This action might not be possible to undo. Are you sure you want to continue?
eMedicine Specialties > Rheumatology > Spondyloarthropathies
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
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.
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 immunemediated 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
reactive arthritis has a high tendency to recur. with minimal differences between countries.000 adults. partly because of a lack of a disease definition and diagnosis criteria. Clinical . HLA-B27 and reactive arthritis are more common in white people than in black people. The presence of hip-joint involvement.[8 ]The reported annual incidence of reactive arthritis is approximately 30-40 cases per 100. but this varies greatly among different geographic locations.11 ] Mortality/Morbidity Reactive arthritis typically follows a self-limited course. with a prevalence of 1%-7%. even in patients who are acutely incapacitated. and unresponsiveness to nonsteroidal anti-inflammatory drugs (NSAIDs) probably portend a severe outcome or chronicity in reactive arthritis. an erythrocyte sedimentation rate (ESR) higher than 30. India.[10. and Thailand showed low prevalence. About 15% of patients with reactive arthritis develop a long-term. Race As with other spondyloarthropathies. particularly with ocular and urogenital inflammation. these factors complicate differentiation of reactive arthritis from other arthritides. This association points out the likely importance of CD8+ cytotoxic T cells compared to CD4+ helper T cells in the pathogenesis of reactive arthritis. arthritis or enthesitis or spondylitis. Age Most patients with reactive arthritis are aged 20-40 years. The frequency of HLA-B27 is the same of that associated with non±AIDSrelated reactive arthritis in a similar demographic group.[12 ]The number of patients with reactive arthritis in this study was low. North Africa.of reactive arthritis in these patients tends to be severe. 7 factors were analyzed as predictors of long-term outcome in spondyloarthropathies. A new infection or other stress factor could cause reactivation of the disease. Frequency International Data on the incidence and prevalence of reactive arthritis are scarce. with a generalized rash that resembles psoriasis. profound arthritis.[9 ]Reports from Latin America. The male-tofemale ratio of disease associated with venereally acquired infections is 9:1. and a valid subgroup analysis was impossible. However. and frank AIDS. with resolution of symptoms by 3-12 months. Individuals who are HLA-B27±positive are at a higher risk of recurrence. sometimes destructive. Sex Reactive arthritis following foodborne enteric infections is equally common in males and females. In a study by Amor et al (1994).
dactylitis (ie. knees. Low-back pain occurs in 50% of patients. predominately lower-extremity. The complete Reiter triad of urethritis. and elbows may also be affected.[3 ]About 10% of patients do not have a preceding symptomatic infection. ankles. and mucosa of the cheeks and lips have been described. wrists. In more chronic and severe cases. Recent evidence indicates that a preceding respiratory infection with Chlamydia pneumoniae may also trigger the disease. resembling mycotic infection or psoriatic onychodystrophy. An asymmetrical. iliac crests. Mild dysuria. and fever. fatigue. As in other spondyloarthropathies. Physical y Joints. Ocular findings . and arthritis may occur. ischial tuberosities. Circinate balanitis may also develop. Both postvenereal and postenteric forms of reactive arthritis may manifest initially as nongonococcal urethritis. tibial tuberosities. and ribs. tenderness. most physical examination findings in patients with acute disease are minimal except for decreased lumbar flexion. the enthesopathy of reactive arthritis may be associated with findings of inflammation (ie. but the shoulders. Erythema nodosum may develop but is uncommon. hips). but nail pitting is not observed. Heel pain is common because of enthesopathies at the Achilles or plantar aponeurosis insertion on the calcaneus. conjunctivitis. swelling) at the Achilles insertion. axial skeleton. entheses o Peripheral joint involvement associated with reactive arthritis is typically asymmetric and usually affects the weight-bearing joints (ie. pain. o o o y y Other mucosal signs and symptoms: Painless shiny patches in the palate.History Reactive arthritis usually develops 2-4 weeks after a genitourinary or gastrointestinal infection. Nails can become thickened and crumble. and vaginal discharge and/or cervicitis in women are other possible manifestations. oligoarthritis is the major presenting symptom. o o o y Skin and nails o Keratoderma blennorrhagica on the palms and soles is indistinguishable from pustular psoriasis and is highly suggestive of chronic reactive arthritis. sausage digits) may develop. As with other spondyloarthropathies. prostatitis and epididymitis in men. the small joints of the hands and feet may also be involved. Other sites include the plantar fascial insertion on the calcaneus. tongue. The onset of reactive arthritis is usually acute and characterized by malaise. While 50% of patients with reactive arthritis may develop low-back pain. mucopurulent discharge. Patients with more chronic and severe axial disease may develop physical findings similar to ankylosing spondylitis.
