Reactive Arthritis in Emergency Medicine 

  • Author: Nima Sarani, MD; Chief Editor: Robert E O'Connor, MD, MPH   more...
 
Updated: May 21, 2012
 

Background

In 1916, Hans Reiter described the classic triad of arthritis, nongonococcal urethritis, and conjunctivitis.[1] However, he mistakenly dubbed this disease as "spirochetosis arthritica."[2] This condition used to be known as Reiter syndrome but is now referred to as reactive arthritis (ReA).[1] This change has occurred in part because of Hans Reiter's affiliation and activities with the Nazis during WWII.

Cases of "Reiter's disease" have likely been described dating back many centuries. In fact, Christopher Columbus may have suffered from its effects having described symptoms such as fever, arthritis, eye hemorrhage, and pain, following a bout of dysentery. His arthritis later progressed to a chronic bedridden state he attributed to "gout."[2]

Reactive arthritis refers to acute nonpurulent arthritis complicating an infection elsewhere in the body.

Reactive arthritis falls under the rheumatic disease category of seronegative spondyloarthropathies, which includes ankylosing spondylitis, psoriatic arthritis, the arthropathy of associated inflammatory bowel disease, juvenile-onset ankylosing spondylitis, juvenile chronic arthritis, and undifferentiated spondyloarthritis.[3]

A study by Kaarela et al reported that reactive arthritis and ankylosing spondylitis appear to be identical. They assessed long-term outcome of reactive arthritis and ankylosing spondylitis to identify similarities in manifestations of disease. A number of similarities were found; among them, sacroiliitis, peripheral arthritis, and iritis developed most often in both chronic reactive arthritis and ankylosing spondylitis.[4]

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Pathophysiology

Reactive arthritis is triggered following enteric or urogenital infections. Reactive arthritis is associated with human leukocyte antigen (HLA)–B27, although HLA-B27 is not always present in an affected individual, particularly in the presence of HIV. It appears that HLA-B27 is also related to the chronicity of disease.[4]

Rihl et al found a high proportion of proangiogenic factors accounting for a genetically determined susceptibility to reactive arthritis.[5] Bacteria associated with reactive arthritis are generally enteric or venereal and include the following: Shigella flexneri, Salmonella typhimurium, Salmonella enteritidis,[6] Streptococcus viridans, Mycoplasma pneumonia, Cyclospora,[7] Chlamydia trachomatis,Yersinia enterocolitica, Yersinia pseudotuberculosis, Campylobacter,[8] and group A Streptococcus.[9] In fact, the incidence of acute rheumatic fever in the United States and Western Europe is decreasing and poststreptococcal reactive arthritis is becoming more prevalent.[10]

Bacteria or their components (RNA, DNA) have been identified in synovial fluid cells, synovial biopsy specimens, and circulatory monocytes.Interestingly, severely symptomatic enteric infections are associated with an increased likelihood of developingreactivearthritis,[2, 11] where as ,more frequently, asymptomatic venereal infections cause this disease.[2]

Reactive arthritis has an axial and ascending nature. It is sterile inflammation triggered by a distal mucosal infection.[12] It has been proposed that damage associated molecular patterns, either exogenous pathogen-associated molecular patterns or endogenous material such as uric acid that are released from necrotic cells, can travel upwards via the pelvic and spinal lymphatic pathways and activate Toll-like receptors (TLRs). TLRs, when stimulated on target mesenchymal stem cells, propagate responses that can eventually lead to syndesmophytes and bamboo spine.[13]

Inflammatory synovitis in reactive arthritis is mediated by proinflammatory cytokines. Native T cells under the influence of TGF-beta and other cytokines such IL-6, differentiate into Th17 effector cells, which then produce IL-17. IL-17 is one of the major cytokines elevated in the synovial fluid of these patients.[14, 15] Furthermore, deficiencies in regulatory mechanisms can result in increased proinflammatory cytokine production and worst outcome. For example, it has been shown in mice with Yersinia enterocolitica –induced reactive arthritis that in the absence of TNFRp55 regulatory signaling, Th17 effector cells sustain the inflammatory response.[16]

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Epidemiology

Frequency

United States

Frequency is estimated at 3.5 cases per 100,000. (Because of uncertainty of diagnosis and variations in definitions, epidemiologic features are difficult to calculate.)

