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Reactive Arthritis

  • Author: Carlos J Lozada, MD; Chief Editor: Herbert S Diamond, MD  more...
 
Updated: Oct 31, 2015
 

Practice Essentials

Reactive arthritis (ReA), formerly termed Reiter syndrome, is an autoimmune condition that develops in response to an infection. It has been associated with gastrointestinal (GI) infections with Shigella, Salmonella, Campylobacter, and other organisms, as well as with genitourinary (GU) infections (especially with Chlamydia trachomatis). See the image below.

Painful erosions on fingers in patient with reacti Painful erosions on fingers in patient with reactive arthritis.

Signs and symptoms

The classic triad of ReA symptoms (found in only one third of patients) consists of the following:

  • Noninfectious urethritis
  • Arthritis
  • Conjunctivitis

In postenteric ReA, diarrhea and dysenteric syndrome (usually mild) is commonly followed by the clinical triad in 1-4 weeks. Some add a fourth component (mucocutaneous findings) to make up a diagnostic tetrad.

The following may be noted:

  • Acute onset of ReA, with malaise, fatigue, and fever
  • Asymmetrical, predominately lower-extremity, oligoarthritis as the major presenting symptom, sometimes with early myalgias
  • Initial nongonococcal urethritis, with frequency, dysuria, urgency, and urethral discharge
  • In addition to conjunctivitis, ophthalmologic symptoms that include erythema, burning, tearing, photophobia, pain, and decreased vision (rare)
  • Mild recurrent abdominal complaints after a precipitating episode of diarrhea
  • In HIV-positive patients, severe psoriasiform dermatitis, commonly involving the flexures, scalp, palms, and soles

Physical findings in ReA may include the following:

  • Musculoskeletal system - Asymmetric oligoarthritis affecting the weight-bearing joints, predominantly the lower extremity; sausage-shaped finger (dactylitis); enthesopathy; sacroiliitis
  • Skin and nails - Keratoderma blennorrhagicum; erythema nodosum (uncommon); onychodystrophy
  • Eyes - Conjunctivitis; anterior uveitis; keratitis; scleritis; episcleritis; cataracts; hypotony; glaucoma; corneal ulceration; disc or retinal edema; retinal vasculitis; optic neuritis; dacryoadenitis
  • GU tract - Meatal edema and erythema and clear mucoid discharge; prostatitis; vulvovaginitis; circinate balanitis (balanitis circinata); cervicitis; cystitis; salpingo-oophoritis; pyelonephritis; bartholinitis
  • GI tract - Diarrhea; abdominal pain; lesions resembling inflammatory bowel disease on ileocolonoscopy
  • Other systems - Cardiac (aortitis, aortic regurgitation, transient conduction abnormalities, myocarditis, pericarditis); renal (proteinuria, microhematuria, amyloid deposits, immunoglobulin A [IgA] nephropathy)

See Clinical Presentation for more detail.

Diagnosis

The diagnosis of ReA is clinical, based on the history and physical examination. No laboratory study or imaging finding is diagnostic.

The following laboratory studies may be helpful:

  • White blood cell (WBC) and red blood cell (RBC) counts
  • Erythrocyte sedimentation rate (ESR)
  • C-reactive protein (CRP) and other acute-phase reactants
  • IgA antibodies to specific bacterial antigens
  • Serology and cultures (blood, urine, stool, cervix, urethra), particularly for Chlamydia
  • Human leukocyte antigen (HLA)–B27
  • Tuberculin skin test
  • HIV
  • Urinalysis

Imaging modalities that may be considered include the following:

  • Plain radiography (reveals findings in only 40-70% of cases)
  • Whole-body scintigraphy
  • Positron emission tomography
  • Magnetic resonance imaging (MRI), especially of the sacroiliac joints
  • Computed tomography (CT)
  • Ultrasonography or echocardiography

Other studies to be considered include the following:

  • Arthrocentesis, synovial fluid analysis, and synovial biopsy (often needed to rule out an infectious process, especially in monoarticular arthritis with constitutional symptoms)
  • Antistreptolysin O (ASO) or anti-DNase B testing (if poststreptococcal infection is suspected)
  • Electrocardiography (ECG; in patients with a prolonged course of ReA)

See Workup for more detail.