case reports have described reactive arthritis after vaccination with live vaccines[18. Bacteria postulated to be potential causes of reactive arthritis include Ureaplasma urealyticum. The lesions tend to recur. and Campylobacter species. episcleritis. Lesions resembling ulcerative colitis or Crohn disease have been described when ileocolonoscopy is performed in patients with established reactive arthritis.[20 ] Differential Diagnoses Ankylosing Spondylitis and Undifferentiated Spondyloarthropathy Gonococcal Arthritis Gout Inflammatory Bowel Disease Psoriatic Arthritis Rheumatic Fever Rheumatoid Arthritis Septic Arthritis Workup Laboratory Studies y The values of acute-phase reactants. .[14 ] Some patients with reactive arthritis continue with intermittent bouts of diarrhea and abdominal pain. Shigella. o y Enteric infections o Enteric infections may trigger reactive arthritis. and corneal ulcerations.[13 ] o y Other manifestations o Other manifestations of reactive arthritis include mild renal pathology with proteinuria and microhematuria.[16 ]and Mycobacterium tuberculosis. keratitis. In severe chronic cases.[17 ]In addition. Yersinia. o Causes Reactive arthritis is usually triggered by a genitourinary or gastrointestinal infection. are usually elevated markedly but later return to the reference range when the inflammation subsides. Other enteric bacteria that have been associated with reactive arthritis include Clostridium difficile.[15 ]beta-hemolytic streptococci.o Conjunctivitis is part of the classic triad of Reiter syndrome and can occur before or at the onset of arthritis. C trachomatis L2b serotype. and Helicobacter pylori. amyloid deposits and immunoglobulin A (IgA) nephropathy have been reported. and aortitis with aortic regurgitation occurs in 1%-2% of reactive arthritis cases. The frequency of reactive arthritis after these enteric infections is about 1%-4%.19 ]and after intravesical therapy with Bacillus Calmette-Guérin (BCG). Cardiac conduction abnormalities may develop.[13 ] Escherichia coli. including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Pathogens include Salmonella. Other ocular lesions include acute uveitis (20% of patients).
or urogenital tract cultures can be performed in an attempt to isolate the causative organism. IgA antibodies to specific bacterial antigens have been reported. y y y Imaging Studies y Radiography o o Early in the disease process. Throat. In the hands and feet. stool. radiography reveals no abnormalities. Microbial components and antigens have been identified in joint fluid using sophisticated laboratory techniques. Other serologic techniques for the detection of Chlamydia species. Severe ankylosing spondylitis occurs in less than 5% of cases. Exuberant plantar spurs are a common sign in long-term reactive arthritis. Treatment Medical Care . Gram stain and culture results are negative and are necessary to exclude septic arthritis. periosteal reaction and proliferation at sites of tendon insertion are visible. Spinal radiographic findings include sacroiliitis and syndesmophytes. including PCR. Synovial fluid analysis reveals a high WBC count. o o o o o y MRI: MRI of the sacroiliac joints may reveal disease earlier than conventional radiography. In more advanced or long-term reactive arthritis. HLA-B27 testing results are positive in 65%-96% of cases. marginal erosions with adjacent bone proliferation occur. Procedures y Needle aspiration of a joint may be necessary to rule out septic or crystal-induced arthritis. may be considered. Syndesmophytes are usually asymmetrical and are found most commonly in the thoracolumbar region.y Other laboratory findings include a normocytic normochromic anemia along with mild leukocytosis and thrombocytosis during the acute phase. most often with elevated polymorphonuclear leukocytes acutely. Sacroiliitis occurs in less than 10% of acute cases but develops in half of patients with chronic severe disease. HLA-B27 testing is not necessary in classic Reiter syndrome but may be helpful to support the diagnosis of reactive arthritis in patients with jointrestricted symptoms. Test results for rheumatoid factor and antinuclear antibodies are negative. Other Tests y y ECG should be performed in patients with a prolonged course of reactive arthritis to evaluate for conduction disturbances. Urinalysis may reveal aseptic pyuria.
