Reactive Arthritis Clinical Presentation

  • Author: Carlos J Lozada, MD; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: Mar 27, 2012
 

History

ReA usually develops 2-4 weeks after a genitourinary or gastrointestinal infection. Recent evidence indicates that a preceding respiratory infection with Chlamydia pneumoniae may also trigger the disease.[3] About 10% of patients do not have a preceding symptomatic infection.

Both postvenereal and postenteric forms of ReA may manifest initially as nongonococcal urethritis. Mild dysuria, mucopurulent discharge, prostatitis and epididymitis in men, and vaginal discharge and/or cervicitis in women are other possible manifestations.

The onset of ReA is usually acute and characterized by malaise, fatigue, and fever. An asymmetrical, predominately lower-extremity, oligoarthritis is the major presenting symptom. Low-back pain occurs in 50% of patients. Heel pain is common because of enthesopathies at the Achilles or plantar aponeurosis insertion on the calcaneus. The complete Reiter triad of urethritis, conjunctivitis, and arthritis may occur.

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Physical

  • Joints, axial skeleton, entheses
    • Peripheral joint involvement associated with ReA is typically asymmetric and usually affects the weight-bearing joints (ie, knees, ankles, hips), but the shoulders, wrists, and elbows may also be affected.
    • In more chronic and severe cases, the small joints of the hands and feet may also be involved. As in other spondyloarthropathies, dactylitis (ie, sausage digits) may develop.
    • While 50% of patients with ReA may develop low-back pain, most physical examination findings in patients with acute disease are minimal except for decreased lumbar flexion. Patients with more chronic and severe axial disease may develop physical findings similar to ankylosing spondylitis.
    • As with other spondyloarthropathies, the enthesopathy of ReA may be associated with findings of inflammation (ie, pain, tenderness, swelling) at the Achilles insertion. Other sites include the plantar fascial insertion on the calcaneus, ischial tuberosities, iliac crests, tibial tuberosities, and ribs.
  • Skin and nails
    • Keratoderma blennorrhagica on the palms and soles is indistinguishable from pustular psoriasis and is highly suggestive of chronic ReA.
    • Erythema nodosum may develop but is uncommon.
    • Nails can become thickened and crumble, resembling mycotic infection or psoriatic onychodystrophy, but nail pitting is not observed.
    • Circinate balanitis may also develop.
  • Other mucosal signs and symptoms: Painless shiny patches in the palate, tongue, and mucosa of the cheeks and lips have been described.
  • Ocular findings
    • Conjunctivitis is part of the classic triad of Reiter syndrome and can occur before or at the onset of arthritis.
    • Other ocular lesions include acute uveitis (20% of patients), episcleritis, keratitis, and corneal ulcerations. The lesions tend to recur.
  • Enteric infections
    • Enteric infections may trigger ReA. Pathogens include Salmonella, Shigella, Yersinia, and Campylobacter species. The frequency of ReA after these enteric infections is about 1%-4%. Other enteric bacteria that have been associated with ReA include Clostridium difficile,[13] Escherichia coli, and Helicobacter pylori.[14]
    • Some patients with ReA continue with intermittent bouts of diarrhea and abdominal pain. Lesions resembling ulcerative colitis or Crohn disease have been described when ileocolonoscopy is performed in patients with established ReA.[13]
  • Other manifestations
    • Other manifestations of ReA include mild renal pathology with proteinuria and microhematuria.
    • In severe chronic cases, amyloid deposits and immunoglobulin A (IgA) nephropathy have been reported. Cardiac conduction abnormalities may develop, and aortitis with aortic regurgitation occurs in 1%-2% of ReA cases.
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Causes

ReA is usually triggered by a genitourinary or gastrointestinal infection.

Bacteria postulated to be potential causes of reactive arthritis include Ureaplasma urealyticum, C trachomatis L2b serotype,[15] beta-hemolytic streptococci,[16] and Mycobacterium tuberculosis.[17] In addition, case reports have described reactive arthritis after vaccination with live vaccines[18, 19] and after intravesical therapy with Bacillus Calmette-Guérin (BCG).[20]

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Contributor Information and Disclosures
Author

Carlos J Lozada, MD  Director of Rheumatology Fellowship Program, Professor, Department of Medicine, Division of Rheumatology and Immunology, University of Miami, Leonard M Miller School of Medicine

Carlos J Lozada, MD is a member of the following medical societies: American College of Physicians and American College of Rheumatology

Disclosure: Pfizer Honoraria Speaking and teaching; Amgen Honoraria Speaking and teaching

Coauthor(s)

Maria F Carpintero, MD  Fellow, Department of Rheumatology, University of Miami, Jackson Memorial Medical Center, Miami Veterans Affairs Medical Center

Maria F Carpintero, MD is a member of the following medical societies: American College of Physicians and American College of Rheumatology

Disclosure: Nothing to disclose.

Specialty Editor Board

John Varga, MD  Professor, Department of Internal Medicine, Division of Rheumatology, Northwestern University

John Varga, MD is a member of the following medical societies: American College of Physicians, American College of Rheumatology, Central Society for Clinical Research, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Elliot Goldberg, MD  Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine

Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology

Disclosure: Nothing to disclose.

Alex J Mechaber, MD, FACP  Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD  Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

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