Management

No curative treatment exists; instead, treatment aims at relieving symptoms and is based on symptom severity. Almost two thirds of patients have a self-limited course; as many as 30% develop chronic symptoms, posing a therapeutic challenge.

Pharmacologic agents that may be used in treating ReA include the following:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs) - These are the mainstays of therapy
  • Corticosteroids (topical, intra-articular, and systemic)
  • Antibiotics (for Chlamydia -related ReA in particular) - Tetracyclines are commonly given
  • Disease-modifying antirheumatic drugs (DMARDs) - Typically given when NSAIDs are ineffective or contraindicated, these include sulfasalazine, methotrexate, and anti−tumor necrosis factor (TNF) medications, such as etanercept and infliximab

No specific surgical treatment is indicated, though ophthalmologic surgery may be warranted to treat certain ocular manifestations of disease.

Physical therapy may be instituted to avoid muscle wasting and to reduce pain.

See Treatment and Medication for more detail.

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Background

Reactive arthritis (ReA), or Reiter syndrome (this eponym is not used because of Reiter’s activities as a Nazi war criminal[1] ) is an autoimmune condition that develops in response to an infection. ReA has been associated with gastrointestinal (GI) infections with Shigella, Salmonella, Campylobacter, and other organisms, as well as with genitourinary (GU) infections (especially with Chlamydia trachomatis).

As currently understood, the term ReA encompasses the older concepts of complete and incomplete reactive arthritis and a clinical syndrome of arthritis with or without extra-articular features that develop within 1 month of infectious diarrhea or GU infection. The classic triad characteristically associated with this condition comprises noninfectious urethritis, arthritis, and conjunctivitis (though this triad is not found in all cases).

ReA is frequently associated with the human leukocyte antigen (HLA)–B27 (HLA-B27) haplotype and is classified in the 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.[2]

A study by Kaarela et al reported that ReA and ankylosing spondylitis appear to be identical.[3] When assessing long-term outcomes of reactive arthritis and ankylosing spondylitis to identify similarities in manifestations of disease, the investigators found a number of similarities. Among these was the determination that sacroiliitis, peripheral arthritis, and iritis developed most often in both chronic ReA and ankylosing spondylitis.

Most ReA patients are young men. Young children tend to have the postdysenteric form, whereas adolescents and young men are most likely to develop ReA after a genitourinary infection. Some authors, interpreting the mucocutaneous findings as pustular psoriasis and the seronegative arthritis as psoriatic arthritis, believe that ReA is best classified as a type of psoriasis.[4]

Defining criteria

The classic triad of ReA—namely, arthritis, conjunctivitis, and noninfectious urethritis—occurs in only about one third of patients at onset. Less stringent diagnostic criteria from the American College of Rheumatology have specified a 1-month duration of arthritis in association with urethritis, cervicitis, or both.

It has been suggested, however, that the syndrome is better described as a triad consisting of arthritis, conjunctivitis or iridocyclitis, and nonbacterial urethritis or cervicitis. Some prefer to describe it as a tetrad, adding the mucocutaneous findings of balanitis circinata and keratoderma blennorrhagicum to the classic triad. In this view, the complete and incomplete forms of ReA can be identified by the presence or absence of the mucocutaneous involvement.

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Pathophysiology

ReA is usually triggered by a GU or GI infection (see Etiology). Evidence indicates that a preceding Chlamydia respiratory infection may also trigger ReA.[5] The frequency of ReA after enteric infection averages 1-4% but varies greatly, even among outbreaks of the same organism. Although severely symptomatic GI infections are associated with an increased risk of ReA,[6, 7] asymptomatic venereal infections more frequently cause this disease.[6] About 10% of patients have no preceding symptomatic infection.