Physical therapy needs to be implemented to help reduce pain and to avoid muscle wasting in severe cases of reactive arthritis. in a recent abstract presentation. although the general impression is that indomethacin has greater potency.[23 ] Quinolones have been studied because of their broad coverage. 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. Azithromycin was shown to be ineffective in a placebo-controlled trial. but specific treatment guidelines for reactive arthritis are lacking. o y Antibiotics o The current concepts on the pathogenesis of reactive arthritis indicate that an infectious agent is the trigger of the disease.[21 ] Systemic corticosteroids can be used. antibiotics are used to treat the underlying infection. particularly in patients in whom NSAIDs elicit a poor response or in those who develop adverse effects related to their use. Prednisone 0.[22 ]Nevertheless. Sacroiliac joints can be injected. y Nonsteroidal anti-inflammatory drugs o NSAIDs are the foundation of therapy. but antibiotic treatment does not change the course of the disease. The starting dose is guided by a patient's symptoms and objective evidence of inflammation. However. o o o o y Disease-modifying antirheumatic drugs . in chlamydia-induced reactive arthritis. Lymecycline was studied in a double-blind placebo-controlled study of patients with chronic reactive arthritis for a treatment period of 3 months.5-1 mg/kg/d can be used initially and tapered according to response. but no clear benefit has been reported. usually under fluoroscopic guidance. 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. The choice of a specific agent depends on the individual response to treatment.4 The duration of illness was significantly decreased in patients with chlamydia-induced disease. o o y Corticosteroids o o These agents can be used as either intra-articular injection or systemic therapy.The treatment of reactive arthritis is depends on the severity of symptoms. even when a microorganism is isolated. These agents should be used regularly to achieve a good anti-inflammatory effect. In these cases.[24 ] More studies are needed before definite recommendations can be made for the role of antibiotics in the management of reactive arthritis. Joint injections can produce long-lasting symptomatic improvement and help avoid the use of other systemic therapy. as opposed to those with disease triggered by enteric infections.
29. to prevent joint damage. large studies have not been published. 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. patients with reactive arthritis who were taking sulfasalazine had a 62. 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. and to alleviate extra-articular disease. other second-line drugs may be used.30 ] o o o Surgical Care No surgical treatment of reactive arthritis is recommended.3% response rate compared to 47. Consultation with a urologist may be necessary if particularly prominent genitourinary manifestations develop. Activities should otherwise be as tolerated by the patient. randomized trials have not been performed to prove clinical benefit in reactive arthritis or in undifferentiated spondyloarthropathy. . In a 36-week trial of sulfasalazine versus a placebo in the spondyloarthropathies.7% for the placebo group in peripheral arthritis (P = 0.27 ]Patients with reactive arthritis and HIV/AIDS should not receive methotrexate or other immunosuppressive agents. DMARDs have also been used in reactive arthritis.[28. Sulfasalazine is more widely used in ankylosing spondylitis. Medication The goals of pharmacotherapy are to reduce morbidity. Clinical experience with these so-called disease-modifying antirheumatic drugs (DMARDs) has been mostly in rheumatoid arthritis and in psoriatic arthritis. Sulfasalazine may be beneficial in some patients. 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. doubleblind.[26. Case reports using the chimeric monoclonal antibody infliximab have shown potential efficacy in symptom relief in patients in whom other therapies failed.09).o In patients with chronic symptoms or in patients with persistent inflammation despite the use of the agents mentioned above. Reports also describe the use of azathioprine and bromocriptine in reactive arthritis. but controlled studies are lacking. again. although their disease-modifying effects in the reactive arthritis setting are uncertain.[25 ] Methotrexate can be used in patients who present with rheumatoidlike disease. Consultations A rheumatologist should be consulted for confirmation of diagnosis and formulation of management plan. Several reports have shown good response. but.