An estimated 1-3% of all patients with a nonspecific urethritis develop an episode of arthritis. The incidence is 1-4% following enteric infection. This number jumps to 20-25% following bacterial enteritis in HLA-B27-positive individuals.[17] Prevalence of inapparent chlamydial infections, underdiagnosis, and underreporting may make incidence even higher.[11]

After outbreak of S enteritidis, 29% had reactive arthritis.[6]

It has been noted that worse functional capacity and higher disease activity are observed in the lower socioeconomic classes.[18]

International

The annual incidence of reactive arthritis is roughly the same in different countries. In Norway, an annual incidence of chlamydial reactive arthritis of 4.6 cases per 100,000 population and an incidence of enteric bacteria–induced reactive arthritis of 5 cases per 100,000 population were reported in 1988-1990. In the Czech Republic, the annual incidence of reactive arthritis in adults during 2002-2003 was reported at 9.3 cases 100,000 population.[19]

Inciting infections may be endemic to certain geographic locations. For example, the incidence of Yersiniaenterocolitica is higher in Europe than in North America and thus is responsible for cases of reactive arthritis in countries such as Finland and Norway.[2] Occurrence appears to be related to the prevalence of HLA-B27 in a population and the rate of urethritis/cervicitis and infectious diarrhea. More than 40 subtypes of HLA-B27 are known. Those associated with the spondyloarthropathies are HLA-B2702, B2704, and B2705.[20] These subtypes may be somewhat geographically segregated. For example, the subtype B2705 is predominantly found in Latin America, Brazil, Taiwan, and parts of India. Interestingly, subtypes HLA-B2706 and B2709, found in native Indonesia and Sardinia, respectively, may be partially protective from reactive arthritis.[21]

Mortality/Morbidity

Most patients have severe symptoms lasting weeks to 6 months. Approximately 15-50% have recurrent bouts of arthritis. Chronic arthritis or sacroiliitis occurs in 15-30% of cases. Predictors of chronicity include HLA-B27 positivity and triggering infections with Yersinia, Salmonella, Shigella, or Chlamydia species.[22]

Race

Reactive arthritis is reported most frequently in whites. When reactive arthritis occurs in black persons, it is frequently B27-negative.

Occurrence appears to be related to HLA-B27 prevalence in the population.

Sex

The male-to-female postvenereal ratio is traditionally 5-10:1. The postenteric ratio is 1:1.

Age

The peak onset is in persons aged 15-35 years; reactive arthritis is rarely seen in children. Cases in children are almost entirely postenteric. Duration of diarrhea and weight loss are also considered risk factors in developing reactive arthritis postenteric infections.[23]

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Contributor Information and Disclosures
Author

Nima Sarani, MD  Resident Physician, Department of Emergency Medicine, Oklahoma University College of Medicine

Nima Sarani, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physicians, and Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

Coauthor(s)

Bo Burns, DO, FACEP, FAAEM  Assistant Professor, Associate Residency Director, Medical Clerkship Director, Department of Emergency Medicine, University of Oklahoma School of Community Medicine; Attending Physician, Department of Emergency Medicine

Bo Burns, DO, FACEP, FAAEM, is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Dana A Stearns, MD  Assistant Director of Undergraduate Education, Department of Emergency Medicine, Massachusetts General Hospital; Assistant Professor of Surgery, Harvard Medical School

Dana A Stearns, MD is a member of the following medical societies: American College of Emergency Physicians

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

Gino A Farina, MD, FACEP, FAAEM  Associate Professor of Clinical Emergency Medicine, Albert Einstein College of Medicine; Program Director, Department of Emergency Medicine, Long Island Jewish Medical Center

Gino A Farina, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Robert E O'Connor, MD, MPH  Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Thomas Scoggins, MD, and Igor Boyarsky, DO, to the development and writing of this article.

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Circinate balanitis in a patient with reactive arthritis.
Plaques on the soles of a patient with reactive arthritis.
Painful erosions on the fingers in a patient with reactive arthritis.
Plaques and erosions of the tongue in a patient with reactive arthritis.
Radiograph of the feet in a 27-year-old man shows erosions in all the left metatarsophalangeal (MTP) joints with subluxation and valgus deformity of most of the toes. Smaller erosions in the four and fifth MTP joints of the right foot are also shown.
Lateral radiograph of the foot (same patient as in the photo above) reveals a calcaneal spur and enthesitis.
Radiograph of both hands shows small erosive changes in both first metacarpal heads associated with minimal subluxation. Bone density is normal.
Radiography of the pelvis reveals bilateral asymmetric sacroiliitis.
Image in 40-year-old man with nonmarginal syndesmophytes predominantly in the lower thoracic and upper lumbar spine.
 
 
 
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