ReA is associated with HLA-B27, an MHC class I molecule involved in T-cell antigen presentation. Results for HLA-B27 are positive in 65-96% of patients (average, 75%) with ReA.[8] Patients with HLA-B27, as well as those with a strong family clustering of the disease, tend to develop more severe and long-term disease.[3]

The mechanism by which the interaction of the inciting organism with the host (often HLA-B27–positive) leads to the development of ReA is not known. It is unclear if microbial antigens cross-react with self-proteins, stimulating and perpetuating an autoimmune response mediated by type 2 T helper (Th2) cells. Chronicity and joint damage have been associated with a Th2 cytokine profile that leads to decreased bacterial clearance.[6]

Synovial fluid cultures are negative for enteric organisms or Chlamydia species. However, a systemic and intrasynovial immune response to the organisms has been found with intra-articular antibody and bacterial reactive T cells. Furthermore, bacterial antigen has been found in the joints. Thus, the elements for an immune-mediated synovitis are present.

Synovitis in ReA is mediated by proinflammatory cytokines. Native T cells under the influence of transforming growth factor (TGF)-β and other cytokines, such as interleukin (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.[9, 10] Deficiencies in regulatory mechanisms can result in increased proinflammatory cytokine production and worse outcome.[11]

The Toll-like receptors (TLRs) recognize different extracellular antigens as part of the innate immune system.[12] TLR-4 recognizes gram-negative lipopolysaccharide (LPS). Studies in mice and humans showed abnormalities in antigen presentation due to downregulation of TLR-4 costimulatory receptors in patients with ReA. Subsequent studies implicated TLR-2 polymorphism associated with acute ReA; however, its role is still disputed.[6, 13]

Molecular evidence of bacterial DNA (obtained via polymerase chain reaction [PCR] assay) in synovial fluids has been found only in Chlamydia -related ReA, and a single placebo-controlled trial of a tetracycline derivative (ie, lymecycline) has shown a reduction in the duration of acute Chlamydia -related, but not enteric-related, ReA.[14] This suggests that persistent infection may play a role, at least in some cases of chlamydial-associated ReA.

In a subsequent trial, the combination of doxycycline and rifampin was superior to doxycycline alone in reducing morning stiffness and swollen and tender joints in patients with undifferentiated spondyloarthropathy.[15]

The role of HLA-B27 in this scenario remains to be fully defined. The following theories have been proposed:

  • Molecular mimicry - This hypothesis suggests that a similarity exists at the molecular level between the HLA-B27 molecule and the inciting organisms, allowing the triggering of an immune response and the subsequent development of clinical disease [16]
  • HLA-B27 as a receptor for certain bacteria - At present, there is little evidence either to confirm or to refute this hypothesis
  • Defective class I antigen-mediated cellular response - This hypothesis suggests that the HLA-B27 molecule may be a defective molecule associated with an aberrant cytotoxic T-cell response

ReA can occur in patients with HIV infection or AIDS—most likely because both conditions can be sexually acquired, rather than because ReA is triggered by HIV. The course of ReA in these patients tends to be severe, with a generalized rash resembling psoriasis, profound arthritis, and frank AIDS. HLA-B27 frequency is the same as that associated with non–AIDS-related ReA in a similar demographic group. This association points out the likely importance of CD8+ cytotoxic T cells as compared with CD4+ Th cells in the pathogenesis of ReA.

ReA is sometimes divided into epidemic and endemic forms. Whereas a triggering agent can be identified for epidemic ReA, none has been identified for endemic ReA. Differentiation between the 2 types of ReA may be difficult in some cases; however, it is not essential to either diagnosis or treatment.