probenecid may increase concentrations and. captopril. toxicity of NSAIDs. although indomethacin may be more effective in the spondyloarthropathies. possibly.Nonsteroidal anti-inflammatory drugs (NSAIDs) Several NSAIDs are available and have similar effectiveness. These agents are used to treat symptoms.Fetal risk shown in humans. hypertension.Fetal risk not confirmed in studies in humans but has been shown in some studies in animals D . may decrease diuretic effects of furosemide and thiazides. may decrease effect of hydralazine. recent GI bleeding or perforation. Cyclooxygenase-2 (COX-2)±specific inhibitors can be used in patients at high risk for GI complications. use only if benefits outweigh risk to fetus Precautions Caution in CHF. may increase risk of methotrexate toxicity. 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. and in PT with decreased renal and hepatic function. Advil) Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. monitor PT closely (instruct patients to watch for signs of bleeding). phenytoin levels may be increased when administered concurrently Contraindications Documented hypersensitivity. and beta-blockers. renal insufficiency. caution in anticoagulation abnormalities or during anticoagulant therapy . Ibuprofen (Motrin. peptic ulcer disease. high risk of bleeding Precautions Pregnancy B .
or thrombocytopenia occurs) Tetracyclines . granulocytopenia. and glucuronide conjugation. Inhibits prostaglandin synthesis. may decrease effect of hydralazine. Metabolism occurs in liver by demethylation. deacetylation. increases risk of acute renal failure in patients with pre-existing renal disease or compromised renal perfusion. hyponatremia.Fetal risk not confirmed in studies in humans but has been shown in some studies in animals D . not to exceed 200 mg/d Pediatric 1-2 mg/kg/d PO divided bid/qid. hyperkalemia. captopril. 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. GI bleeding.Indomethacin (Indocin. may increase risk of methotrexate toxicity. renal insufficiency Precautions Pregnancy B . Indochron E-R) Rapidly absorbed. toxicity of NSAIDs. Dosing Adult 25-50 mg PO bid/tid 75 mg SR PO bid. probenecid may increase concentrations and. may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding). reversible leukopenia may occur (discontinue if persistent leukopenia.Fetal risk shown in humans. interstitial nephritis. phenytoin levels may be increased when administered concurrently Contraindications Documented hypersensitivity. use only if benefits outweigh risk to fetus Precautions Acute renal insufficiency. may decrease diuretic effects of furosemide and thiazides. and beta-blockers. and renal papillary necrosis may occur. possibly.
tetracycline use during tooth development (ie. Vibramycin) Inhibits protein synthesis and. consider drug serum level determinations in prolonged therapy. Corticosteroids modify the body's immune response to diverse stimuli. thus. bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. causing breakthrough bleeding and increased risk of pregnancy Contraindications Documented hypersensitivity. Collagenase inhibitors have been used to treat early rheumatoid arthritis. Some evidence shows that. severe hepatic dysfunction Precautions Pregnancy D . magnesium. <8 y) can cause permanent discoloration of teeth.These agents are used to treat urethritis or cervicitis caused by chlamydial organisms. in chlamydia-induced Reiter syndrome. 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.Fetal risk shown in humans. tetracyclines can increase hypoprothrombinemic effects of anticoagulants. iron. or bismuth subsalicylate. calcium. tetracyclines can decrease effects of PO contraceptives. use only if benefits outweigh risk to fetus Precautions Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment. Doxycycline (Bio-Tab. Fanconilike syndrome may occur with outdated tetracycline Corticosteroids These agents have anti-inflammatory properties and cause profound and varied metabolic effects. tetracycline treatment may reduce duration and perhaps severity of illness. . reduce dose in renal impairment.
osteoporosis. peptic ulcer disease. edema. hypokalemia. Dosing Adult 0. and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose). infections may occur with glucocorticoid use Aminosalicylic acid derivatives These agents are used to reduce inflammation. myopathy. hepatic dysfunction. GI disease Precautions Pregnancy B . fungal or tubercular skin infections. monitor for hypokalemia with coadministration of diuretics Contraindications Documented hypersensitivity. phenytoin. euphoria. .5 mg/kg/d PO initially. connective tissue infections. viral infection. phenobarbital. osteonecrosis. concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia. Sulfasalazine (Azulfidine. myasthenia gravis. hyperglycemia. growth suppression. peptic ulcer disease.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. EN-tabs) Acts locally in colon to decrease the inflammatory response and systemically inhibits prostaglandin synthesis. taper according to response Pediatric Not established Interactions Coadministration with estrogens may decrease prednisone clearance.Prednisone (Sterapred) May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. psychosis.
