identified.[4] However, some studies suggest that long-term treatment with antibiotics may help to reduce the length of the arthritis in some cases, particularly if chlamydia is the triggering infection. The use of long-term treatment with antibiotics in reactive arthritis is currently being investigated.
  • Disease-modifying anti-rheumatic drugs (DMARDS):
    • Clinical experience with DMARDs in reactive arthritis is limited.
    • Sulfasalazine has been shown to be beneficial in some patients.
    • Experiences with other DMARDs, eg azathioprine, methotrexate and ciclosporin, have been anecdotally reported and they may be used in patients unresponsive to standard treatments (NSAIDs and physiotherapy).
    • Antibiotics (tetracyclines) may be useful in uroarthritis but have not been successful in enteroarthritis. In more aggressive cases, or when reactive arthritis evolves towards ankylosing spondylitis, TNF alpha-blockers may represent an effective choice.[5]
  • Reactive arthritis is usually self-limiting with resolution of symptoms by 3-12 months, but symptoms may persist for 12 months or more.
  • About 15% of patients develop a long-term, and sometimes destructive arthritis, enthesitis or spondylitis.
  • There is a high incidence of recurrence, especially in those who are HLA-B27 positive.
  • Recurrence of disease may be triggered by a new infection or other stress factor.
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Further reading & references

  1. Hannu T, Mattila L, Rautelin H, et al; Campylobacter-triggered reactive arthritis: a population-based study. Rheumatology (Oxford). 2002 Mar;41(3):312-8.
  2. Kvien TK, Glennas A, Melby K, et al; Reactive arthritis: incidence, triggering agents and clinical presentation. J Rheumatol. 1994 Jan;21(1):115-22.
  3. Yu D, Kuipers JG; Role of bacteria and HLA-B27 in the pathogenesis of reactive arthritis. Rheum Dis Clin North Am. 2003 Feb;29(1):21-36, v-vi.
  4. Lozada CJ et al, Reactive Arthritis, Medscape, Jan 2010
  5. Palazzi C, Olivieri I, D'Amico E, et al; Palazzi C, Olivieri I, D'Amico E, et al; Management of reactive arthritis. Expert Opin Pharmacother. 2004 Jan;5(1):61-70.
Original Author: Dr Colin Tidy Current Version: Peer Reviewer: Dr John Cox
Last Checked: 19/08/2011 Document ID: 2700  Version: 22 © EMIS

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

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