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Etiology

Infectious causes

ReA is usually triggered by a GU or GI infection and thus is sometimes classified as venereal or dysenteric. Such infections are mostly the result of gram-negative, obligate, or facultative intracellular pathogens.[17] Organisms that have been associated with ReA include the following:

  • C trachomatis (L2b serotype) [18]
  • Ureaplasma urealyticum
  • Neisseria gonorrhoeae
  • Shigella flexneri
  • Salmonella enterica serovars Typhimurium, Enteritidis, [19] and Hadar [20]
  • Mycoplasma pneumoniae
  • Mycobacterium tuberculosis [21]
  • Cyclospora [22]
  • Yersinia enterocolitica and pseudotuberculosis
  • Campylobacter jejuni [23] and coli
  • Clostridium difficile
  • Beta-hemolytic [11] (eg, group A [24] ) and viridans streptococci

Data suggest that chlamydial ReA is underdiagnosed and that asymptomatic chlamydial infections might be a common cause.[25] An important difference between Chlamydia -induced (postvenereal) ReA and postenteric ReA is the presence of viable but aberrant chlamydial organisms in the synovial fluid[26] (so-called Chlamydia persistence[27] ). PCR assay to detect C trachomatis DNA in synovial samples may be a good method for establishing the diagnosis of Chlamydia -induced arthritis in patients with ReA.[28]

The prevalence of different serotypes of C trachomatis antibodies and the incidence of Chlamydia- induced ReA was studied among patients with early arthritis in a defined population in Finland.[8] Antibodies against C trachomatis were most common in patients with arthritis because cases with Chlamydia -induced ReA are included in this subgroup.

Ureaplasma organisms are known to be capable of causing experimental and clinical nongonococcal urethritis. Synovial mononuclear cells from arthritic joints of patients with ReA react with Ureaplasma antigens; this organism has been isolated from an ReA patient.

The enteric pathogen that most commonly results in ReA is Campylobacter (C jejuni, 90-95%; C coli, 5-10%).[29] ReA patients with arthritic symptoms are more frequently infected with C jejuni strains with sialic acid lipo-oligosaccharide. In addition, sialylation of C jejuni lipo-oligosaccharide is associated with more severe enteric disease.[30]

Group A streptococci are known to be capable of causing poststreptococcal ReA.[31] Patients with this condition demonstrate increase antistreptolysin O (ASO) antibodies and an increased erythrocyte sedimentation rate (ESR).[32] ReA can also be induced by tonsillitis. In one study, 13 of 21 patients were positive for ASO and 12 were positive for group A Streptococcus.[33]

Acute tuberculosis can sometimes cause ReA. The resulting condition is known as Poncet disease, which is a different entity from tuberculous arthritis.[34, 35, 36]

Other possible linkages include infection with C difficile[37, 38] and with bacillus Calmette-Guérin (BCG).[39, 40] Intravesical instillation of BCG for bladder cancer has been associated with reactive arthritis.[41, 42, 43] ReA has also been shown to occur after tetanus and rabies vaccination.[44, 45]

Genetic factors

ReA has an important genetic component; it tends to cluster in certain families and almost exclusively affects males, and HLA-B27 is identified in 70-80% of patients.[8] HLA-B27 may share molecular characteristics with bacterial epitopes, facilitating an autoimmune cross-reaction instrumental in pathogenesis. HLA-B27 contributes to the pathogenesis of the disease and reportedly increases the risk of ReA 50-fold.[46] HLA-B51 and HLA-DRB1 alleles have also been shown to be associated with ReA.[28]

Rihl et al found a high proportion of proangiogenic factors accounting for a genetically determined susceptibility to ReA.[47]

Other factors

ReA triggered by adalimumab and leflunomide in a patient with ankylosing spondyloarthropathy and Crohn disease has been described.[48]

Duration of diarrhea and weight loss are also considered risk factors in the development of ReA after enteric infections.[7]

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Epidemiology

United States statistics

Data on the incidence and prevalence of ReA are scarce, partly because of a lack of a disease definition and classification criteria; these factors complicate differentiation of ReA from other arthritides.[49] The frequency is estimated to be 3.5-5 cases per 100,000. The incidence reported in US Navy personnel over a 10-year period was 4 cases per 100,000 men per year. The prevalence of ReA may be relatively high among patients with AIDS, especially men who are seropositive for HLA-B27. ReA develops in almost 75% of HIV-positive men with HLA-B27.

