Enteropathic Spondylitis: Difference between revisions

Enteropathic spondylitis, or EA, is a form of chronic, inflammatory arthritis associated with the occurrence of an inflammatory bowel disease (IBD), the two best-known types of which are ulcerative colitis and Crohn’s disease.

  • About one in five people with Crohn’s or ulcerative colitis will develop enteropathic arthritis.
  • The most common areas affected by EnA are the peripheral (limb) joints and, in some cases, the entire spine can become involved, as well[1].

The results from epidemiologic studies on AE affected by several factors, including the lack of validated sets of diagnostic criteria, the frequency of IBD in different geographic areas, the age cut-off and case definition, and different study designs.

The incidence and prevalence of IBD

  • Western Countries is estimated to be 6-15/100,000
  • 50-200/100,000 for developed countries CD
  • 8-14/100,000 and 120-200/100,000 for underdeveloped countries UC.

Rheumatic manifestations are the most frequent extraintestinal manifestation in IBD patients with a prevalence ranging between 17% and 39%

  • The joint involvement observed in IBD is usually classified in two subsets: axial (including sacroiliitis with or without spondylitis) and peripheral.
  • The axial involvement is found to be present in 2%–16% of IBD patients, with a higher prevalence in CD patients than in UC ones.
  • The prevalence of sacroiliitis (asymptomatic and symptomatic) is between 12% and 20% and association with HLA-B27 ranged from 3.9% to 18.9%.
  • Women show more frequently a peripheral joint involvement, whereas men tend to have an axial involvement.
  • Potential risk factors for arthritis in IBD patients are active bowel disease, family history of IBD, appendectomy, cigarette smoking, and the presence of others extraintestinal manifestations, such as erythema nodosum or pyoderma gangrenosum[2]

Mechanism of Injury / Pathological Process[edit | edit source]

  • Cells of the immune system.jpg

    The pathogenesis of EA is not fully understood – observationally joint inflammation occurs in genetically predisposed subjects with bacterial gut infections (providing important evidence for a possible relationship between inflammation of the gut mucosa and arthritis).

  • More than two-third of patients with SpA (spondyloarthritis) show microscopic inflammatory changes of gut mucosa without clinical signs of gastrointestinal disease.
  • Current theories prepose that genetically predisposed subjects have an aberrant migration of intestinal lymphocytes or macrophages from inflamed gut mucosa to joints.
  • A dysfunctional interaction between the mucosal immune system and gut bacteria could result in an abnormal state of immunological tolerance toward flora by alterations in mucosal effector cells or by affecting regulatory cells.[2]
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The symptoms of enteropathic arthritis (EnA) can be divided in two groups:

  1. Symptoms of inflammatory bowel disease (IBD) see Link
  2. Arthritic symptoms in the joints and, possibly, see below.[1]
  • About one in five people with EnA will have inflammatory arthritis in one or more peripheral (limb) joints eg an arm or leg, lower limbs are more commonly affected.
  • The severity of the peripheral arthritis normally coincides with the severity of the IBD, thus when diarrhea and abdominal pain are flaring, the peripheral arthritis tends to flare, as well.
  • About one in six people with IBD also has spinal inflammation, this is independent of the severity of the bowel disease symptoms.
  • In many people, this may just be arthritis in the sacroiliac (SI) joints, but in about five percent of people, the entire spine is involved.

Note that arthritis symptoms may precede the IBD symptoms[1].

A diagnosis of enteropathic arthritis is made through a complete medical examination including a history of symptoms and taking into account family history. Various tests may also be done:

  • A stool culture may be taken if a diagnosis of an inflammatory bowel disease (IBD) such as ulcerative colitis and Crohn’s disease has not yet been established.
  • A colonoscopy with or without bowel biopsies.
  • Blood tests may be done including an erythrocyte sedimentation rate (ESR or SED Rate), which may help in detecting inflammation, a test to determine the presence of the HLA-B27 genetic marker, and/or a C-reactive protein, which is another test that may help detect the presence of inflammation in the body.
  • Synovial fluid may be taken from affected joints for study.
  • X-rays of affected joints.[2]

Management / Interventions[edit | edit source]

A common treatment regimen for the various forms of spondyloarthritis (ankylosing spondylitis, psoriatic arthritis, enteropathic arthritis, reactive arthritis, juvenile spondyloarthritis, and undifferentiated spondyloarthritis) and MAS involves

Medication –

  • In enteropathic arthritis (spondylitis/arthritis associated with inflammatory bowel disease), medications may need to be adjusted so the gastrointestinal component of the disease is also treated and not exacerbated.
  • The use of corticosteroids and/or DMARDs and/or of anti-TNFα, helpful to contain intestinal inflammation, usually leads also to the reduction of peripheral arthritis symptoms.
  • Intra-articular injections of steroids[2]
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Physical therapy – including

  • Exercise (strength and range of movement)
  • Good posture practices
  • Mobilisations and massage
  • Other options eg heat/cold to help relax muscles and reduce joint pain[1].
  • Enteropathic spondyloarthritis encompasses a group of rheumatic disorders that share overlapping pathophysiology with other immune system disorders, particular those of the gut.
  • A multidisciplinary approach is important in recognizing the varied manifestations of ESpA in order to achieve a prompt and accurate diagnosis leading to the comprehensive care required to manage these diseases effectively.
  • Clinical goals are to maximize long-term quality of life through the management and control of inflammation of the gut and joints, manage peripheral involvement of the eyes and skin, and prevent progression to structural damage.

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