Deterrence/Prevention Even when a causal microorganism is isolated. or urinary obstruction Follow-up Further Inpatient Care Hospitalization of a patient with uncomplicated reactive arthritis is not indicated. blood dyscrasias. antibiotic therapy does not change the course of the disease. 1000 mg PO bid Pediatric Not established Interactions Decreases effects of iron. visit eMedicine's Arthritis Center. hypersensitivity to sulfa drugs or any component.Dosing Adult 500 mg PO bid initially. and methotrexate Contraindications Documented hypersensitivity. digoxin. PO hypoglycemic agents. and folic acid. increases effect of PO anticoagulants. Also. see eMedicine's patient education article Psoriatic Arthritis. Miscellaneous Medicolegal Pitfalls . 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. conversely. Patient Education For excellent patient education resources.
Ankylosing spondylitis and reactive arthritis in the developing world. Lu DW. Reactive arthritis: clinical aspects and medical management. [Medline]. Lähdevirta J. Arthritis Rheum. [Medline].53(2):100-5.35(1):21-44. Treharne J. with special reference to chlamydia-induced arthritis.22(4):709-23. Berlin. [Medline]. J Rheumatol. . Adv Exp Med Biol. Feb 1994. Saikku P. Failure to appropriately treat septic arthritis in a timely manner could result in joint destruction. Burgos-Vargas R. Aug 2008. 1999. Repo H. Hajjaj-Hassouni N. [Medline]. Jan 1991. 1916. Results and discussion of a questionnaire prepared for the 4th International Workshop on Reactive Arthritis. July 3-6. Feb 2009. placebo-controlled study of three-month treatment with lymecycline in reactive arthritis. Germany. Carter JD. [Medline]. [Medline]. Chlamydia pneumoniae--a new causative agent of reactive arthritis and undifferentiated oligoarthritis. 6. 3. Oct 2005. Leirisalo-Repo M. 4.y Septic arthritis must be ruled out if suspected before a diagnosis of reactive arthritis is made. Dtsche Med Wschr. J Am Acad Dermatol. Braun J. Double-blind. Sieper J.53(4):720-3. Best Pract Res Clin Rheumatol. Laitko S. 19982003. Carter JD. Sep 2000. 8. 2009. Hudson AP. Declining use of the eponym "Reiter's syndrome" in the medical literature. [Medline]. HIV/AIDS should be considered before instituting immunosuppressive therapy in severe cases of reactive arthritis. Inman RD. J Rheumatol. Ann Rheum Dis.21(4):386-90.649:300-9. On the difficulties of establishing a consensus on the definition of and diagnostic investigations for reactive arthritis. A prospective. Kingsley G.42:1535-6. [Medline]. Medicolegal liability could result from this oversight. Katz KA. y References 1. Oct 2004.27(9):2185-92. Ueber cine bisher unbekannte spirochaeten-infektion (spirochaetosis arthritica). with special reference to Chlamydia arthritis. Lauhio A. Curr Opin Rheumatol. et al. Vasey FB. Braun J. Innate immunity of spondyloarthritis: the role of toll-like receptors.31(10):1973-80. van der Heijde D. Doxycycline versus doxycycline and rifampin in undifferentiated spondyloarthropathy.34(1):6-14. 10. Reiter H. Jul 2009. Epidemiologic approaches to infection and immunity: the case of reactive arthritis. Rohekar S. 2. 9. [Medline]. Pope J. Rheum Dis Clin North Am. 7. Valeriano J. 5. randomized 9-month comparison.