An estimated 1-3% of all patients with a nonspecific urethritis develop an episode of arthritis. The incidence is 1-4% after enteric infection. This number jumps to 20-25% after bacterial enteritis in HLA-B27-positive individuals.[29] Prevalence of asymptomatic chlamydial infections, underdiagnosis, and underreporting may make the incidence even higher.[50] It has been noted that worse functional capacity and higher disease activity are observed in the lower socioeconomic classes.[51]

A population-based study assessed ReA after culture-confirmed infections with bacterial enteric pathogens in Minnesota and Oregon.[52] The estimated incidence after culture-confirmed Campylobacter, Escherichia coli O157, Salmonella, Shigella, and Yersinia infections in Oregon was 0.6-3.1 cases per 100,000 population. ReA may occur in 1.5% of Shigella enterocolitis cases and 25% of HLA-B27–positive Shigella cases. After an outbreak of S enterica serovar Enteritidis, 29% had reactive arthritis.[19]

International statistics

The infections that incite ReA may vary with geographic location. For example, Y enterocolitica is more commonly identified in Europe than in North America and thus is responsible for more cases of ReA in countries such as Finland and Norway.[6] The occurrence of ReA appears to be related to the prevalence of HLA-B27 in a population and to 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.[17] These subtypes may be somewhat geographically segregated. For example, the subtype B2705 is found predominantly in Latin America, Brazil, Taiwan, and parts of India. It is noteworthy that subtypes HLA-B2706 and B2709—found in native Indonesia and Sardinia, respectively—may be partially protective against ReA.[53]

In Norway, an annual incidence of 4.6 cases per 100,000 population for chlamydial ReA and an incidence of 5 cases per 100,000 population for enteric bacteria–induced ReA were reported in 1988-1990. In Finland, nearly 2% of males were found to have ReA after nongonococcal urethritis; the incidence of HLA-B27 is higher in the Finnish population. In the United Kingdom, the incidence of ReA after urethritis is about 0.8%. In the Czech Republic, the annual incidence of ReA in adults during 2002-2003 was reported at 9.3 cases per 100,000 population.[54]

Age-, sex-, and race-related demographics

ReA is most common in young men, with the peak onset in the third decade of life. It rarely occurs in children; when it does, the enteric form of the disease is predominant. Most pediatric patients present with symptoms after the age of 9 years.[41]

In a study of 100 patients with ReA, Lahu and colleagues found that most patients were between 20 and 40 years old and that the first attack occurred earlier in males than females. Of the 100 patients studied, 66% were male.  Urogenital and nasopharyngeal infections were more common among male patients.[55]

ReA after foodborne enteric infections is equally common in males and females. However, the male-to-female ratio for disease associated with venereally acquired infections has been estimated to range from 5:1 to 10:1. A possible prostatic focus of persistent infection is postulated to explain the male predominance of ReA.

The frequency of ReA appears to be related to the prevalence of HLA-B27 in the population. As with other spondyloarthropathies, HLA-B27 and ReA are more common in white people than in black people. When ReA occurs in black persons, it is frequently B27-negative.

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Prognosis

ReA has a variable natural history[50] but typically follows a self-limited course, with resolution of symptoms by 3-12 months, even in patients who are acutely incapacitated. A fatal outcome is seldom reported, but death can occur, and it is usually related to the adverse effects of treatment. Postdysenteric cases are associated with a better prognosis than postvenereal cases. The presence of HLA-B27 may predict a more prolonged course and severe outcome, as may infections triggered by Yersinia, Salmonella, Shigella, or Chlamydia.[56]

ReA has a high tendency to recur (15-50% of cases), particularly in individuals who are HLA-B27–positive. A new infection or other stress factor could cause reactivation of the disease.

