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Reactive Arthritis
Carlos J Lozada, MD, Director of Rheumatology Fellowship Program, Associate Professor, Department of
Medicine, Division of Rheumatology and Immunology, Jackson Memorial Medical Center, University of Miami
School of Medicine
Maria F Carpintero, MD, Fellow, Department of Rheumatology, University of Miami, Jackson Memorial
Medical Center, Miami Veterans Affairs Medical Center
Updated: Jan 5, 2010

Introduction

Background
Reactive arthritis (ReA), also known as Reiter syndrome, is an autoimmune condition that develops in response
to an infection. In 1916, Hans Reiter described the triad of nongonococcal urethritis, conjunctivitis, and arthritis
in a young German officer with bloody dysentery.[1 ]In 1916, Fiessinger and Leroy described 4 patients with what
they called oculo-urethro-synovial syndrome and associated the syndrome with an outbreak of Shigella
dysentery.

Since then, many cases of what is now known as reactive arthritis have been described. The older term
Reiter's syndrome, used in the past to describe the same clinical presentations, is being used less frequently.
This is because Reiter was a physician leader of the Nazi party in Germany during World War II and authorized
medical experiments on prisoners in concentration camps.[2 ]

Reactive arthritis has been associated with gastrointestinal infections with Shigella , Salmonella , and
Campylobacter species and other microorganisms, as well as with genitourinary infections (especially with
Chlamydia trachomatis).

Outbreaks of enteric Reiter syndrome have been reported aboard military vessels, cruise ships, and vessels
transporting immigrants to the United States. In 1967, the term reactive arthritis was first used in cases
associated with Yersinia gastroenteritis. A strong association with human leukocyte antigen (HLA)–B27 was
found. This finding helped to confirm the concept of an incomplete Reiter syndrome, in which arthritis can occur
in the absence of urethritis and conjunctivitis. Because of the association with HLA-B27 and its clinical overlap
with ankylosing spondylitis and psoriatic arthritis, reactive arthritis is classified as a type of seronegative
spondyloarthropathy.

In this article, reactive arthritis encompasses the older concepts of complete and incomplete Reiter syndrome
and a clinical syndrome of arthritis with or without extra-articular features that develop within one month of
infectious diarrhea or genitourinary infection.

Pathophysiology
Reactive arthritis usually develops 2-6 weeks after a genitourinary or gastrointestinal infection. Recent
evidence indicates that a preceding Chlamydia respiratory infection may also trigger reactive arthritis.[3 ]About
10% of patients do not have a preceding symptomatic infection.

Inflammation of joints, entheses, axial skeleton, skin, mucous membranes, gastrointestinal tract, and eyes may
occur. Results for HLA-B27 are positive in 65%-96% of patients (average, 75%) with reactive arthritis. The
likelihood of developing reactive arthritis is increased 50-fold in patients who are HLA-B27–positive, but this
syndrome can also occur in patients who are HLA-B27 negative.

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. The frequency of reactive arthritis after enteric infection averages 1%-4% but
varies greatly, even among outbreaks of the same organism.

The mechanism of the interaction of the inciting organism with the host (often HLA-B27–positive) leading to the
development of reactive arthritis is not known. It is unclear if microbial antigens cross-react with self-proteins,
stimulating (molecular mimicry) and perpetuating a Th2-cell–mediated autoimmune response. Chronicity and
joint damage have been associated with a Th2 cytokine profile that leads to decreased bacterial clearance.[4 ]

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.

Molecular evidence of bacterial DNA (by polymerase chain reaction [PCR]) in synovial fluids has been found
only in Chlamydia -related reactive arthritis, and one placebo-controlled trial of a tetracycline derivative (ie,
lymecycline) showed a reduction in the duration of acute Chlamydia -related, but not enteric-related, reactive
arthritis.[5 ]This suggests that persistent infection may play a role, at least in some cases of chlamydial reactive
arthritis. In a more recent 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.[6 ]

The Toll-like receptors (TLRs) recognize different extracellular antigens as part of the innate immune system.
TLR-4 recognizes gram-negative lipopolysaccharide (LPS). Studies in mice and humans showed abnormalities
in antigen presentation due to down-regulation of TLR-4 costimulatory receptors in patients with reactive
arthritis. More recent studies implicated TLR-2 polymorphism associated with acute reactive arthritis; however,
its role is still disputed.[4,7 ]

The role of HLA-B27 in this scenario remains to be defined but, as discussed elsewhere (Ankylosing
Spondylitis and Undifferentiated Spondyloarthropathies), molecular mimicry, presentation of pathogenic
peptides, and an altered host response to the bacteria are all possible.