Viard JP. Mar 1999. Mathis C.35(5):564-8. J Intern Med.27(2):209-10. Sibilia J. 23. Maugars Y. placebo controlled study. Janssen M. Three month treatment of reactive arthritis with azithromycin: a EULAR double blind. 13. Mod Rheumatol. El Karoui K. Clin Rheumatol. [Medline]. Listrat V. Hazes JM. Feb 2008. Gelber AC. [Medline]. 12. Rheumatol Int. Jeurissen ME.46(3):484-9. [Medline]. Gaston H. Lecuit M.85(3):1801. [Medline]. Sex Transm Infect. Mielants H. Philadelphia PA. Ann Rheum Dis. De Vos M. Jan 2009. Dijkmans BA. et al. Colin EM. [Medline]. Ribadeau-Dumas F. Bas S. Arthritis Rheum. Sahin N. revealing its distinction from acute rheumatic fever. Leirisalo-Repo M. J Rheumatol. Elewaut A. 14. Two case reports and a review of the literature. Veys E. Enginar AU. 20. Bartlett JG.63(9):1113-9. Birnbaum J. Reactive and undifferentiated arthritis in North Africa: use of PCR for detection of Chlamydia trachomatis. Bardin T. October 19. Clin Rheumatol. [Medline].96(2 Pt 1):339-44. [Medline]. Méchaï F. de Barbeyrac B. Vilon P. Post-streptococcal reactive arthritis: a clinical and serological description. Mar 2007. 16. [Medline]. Predictive factors for the longterm outcome of spondyloarthropathies. Ugurlu H. Doganavsargil E. Sep 2004. Corticosteroid injection of the sacroiliac joint in patients with seronegative spondylarthropathy. Reactive arthritis associated with L2b lymphogranuloma venereum proctitis. May 1992. Kvien TK. [Medline]. 15. 2009. Dolhain RJ. Salli A. 19. Rheumatology (Oxford). Carter JD et al. Aug 2007. Poncet's disease: reactive arthritis accompanying tuberculosis. (abstract 1152). . [Medline].19(2):209-11.26(8):1368-9. Butrimiene I. Clostridium difficile: an under-recognized cause of reactive arthritis?. Reactive arthritis following tetanus and rabies vaccinations. Aksu K. 2009. 21. Combination Antibiotics as a Treatment for Chronic Chlamydia-Induced Reactive Arthritis. 18. 22. Tektonidou MG. Ileocolonoscopy in seronegative spondylarthropathy. Kroot EJ. ACR/ARHP Annual Scientific Meeting. Prost A. Granfors K. Cuvelier C. Jun 2009. Reiter's syndrome during intravesical BCG therapy for bladder carcinoma. Dougados M. de Jong AJ.27(2):253-5. Nahal R. [Medline]. Keser G.28(1):11-6. Oct 1994. Dec 2006.245(3):261-7. 17. Feb 1989. Gaston JS. Gastroenterology. Vischer TL.11. Kuipers JG. Clin Rheumatol. [Medline]. Barbier F. Jansen TL. Santos RS. Reactive arthritis following tetanus vaccination: a case report.21(10):1883-7. Amor B.
Ahvonen P. Comparison of sulfasalazine and placebo in the treatment of reactive arthritis (Reiter's syndrome). Majithia V. Arnett FC. Schafranski MD. 30. 33. Abdelmoula LC. [Medline]. May 2005. Pa: WB Saunders. Ann Rheum Dis.84(5):564-6. crossover study of azathioprine in Reiter's syndrome. Chaabouni L. [Medline]. Bowel infection predisposing to reactive arthritis.17(3):247-56. Vasey FB. An "experimental" epidemic of Reiter's syndrome revisited. [Treatment of reactive arthritis with infliximab]. Clegg DO. 31. Tekaya R. [Medline]. 27. Ritchlin CT. et al. and unresolved treatment. 25. [Medline]. 1969. Dec 2006. [Medline]. Schumacher HR Jr. Luukkainen R. Weisman MH. Cush JJ. [Medline]. 1979.45(8):653-5. 37. May 1976.3(2):30319. A Department of Veterans Affairs Cooperative Study. Tunis Med. [Medline]. Acta Rheumatol Scand. A placebo controlled.27(1):121-3. Hakola M. Successful use of infliximab in the treatment of Reiter's syndrome: a case report and discussion. Baillieres Clin Rheumatol.19(5):747-50.[Medline]. Bravo G. Ann Rheum Dis. Rheumatol Int.15(3):232-53. Ben M'barek R. [Medline]. Reactive arthritis: defined etiologies. Korpela M. Yahia CB. 32. 35. Yli-Kerttula U. 36. et al. 34. Arthritis in Black and White. Infect Dis Clin North Am. Testouri N. Aug 1989. [Medline]. J Rheumatol. Gill H. Fries JF. Ann Intern Med. Sep 2003. Calin A. Dec 2008. . Calin A. Sievers K. May 1992. 2nd ed. Reda DJ. Clin Rheumatol. 1997:252.20(4):827-47. 29. An acute remission of Reiter's syndrome in male patients treated with bromocriptine. Incomplete Reiter's syndrome: clinical comparisons with classical triad. [Medline]. Aho K.39(12):2021-7. Aho K. Ann Rheum Dis. [Medline].38 Suppl 1:suppl 73-8. Arthritis Rheum.24. Follow-up evidence on genetic and environmental factors. [Medline].86(12):1095-7. Curr Opin Rheumatol. Carter JD. Zazueta B. Treatment update on spondyloarthropathy. emerging pathophysiology. Dec 1996. 26. Anandarajah A. Infliximab for reactive arthritis secondary to Chlamydia trachomatis infection. Effect of a three month course of ciprofloxacin on the late prognosis of reactive arthritis. Yli-Kerttula T. 28. Arthritis associated with Yersinia enterocolitica infection. Philadelphia. Jan 2008. May 23 2009.62(9):8804. Brower A. Aug 1986. Möttönen T. Lavalle C.