Approximately 15-30% of patients with ReA develop a long-term, sometimes destructive, arthritis or enthesitis or spondylitis. A 1994 study analyzed 7 factors as predictors of long-term outcome in spondyloarthropathies.[57] The number of patients with ReA in this study was low, and a valid subgroup analysis was impossible. The presence of hip-joint involvement, an ESR higher than 30, and unresponsiveness to nonsteroidal anti-inflammatory drugs (NSAIDs) probably portend a severe outcome or chronicity in ReA.

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Patient Education

Poor health-related quality of life and impaired daily physical functioning are observed in patients with refractory or chronic ReA, and strategies focused on improving or maintaining functional status are important in treatment.[13] Educational measures that may be helpful include the following:

  • Encourage patients to monitor themselves for any changes in symptoms.
  • Help patients to become awareness of the chronic or recurrent nature of this syndrome and to accept the need for long-term medications
  • Inform patients that their condition places them at a higher than usual risk for elective ocular surgery
  • Discourage inactivity and immobilization
  • Encourage stretching exercises and range of motion
  • Provide adolescent patients with information on the prevention of sexually transmitted diseases and the use of condoms

For patient education resources, see the Arthritis Center, the Sexually Transmitted Diseases Center, and the Bacterial and Viral Infections Center, as well as Knee Pain, Chlamydia, and Gonorrhea. The American College of Rheumatology also provides patient information on reactive arthritis.

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Contributor Information and Disclosures
Author

Carlos J Lozada, MD Director of Rheumatology Fellowship Training Program, Professor of Clinical Medicine, 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, American College of Rheumatology

Disclosure: Received honoraria from Pfizer for consulting; Received grant/research funds from AbbVie for other; Received honoraria from Heel for consulting.

Coauthor(s)

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.

Maria F Carpintero, MD Assistant Professor of Clinical Medicine, Division Rheumatology/Immunology, University of Miami, Leonard M Miller School of Medicine

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

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate Medical Center; 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, Phi Beta Kappa

Disclosure: Nothing to disclose.

Acknowledgements

Mounir Bashour, MD, CM, FRCS(C), PhD, FACS Assistant Professor of Ophthalmology, McGill University; Clinical Assistant Professor of Ophthalmology, Sherbrooke University; Medical Director, Cornea Laser and Lasik MD

Mounir Bashour, MD, CM, FRCS(C), PhD, FACS is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American College of International Physicians, American College of Surgeons, American Medical Association, American Society of Cataract and Refractive Surgery, American Society of Mechanical Engineers, American Society of Ophthalmic Plastic and Reconstructive Surgery, Biomedical Engineering Society, Canadian Medical Association,Canadian Ophthalmological Society, Contact Lens Association of Ophthalmologists, International College of Surgeons US Section, Ontario Medical Association, Quebec Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Igor Boyarsky, DO Emergency Room Physician, Kaiser Permanente Southern California

Igor Boyarsky, DO is a member of the following medical societies: American Academy of Anti-Aging Medicine, American Academy of Emergency Medicine, American College of Emergency Physicians, and American Osteopathic Association

Disclosure: Nothing to disclose.

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.

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.

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.

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Lawrence K Jung, MD Chief, Division of Pediatric Rheumatology, Children's National Medical Center

Lawrence K Jung, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Rheumatology, Clinical Immunology Society, and New York Academy of Sciences

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society

Disclosure: Nothing to disclose.