Reactive arthritis, including classic Reiter syndrome, can occur in patients infected with HIV or who have AIDS.
This is likely because both conditions can be sexually acquired rather than being triggered by HIV. The course
of reactive arthritis in these patients tends to be severe, with a generalized rash that resembles psoriasis,
profound arthritis, and frank AIDS. The frequency of HLA-B27 is the same of that associated with non–AIDS-
related reactive arthritis in a similar demographic group. This association points out the likely importance of
CD8+ cytotoxic T cells compared to CD4+ helper T cells in the pathogenesis of reactive arthritis.

Frequency
International

Data on the incidence and prevalence of reactive arthritis are scarce, partly because of a lack of a disease
definition and diagnosis criteria; these factors complicate differentiation of reactive arthritis from other
arthritides.[8 ]The reported annual incidence of reactive arthritis is approximately 30-40 cases per 100,000
adults, with a prevalence of 1%-7%, but this varies greatly among different geographic locations.[9 ]Reports from
Latin America, North Africa, India, and Thailand showed low prevalence, with minimal differences between
countries.[10,11 ]

Mortality/Morbidity
Reactive arthritis typically follows a self-limited course, with resolution of symptoms by 3-12 months, even in
patients who are acutely incapacitated. However, reactive arthritis has a high tendency to recur, particularly
with ocular and urogenital inflammation. Individuals who are HLA-B27–positive are at a higher risk of
recurrence. A new infection or other stress factor could cause reactivation of the disease.

About 15% of patients with reactive arthritis develop a long-term, sometimes destructive, arthritis or enthesitis
or spondylitis. In a study by Amor et al (1994), 7 factors were analyzed as predictors of long-term outcome in
spondyloarthropathies.[12 ]The number of patients with reactive arthritis in this study was low, and a valid
subgroup analysis was impossible. The presence of hip-joint involvement, an erythrocyte sedimentation rate
(ESR) higher than 30, and unresponsiveness to nonsteroidal anti-inflammatory drugs (NSAIDs) probably
portend a severe outcome or chronicity in reactive arthritis.

Race
As with other spondyloarthropathies, HLA-B27 and reactive arthritis are more common in white people than in
black people.

Sex
Reactive arthritis following foodborne enteric infections is equally common in males and females. The male-to-
female ratio of disease associated with venereally acquired infections is 9:1.

Age
Most patients with reactive arthritis are aged 20-40 years.

Clinical

History
Reactive arthritis 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 reactive arthritis 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 reactive arthritis 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.

Physical

 Joints, axial skeleton, entheses

o Peripheral joint involvement associated with reactive arthritis is typically asymmetric and
usually affects the weight-bearing joints (ie, knees, ankles, hips), but the shoulders, wrists,
and elbows may also be affected.
o 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.
o While 50% of patients with reactive arthritis 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.
o As with other spondyloarthropathies, the enthesopathy of reactive arthritis 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
o Keratoderma blennorrhagica on the palms and soles is indistinguishable from pustular
psoriasis and is highly suggestive of chronic reactive arthritis.
o Erythema nodosum may develop but is uncommon.
o Nails can become thickened and crumble, resembling mycotic infection or psoriatic
onychodystrophy, but nail pitting is not observed.
o 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
o Conjunctivitis is part of the classic triad of Reiter syndrome and can occur before or at the
onset of arthritis.
 o Other ocular lesions include acute uveitis (20% of patients), episcleritis, keratitis, and corneal
ulcerations. The lesions tend to recur.
 Enteric infections
o Enteric infections may trigger reactive arthritis. Pathogens include Salmonella, Shigella,
Yersinia, and Campylobacter species. The frequency of reactive arthritis after these enteric
infections is about 1%-4%. Other enteric bacteria that have been associated with reactive
arthritis include Clostridium difficile,[13 ] Escherichia coli, and Helicobacter pylori.[14 ]
o Some patients with reactive arthritis 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 reactive arthritis.[13 ]
 Other manifestations
o Other manifestations of reactive arthritis include mild renal pathology with proteinuria and
microhematuria.
o 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 reactive arthritis cases.