Keat A. Reactive arthritis and enteropathic arthritis. Reactive joint symptoms following an outbreak of Salmonella typhimurium phage type 135a. [Medline]. Meador R. Bull Mem Soc Med Hop Paris. Panayi G. White P. In: Klippel J.25(3):249-59. 45.309(26):1606-15. Skylv G. Incidence of inflammatory rheumatic diseases in Finland. J Rheumatol. Primer on the Rheumatic Diseases. von Essen R.19(4):863-83. Arnett FC. 47. Spondyloarthritis: update on pathogenesis and management. Reiter's syndrome and reactive arthritis in perspective. Iliopoulos A. Decreased pain and synovial inflammation after etanercept therapy in patients with reactive and undifferentiated arthritis: an openlabel trial. Pott HG. Reveille JD. Wright V. Moll JM. Fiessenger N.32(3):524-7. Haslock I. 46. Crofford L. Followup study on patients with Reiter's disease and reactive arthritis. Contribution a l'etude d'une epidemie de dysenterie dans la Somme. Ga: National Arthritis Foundation. Stone J. 41. Feb 1995. Antigenic responses in reactive arthritis. psoriatic arthritis. Hammer M. Change in the epidemiology of Reiter's syndrome (reactive arthritis) in the post-AIDS era? An analysis of cases appearing in the Greek Army. Feb 1992. [Medline]. 43. Comparing 10-day and 4month doxycycline courses for treatment of Chlamydia trachomatis-reactive arthritis: a prospective. [Medline]. Schumacher HR Jr.118(6):592-603. Lee AT. J Rheumatol.40:2030-69. Nissilä M.53(4):613-7. Wollenhaupt J. Sep 1974. the intestinal arthropathies. Isomäki H. N Engl J Med. Suoranta H. 1978. Dec 29 1983. Tsamis N. [Medline]. 2008:217-21. 13th. 49. 42.53(5):343-64.7(3):188-92. Macrae IF. Leirisalo M. Arthritis Rheum. Arthritis Rheum. Rheum Dis Clin North Am. Pile KD. Reiter's disease.18(1):49-66. Dec 2005. Hsia E.38. 1916. with special reference to HLA-B27. [Medline].22(2):252-4. 50. Hall RG. [Medline]. Associations between ankylosing spondylitis. and Behcet's syndrome. Am J Med. Scand J Rheumatol. Leroy E. Inman R. Ioakimidis D. 39. Infect Dis Clin North Am. Putschky N. [Medline]. 40. Voipio-Pulkki LM. Zeidler H. double-blind trial. 48. Jun 2005. Petersel DL. Reactive arthritis. [Medline]. Kingsley G. Kuipers JG. 44. Arvanitis A. Nov 2006. Raunio J. Flagg SD. Sigal LH. Kitumnuaypong T. [Medline]. [Medline]. Karras D. Atlanta. Ann Rheum Dis. Mar 2005. Iakovou I. [Medline]. Hämeenkorpi R. Mar 1982. Aug 15 2005.65(11):1521-4. Kousa M. . Medicine (Baltimore).
