Patient professional reference
Synonym: Reiter's syndrome
Reactive arthritis is a form of seronegative spondyloarthritis clinically associated with inflammatory back pain, additive or migratory oligoarthritis and extra-articular symptoms that typically follow a gastrointestinal or urogenital infection by a minimum of 1 to a maximum of 3-6 weeks.
The presence of large joint oligoarthritis, urogenital tract infection and uveitis characterises Reiter's syndrome as a clinical subtype of reactive arthritis.
There appears to be a strong association with HLA B27 (~75%) and the seronegative arthropathies. The syndrome is sometimes subdivided into two subgroups:
- Post-enteric: the three most commonly associated enteric pathogens are Campylobacter, Salmonella and Shigella species.
- Post-venereal: following Chlamydia trachomatis infection or with human immunodeficiency virus (HIV).
- Reactive arthritis commonly affects young adults, most frequently white and carrying the HLA-B27 allele.
- C. trachomatis and Chlamydia pneumoniae are the most frequent causative pathogens.
- Reactive arthritis may be associated with tuberculosis (Poncet's disease).
- Arthritis may also occur after infection with atypical organisms such as Clostridium difficile and Giardia lamblia.
- 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, predominantly lower extremity, oligoarthritis (usually no more than six joints) is the major presenting symptom.
- Low back pain often occurs.
- 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.
- Ankylosing spondylitis and undifferentiated spondyloarthropathy.
- Gonococcal arthritis.
- Inflammatory bowel disease.
- Psoriatic arthritis.
- Rheumatic fever.
- Rheumatoid arthritis.
- Septic arthritis.
Once arthritis is observed, microbial tests and blood or synovial fluid cultures are negative, and only serum antibodies are detected.
- ESR and CRP are usually very high.
- FBC: normocytic normochromic anaemia, mild leukocytosis and thrombocytosis during the acute phase.
- HLA-B27 is positive in the majority of those affected. 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 - eg, polymerase chain reaction (PCR).Refer to a sexual health clinic for further genitourinary investigation in sexually active patients.
- Serology for other possible infectious triggers - eg, Yersinia, Campylobacter, Salmonella and Shigella species.
- 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.
- ECG: in patients with prolonged disease to assess for conduction disturbances.
- In the acute phase, rest affected joints, aspirate synovial effusions.
- Non-steroidal anti-inflammatory drugs (NSAIDs).
- 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. 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.
- Reactive arthritis is usually self-limiting with resolution of symptoms by 3-12 months, but symptoms may persist for 12 months or more.
- A minority of patients may 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.
Further reading and references
Selmi C, Gershwin ME; Diagnosis and classification of reactive arthritis. Autoimmun Rev. 2014 Apr-May13(4-5):546-9. doi: 10.1016/j.autrev.2014.01.005. Epub 2014 Jan 10.
Ajene AN, Fischer Walker CL, Black RE; Enteric pathogens and reactive arthritis: a systematic review of Campylobacter, salmonella and Shigella-associated reactive arthritis. J Health Popul Nutr. 2013 Sep31(3):299-307.
Zeidler H, Hudson AP; New insights into Chlamydia and arthritis. Promise of a cure? Ann Rheum Dis. 2014 Apr73(4):637-44. doi: 10.1136/annrheumdis-2013-204110. Epub 2013 Dec 2.
Abdulaziz S, Almoallim H, Ibrahim A, et al; Poncet's disease (reactive arthritis associated with tuberculosis): retrospective case series and review of literature. Clin Rheumatol. 2012 Oct31(10):1521-8. doi: 10.1007/s10067-012-2042-0. Epub 2012 Aug 2.
Morris D, Inman RD; Reactive arthritis: developments and challenges in diagnosis and treatment. Curr Rheumatol Rep. 2012 Oct14(5):390-4. doi: 10.1007/s11926-012-0280-4.
Management of sexually aquired reactive arthritis; British Association for Sexual Health and HIV (2008)
Zarco Montejo P; [Diagnosis and treatment of Chlamydia-induced reactive arthritis]. Reumatol Clin. 2012 Mar8 Suppl 1:S20-5. doi: 10.1016/j.reuma.2011.11.003. Epub 2012 Mar 14.
Tuuminen T, Lounamo K, Leirisalo-Repo M; A review of serological tests to assist diagnosis of reactive arthritis: critical appraisal on methodologies. Front Immunol. 2013 Dec 44:418. doi: 10.3389/fimmu.2013.00418.
Carlin EM, Ziza JM, Keat A, et al; 2014 European Guideline on the management of sexually acquired reactive arthritis. Int J STD AIDS. 2014 Nov25(13):901-12. doi: 10.1177/0956462414540617. Epub 2014 Jun 27.
Palazzi C, Olivieri I, D'Amico E, et al; Management of reactive arthritis. Expert Opin Pharmacother. 2004 Jan5(1):61-70.
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