Causes
Reactive arthritis 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 ]

Differential Diagnoses
Ankylosing Spondylitis and Undifferentiated Spondyloarthropathy Psoriatic Arthritis
Gonococcal Arthritis Rheumatic Fever
Gout Rheumatoid Arthritis
Inflammatory Bowel Disease Septic Arthritis
Workup

Laboratory Studies

 The values of acute-phase reactants, including erythrocyte sedimentation rate (ESR) and C-reactive
protein (CRP), are usually elevated markedly but later return to the reference range when the
inflammation subsides.
 Other laboratory findings include a normocytic normochromic anemia along with mild leukocytosis and
thrombocytosis during the acute phase. IgA antibodies to specific bacterial antigens have been
reported. Urinalysis may reveal aseptic pyuria.
  Synovial fluid analysis reveals a high WBC count, most often with elevated polymorphonuclear
leukocytes acutely. Gram stain and culture results are negative and are necessary to exclude septic
arthritis. Microbial components and antigens have been identified in joint fluid using sophisticated
laboratory techniques.
 Throat, stool, or urogenital tract cultures can be performed in an attempt to isolate the causative
organism. Other serologic techniques for the detection of Chlamydia species, including PCR, may be
considered.
 Test results for rheumatoid factor and antinuclear antibodies are negative.

Imaging Studies

 Radiography
o Early in the disease process, radiography reveals no abnormalities.
o In more advanced or long-term reactive arthritis, periosteal reaction and proliferation at sites
of tendon insertion are visible.
o Exuberant plantar spurs are a common sign in long-term reactive arthritis.
o In the hands and feet, marginal erosions with adjacent bone proliferation occur.
o Spinal radiographic findings include sacroiliitis and syndesmophytes. Sacroiliitis occurs in less
than 10% of acute cases but develops in half of patients with chronic severe disease.
o Syndesmophytes are usually asymmetrical and are found most commonly in the
thoracolumbar region.
o Severe ankylosing spondylitis occurs in less than 5% of cases.
 MRI: MRI of the sacroiliac joints may reveal disease earlier than conventional radiography.

Other Tests

 ECG should be performed in patients with a prolonged course of reactive arthritis to evaluate for
conduction disturbances.
 HLA-B27 testing results are positive in 65%-96% of cases. HLA-B27 testing is not necessary in classic
Reiter syndrome but may be helpful to support the diagnosis of reactive arthritis in patients with joint-
restricted symptoms.

Procedures

 Needle aspiration of a joint may be necessary to rule out septic or crystal-induced arthritis.

Treatment

Medical Care
The treatment of reactive arthritis is depends on the severity of symptoms.

 Nonsteroidal anti-inflammatory drugs

 o NSAIDs are the foundation of therapy. These agents should be used regularly to achieve a
good anti-inflammatory effect.
o The choice of a specific agent depends on the individual response to treatment, although the
general impression is that indomethacin has greater potency.
o Physical therapy needs to be implemented to help reduce pain and to avoid muscle wasting in
severe cases of reactive arthritis.
 Corticosteroids
o These agents can be used as either intra-articular injection or systemic therapy.
o Joint injections can produce long-lasting symptomatic improvement and help avoid the use of
other systemic therapy. Sacroiliac joints can be injected, usually under fluoroscopic guidance.
[21 ]