Campylobacter. Susceptibility and HLA-B27 in post-dysenteric arthropathies. J Rheumatol. Toivanen P. Director of Rheumatology Fellowship Program. Reactive arthritis following culture-confirmed infections with bacterial enteric pathogens in Minnesota and Oregon: a populationbased study. [Medline]. 55. ReA. MD is a member of the following medical societies: American College of Physicians and . 54. conjunctivitis. Department of Medicine. 56. [Medline]. Rheumatol Eur. Tsui HW. van Bodegom P. Solitar BM. [Medline]. Yersinia. Reiter's syndrome.35(8):1599-602. Sep 1999. 57. Reiter syndrome. Jul 1995. placebo-controlled study. Chlamydia trachomatis.24(1):5-8. Toivanen P. 1995. infectious diarrhea. Salmonella. psoriatic arthritis. Apr 1998. No benefit of long-term ciprofloxacin treatment in patients with reactive arthritis and undifferentiated oligoarthritis: a threemonth. Deodhar AA. Fendler C. Shigella dysentery. University of Miami School of Medicine Carlos J Lozada. ankylosing spondylitis. [Medline]. Lionarons RJ. Hiepe F. Riarh R. MD. Sieper J. 53. and therapeutic aspects of reactive arthritis and ankylosing spondylitis. 52. Arthritis Rheum. Wakefield D. Verma M. RS. [Medline]. Associate Professor. Dinant HJ. multicenter.67(12):1689-96. Lowe AM. McCluskey P. Lozada CJ.27(5):293-300.42(9):1894-7. Keywords reactive arthritis. Sörensen H. genitourinary infection Contributor Information and Disclosures Author Carlos J Lozada. Curr Opin Rheumatol. Aziz K. Xi N. [Medline]. seronegative spondyloarthropathy. Krug HE. oculourethro-synovial syndrome. Carr G. Nabbe AJ. chlamydial reactive arthritis . Toivanen A. Bilotta R. Rohekar S. Aug 2008. Jackson Memorial Medical Center. Toivanen A. Laitko S. Epidemiologic. Gripenberg-Lerche C. C trachomatis. Division of Rheumatology and Immunology. Oct 1985. Blanchard K. Ann Rheum Dis.51. Barkhuizen A.7(4):279-83. [Medline]. gastrointestinal infections. Townes JM. Tsui FW. double-blind. Landheer JE. nongonococcal urethritis. Semin Arthritis Rheum. Reiter's syndrome among Asian shipboard immigrants: the case of The Golden Venture. van Bohemen CG.56(2):377-9. Dec 2008.42(7):1386-96. Laine ES. randomized. Immunology. clinical. Chlamydia reactive arthritis. Aetiopathogenesis of reactive arthritis. Ciprofloxacin treatment does not influence course or relapse rate of reactive arthritis and anterior uveitis. Symptomatic acute reactive arthritis after an outbreak of salmonella. 58. Tseng CE. Gatus B. Krajewski WM. Smith K. Arthritis Rheum. Jul 1999.
American College of Rheumatology Disclosure: Nothing to disclose. University of Miami Miller School of Medicine Alex J Mechaber. CME Editor Alex J Mechaber. MD is a member of the following medical societies: American College of Physicians Disclosure: Nothing to disclose. Coauthor(s) Maria F Carpintero. MD is a member of the following medical societies: Alpha Omega Alpha. Department of Internal Medicine. Temple University School of Medicine. FACP. MD. Chairman Emeritus. MD is a member of the following medical societies: Alpha Omega Alpha. Central Society for Clinical Research. American College of Physicians. Associate Professor of Medicine. Senior Pharmacy Editor. American Medical Association. Temple University School of Medicine Elliot Goldberg. Western Pennsylvania Hospital Herbert S Diamond. Professor of Medicine. PhD. Fellow. and Society for Investigative Dermatology Disclosure: Nothing to disclose. MD. Northwestern University John Varga. American College of Rheumatology. and Phi Beta Kappa . MD. American College of Physicians-American Society of Internal Medicine. Associate Dean for Undergraduate Medical Education. MD. Chief Editor Herbert S Diamond. Medical Editor John Varga. Jackson Memorial Medical Center. Dean of the Western Pennsylvania Clinical Campus. Pharmacy Editor Francisco Talavera. Professor. MD. FACP is a member of the following medical societies: Alpha Omega Alpha. Department of Internal Medicine. Department of Rheumatology. and American College of Rheumatology Disclosure: Nothing to disclose. University of Miami. American College of Physicians. and Society of General Internal Medicine Disclosure: Nothing to disclose. American College of Rheumatology. Division of Rheumatology. eMedicine Disclosure: eMedicine Salary Employment Managing Editor Elliot Goldberg. PharmD. MD. Department of Medicine. Miami Veterans Affairs Medical Center Maria F Carpintero. Professor. MD is a member of the following medical societies: American College of Physicians.
2010 by Medscape.medscape. All Rights Reserved (http://www.Disclosure: medifocus Honoraria Review panel membership. health dialogs Honoraria Consulting. West Penn Allegheny Health System None Board membership Further Reading © 1994.com/public/copyright) .