Reactive Arthritis in Emergency Medicine 

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]

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.

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, and Yersinia pseudotuberculosis. 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 developing reactive arthritis,^{[2, 8]} whereas, more frequently, asymptomatic venereal infections cause this disease.^[2]

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.^[9] Prevalence of inapparent chlamydial infections, underdiagnosis, and underreporting may make incidence even higher.^[8]

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

International

In Norway, an annual incidence of chlamydia-induced 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. 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.^[10] 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.^[11]

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.

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.