o Systemic corticosteroids can be used, particularly in patients in whom NSAIDs elicit a poor
response or in those who develop adverse effects related to their use. The starting dose is
guided by a patient's symptoms and objective evidence of inflammation. Prednisone 0.5-1
mg/kg/d can be used initially and tapered according to response.
 Antibiotics
o The current concepts on the pathogenesis of reactive arthritis indicate that an infectious agent
is the trigger of the disease, but antibiotic treatment does not change the course of the
disease, even when a microorganism is isolated. In these cases, antibiotics are used to treat
the underlying infection, but specific treatment guidelines for reactive arthritis are lacking.
However, in chlamydia-induced reactive arthritis, studies have suggested that the appropriate
treatment of the acute urogenital infection can prevent reactive arthritis and that treatment of
acute reactive arthritis with a 3-month course of tetracycline reduces the duration of illness.
No evidence indicates that antibiotic therapy benefits enteric-related reactive arthritis or
chronic reactive arthritis of any cause.
o Lymecycline was studied in a double-blind placebo-controlled study of patients with chronic
reactive arthritis for a treatment period of 3 months.4 The duration of illness was significantly
decreased in patients with chlamydia-induced disease, as opposed to those with disease
triggered by enteric infections.
o Azithromycin was shown to be ineffective in a placebo-controlled trial.[22 ]Nevertheless, in a
recent abstract presentation, azithromycin or doxycycline in combination with rifampin for 6
months was reported to be significantly superior to placebo and significantly improved
symptoms associated with chlamydia–induced reactive arthritis.[23 ]
o Quinolones have been studied because of their broad coverage, but no clear benefit has been
reported.[24 ]
o More studies are needed before definite recommendations can be made for the role of
antibiotics in the management of reactive arthritis.
 Disease-modifying antirheumatic drugs
o In patients with chronic symptoms or in patients with persistent inflammation despite the use
of the agents mentioned above, other second-line drugs may be used. Clinical experience
with these so-called disease-modifying antirheumatic drugs (DMARDs) has been mostly in
 rheumatoid arthritis and in psoriatic arthritis. DMARDs have also been used in reactive
arthritis, although their disease-modifying effects in the reactive arthritis setting are uncertain.
o Sulfasalazine may be beneficial in some patients. The use of this drug in reactive arthritis is of
interest because of the finding of clinical or subclinical inflammation of the bowel in many
patients. Sulfasalazine is more widely used in ankylosing spondylitis. In a 36-week trial of
sulfasalazine versus a placebo in the spondyloarthropathies, patients with reactive arthritis
who were taking sulfasalazine had a 62.3% response rate compared to 47.7% for the placebo
group in peripheral arthritis (P = 0.09).[25 ]
o Methotrexate can be used in patients who present with rheumatoidlike disease. Several
reports have shown good response, but controlled studies are lacking. Reports also describe
the use of azathioprine and bromocriptine in reactive arthritis, but, again, large studies have
not been published.[26,27 ]Patients with reactive arthritis and HIV/AIDS should not receive
methotrexate or other immunosuppressive agents.
o Although biologic agents such as TNF-blockers have been demonstrated to be beneficial and
formally approved for the treatment of psoriatic arthritis and ankylosing spondylitis, double-
blind, randomized trials have not been performed to prove clinical benefit in reactive arthritis
or in undifferentiated spondyloarthropathy. Case reports using the chimeric monoclonal
antibody infliximab have shown potential efficacy in symptom relief in patients in whom other
therapies failed.[28,29,30 ]

Surgical Care
No surgical treatment of reactive arthritis is recommended.

Consultations
A rheumatologist should be consulted for confirmation of diagnosis and formulation of management plan.
Consultation with a urologist may be necessary if particularly prominent genitourinary manifestations develop.
An ophthalmologist may be consulted to confirm the diagnosis and to treat the ophthalmologic manifestations
of reactive arthritis.

Activity
Physical therapy may be instituted to avoid muscle wasting and to reduce pain. Activities should otherwise be
as tolerated by the patient.

Medication

The goals of pharmacotherapy are to reduce morbidity, to prevent joint damage, and to alleviate extra-articular
disease.

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Several NSAIDs are available and have similar effectiveness, although indomethacin may be more effective in
the spondyloarthropathies. These agents are used to treat symptoms. Cyclooxygenase-2 (COX-2)–specific
inhibitors can be used in patients at high risk for GI complications.

Ibuprofen (Motrin, Advil)

Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Dosing

Adult

400-600 mg PO qid or 800 mg PO tid

Pediatric

Not established

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may
increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients
to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased
when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high
risk of bleeding

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in CHF, hypertension, and in PT with decreased renal and hepatic function; caution in anticoagulation
abnormalities or during anticoagulant therapy
Indomethacin (Indocin, Indochron E-R)

Rapidly absorbed. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation.
Inhibits prostaglandin synthesis.

