Reactive Arthritis (and Reiter’s syndrome)

Reactive arthritis is a relatively short-lived condition causing painful joint swelling.  It develops in response to and occurs shortly after an infection, usually of the bowel, genital tract or throat.

Background

Previously known as ‘Reiter’s syndrome’ (not commonly used now as Reiter was a Nazi war criminal), reactive arthritis classically presents with a triad of features.

It usually resolves within 3-12 months, but up to 15% of patients can develop chronic, and occasionally destructive/aggressive, arthritis, enthesitis or spondylitis.

ImageNB Although this is the classic description, only one third of patients will present with all three (sensitivity 50%; specificity 99%- i.e. not all patients with ReA have all three, but patients with all three usually have ReA).

Aetiology- which infections?

  • GU
    • Chlamydia trachomatis is generally thought to be the most common aetiological infection.  Particular the L2b serotype.
      • NB Chlamydia may be detectable in the synovial fluid (this is not the case of enteric bacteria)
      • This may be an asymptomatic infection
    • Other possible pathogens include HIV and ureaplasma urealyticum
  • GI
    • Most commonly Campylobacter jejuni, but can also be seen after Salmonella, Shigella and Yersinia infections
    • NB Many patients won’t have a ‘diagnosis’ of which bacteria- but may have a history suggestive of a recent gastroenteritis

Epidemiology

  • Around 5/100,000 patients per year get ReA.
  • Around 1-4% of patients get ReA after enteric infection
  • Around 0.5-1% of patients with urethritis develop ReA

Pathophysiology

  • As with other seronegative arthropathies, there is an association with HLA-B27 allele of the MHC-class I protein.
  • The exact mechanism of how initial infection causes the arthropathy is largely unknown, although it is possible that a systemic infection (or indeed, infiltration of bacteria into the joint space), causes an inflammatory response in the joint which is perpetuated by the presentation of antigens (either auto-antigens or pathological antigens) to an HLA-B27.
  • The inflammation itself is mediated by CD4+ T cells and their inflammatory cytokines e.g. TNF, IL-6, IL-1/1B, IL10

Presentation

  • Symptoms tend to present 2-4 weeks post-infection (note that up to 10% of patients may have been asymptomatic) and onset is generally acute (symptoms develop within several days)
  • For presentation of conjunctivitis and urethritis, see posts
  • Constitutional symptoms are very common- e.g. fatigue, mild fever, muscle aches
  • Musculoskeletal symptoms
    • Typically lower limb, asymmetrical oligoarthritis with a relatively acute onset (swollen, hot, painful, tender, red joints- with associated joint effusions)
    • Tendonitis/enthesitis of the lower limbs (achilles’ tendonitis/ plantar fasciitis) is also relatively common.  The patient may also have dactylitis (sausage digits)
    • Back pain is reported in around 50% of patients with ReA
      • Note that physical examination evidence of active spondylitis/sacroiliitis (e.g. loss of ROM) is not commonly seen.  Examination of the back may even be normal.
  • Extra-articular features
    • Skin/mucosal changes are quite common
      • Keratoderma blennorrhagicum (hyperkeratotic skin presenting as vesicles on erythematous skin of the soles/palms/trunk/scalp, eventually converging- covering a larger plaque of skin.  Usually yellow/brown in colour)
      • rarely erythema nodosum
      • mouth ulcers

Investigations

  • There are no specific investigations for ReA, but inflammatory markers will usually be high in active disease and can be used as an indicator of disease progression.
  • A stool sample or urethral swab may reveal the underlying causal organism (if there is still evidence of underlying infection, this should be treated.  However, the result itself is unlikely to influence the management of ReA).
  • X-rays may be done but can be normal, particularly in early disease.
    • there may be evidence of bony erosion and bony reaction in severe or late disease
  • HLA-B27 may be checked if patients have long-standing symptoms (again, unlikely to affect management)

Management

  • NSAIDs and intra-articular corticosteroid injections are used to manage joint symptoms
    • In patients who do not respond, systemic steroids may also be tried
  • Physiotherapy may also be useful
  • DMARDs may be started in patients who have had symptoms for >3 months (?sulfasalazine (normally used for arthritis associated with IBD) but others e.g. azathioprine, methotrexate may also be used)
    • NB there is a distinct lack of evidence regarding DMARD use in ReA, likely due to its self-limiting nature.
  • Treatment of underlying infection should be started but will not affect prognosis of ReA.

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