Barry L Myones, MD Associate Professor, Departments of Pediatrics and Immunology, Pediatric Rheumatology Section, Baylor College of Medicine; Director of Research, Pediatric Rheumatology Center, Texas Children's Hospital

Barry L Myones, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American College of Rheumatology, American Heart Association, American Society for Microbiology, Clinical Immunology Society, and Texas Medical Association

Disclosure: Nothing to disclose.

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.

Lluís Puig, MD, PhD Program Director, Assistant Professor, Department of Dermatology, Hospital De La Santa Creu I Sant Pau, Universitat Autónoma De Barcelona

Lluís Puig, MD, PhD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, European Academy of Dermatology and Venereology, and International Society of Dermatopathology

Disclosure: Nothing to disclose.

Jorge Romaní, MD Assistant Professor, Department of Dermatology, Hospital De Palamós Faculty of Medicine, Spain

Disclosure: Nothing to disclose.

Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

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.

Thomas Scoggins, MD Consulting Staff, Department of Emergency Medicine, Blount Memorial Hospital

Thomas Scoggins, MD is a member of the following medical societies: American College of Emergency Physicians and Flying Physicians Association

Disclosure: Nothing to disclose.

John D Sheppard Jr, MD, MMSc Professor of Ophthalmology, Microbiology and Molecular Biology, Clinical Director, Thomas R Lee Center for Ocular Pharmacology, Ophthalmology Residency Research Program Director, Eastern Virginia Medical School; President, Virginia Eye Consultants

John D Sheppard Jr, MD, MMSc is a member of the following medical societies: American Academy of Ophthalmology, American Society for Microbiology, American Society of Cataract and Refractive Surgery, American Uveitis Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

David D Sherry, MD Director, Clinical Rheumatology, Attending Physician, Pain Management, The Children's Hospital of Philadelphia; Professor of Pediatrics, University of Pennsylvania School of Medicine

David D Sherry, MD is a member of the following medical societies: American College of Rheumatology and American Pain Society

Disclosure: Nothing to disclose.

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

Akaluck Thatayatikom, MD Associate Professor and Chief, Department of Pediatrics, Division of Pediatric Allergy, Immunology, and Rheumatology, University of Kentucky College of Medicine

Akaluck Thatayatikom, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Rheumatology, Childhood Arthritis and Rheumatology Research Alliance, and Clinical Immunology Society

Disclosure: Nothing to disclose.

Robin Travers, MD Assistant Professor of Medicine (Dermatology), Dartmouth University School of Medicine; Staff Dermatologist, New England Baptist Hospital; Private Practice, SkinCare Physicians

Robin Travers, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Informatics Association, Massachusetts Medical Society, Medical Dermatology Society, and Women's Dermatologic Society

Disclosure: Nothing to disclose.

R Christopher Walton, MD Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, University of Tennessee College of Medicine

R Christopher Walton, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Healthcare Executives, American Uveitis Society, Association for Research in Vision and Ophthalmology, and Retina Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

References
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Balanitis circinata (circinate balanitis) in patient with reactive arthritis.
Plaques on soles of patient with reactive arthritis.
Painful erosions on fingers in patient with reactive arthritis.
Plaques and erosions of tongue in patient with reactive arthritis.
Radiograph of feet of 27-year-old man shows erosions in all left metatarsophalangeal (MTP) joints with subluxation and valgus deformity of most toes. Smaller erosions are also visible in fourth and fifth MTP joints of right foot.
Lateral radiograph of foot reveals 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 pelvis reveals bilateral asymmetric sacroiliitis.
Radiograph in 40-year-old man shows nonmarginal syndesmophytes predominantly in lower thoracic and upper lumbar spine.
Swelling of right knee with effusion caused by arthritis. Image courtesy of Gun Phongsamart, MD.
Remarkable tenderness of left sacroiliac joint caused by sacroiliitis. Image courtesy of Gun Phongsamart, MD.
Balanitis circinata (circinate balanitis). Image courtesy of Gun Phongsamart, MD.
Achilles tendinitis and swelling of retrocalcaneal bursa.
 
 
 
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