Dosing

Adult

25-50 mg PO bid/tid
75 mg SR PO bid; not to exceed 200 mg/d

Pediatric

1-2 mg/kg/d PO divided bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may
increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking
anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity;
phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; GI bleeding; renal insufficiency

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may
occur; increases risk of acute renal failure in patients with pre-existing renal disease or compromised renal
perfusion; reversible leukopenia may occur (discontinue if persistent leukopenia, granulocytopenia, or
thrombocytopenia occurs)

Tetracyclines
These agents are used to treat urethritis or cervicitis caused by chlamydial organisms. Some evidence shows
that, in chlamydia-induced Reiter syndrome, tetracycline treatment may reduce duration and perhaps severity
of illness. Collagenase inhibitors have been used to treat early rheumatoid arthritis.
Doxycycline (Bio-Tab, Vibramycin)

Inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of
susceptible bacteria.

Dosing

Adult

Urethritis or cervicitis: 100 mg PO bid 7d

Decrease severity: 100 mg PO bid for 8-12 wk

Pediatric

Not established

Interactions

Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth
subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can
decrease effects of PO contraceptives, causing breakthrough bleeding and increased risk of pregnancy

Contraindications

Documented hypersensitivity; severe hepatic dysfunction

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal
impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth
development (ie, <8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with
outdated tetracycline

Corticosteroids
These agents have anti-inflammatory properties and cause profound and varied metabolic effects.
Corticosteroids modify the body's immune response to diverse stimuli.
Prednisone (Sterapred)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Dosing

Adult

0.5 mg/kg/d PO initially, taper according to response

Pediatric

Not established

Interactions

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause
digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of
glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of
diuretics

Contraindications

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue
infections; fungal or tubercular skin infections; GI disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia; edema; osteonecrosis;
myopathy; peptic ulcer disease; hypokalemia; osteoporosis; euphoria; psychosis; myasthenia gravis; growth
suppression; infections may occur with glucocorticoid use

Aminosalicylic acid derivatives

These agents are used to reduce inflammation.

Sulfasalazine (Azulfidine, EN-tabs)

Acts locally in colon to decrease the inflammatory response and systemically inhibits prostaglandin synthesis.

Dosing
Adult

500 mg PO bid initially; 1000 mg PO bid

Pediatric

Not established

Interactions

Decreases effects of iron, digoxin, and folic acid; conversely, increases effect of PO anticoagulants, PO
hypoglycemic agents, and methotrexate

Contraindications

Documented hypersensitivity; hypersensitivity to sulfa drugs or any component; GI or GU obstruction

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients with renal or hepatic impairment, blood dyscrasias, or urinary obstruction

Follow-up

Further Inpatient Care

Hospitalization of a patient with uncomplicated reactive arthritis is not indicated.

Deterrence/Prevention
Even when a causal microorganism is isolated, antibiotic therapy does not change the course of the disease.

Patient Education
For excellent patient education resources, visit eMedicine's Arthritis Center. Also, see eMedicine's patient
education article Psoriatic Arthritis.

Miscellaneous

Medicolegal Pitfalls

 Septic arthritis must be ruled out if suspected before a diagnosis of reactive arthritis is made. Failure to
appropriately treat septic arthritis in a timely manner could result in joint destruction. Medicolegal
liability could result from this oversight.
  HIV/AIDS should be considered before instituting immunosuppressive therapy in severe cases of
reactive arthritis.

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Keywords

reactive arthritis, Reiter syndrome, Reiter's syndrome, RS, ReA, nongonococcal urethritis, conjunctivitis, oculo-
urethro-synovial syndrome, Chlamydia reactive arthritis, chlamydial reactive arthritis , Shigella dysentery,
gastrointestinal infections, Salmonella, Campylobacter, Chlamydia trachomatis, C trachomatis, Yersinia,
ankylosing spondylitis, psoriatic arthritis, seronegative spondyloarthropathy, infectious diarrhea, genitourinary
infection

Contributor Information and Disclosures

Author

Carlos J Lozada, MD, Director of Rheumatology Fellowship Program, Associate Professor, Department of

Medicine, Division of Rheumatology and Immunology, Jackson Memorial Medical Center, University of Miami
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: Nothing to disclose.
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
Disclosure: Nothing to disclose.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Managing Editor

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.

CME Editor

Alex J Mechaber, MD, FACP, 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, Professor of Medicine, Temple University 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: medifocus Honoraria Review panel membership; health dialogs Honoraria Consulting; West Penn
Allegheny Health System None Board membership

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