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Reactive arthritis

Reactive arthritis. Reactive arthritis ( ReA ), also known as Reiter syndrome , is an autoimmune condition that develops in response to an infection .

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Reactive arthritis

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  1. Reactive arthritis

  2. Reactive arthritis (ReA), alsoknownasReitersyndrome, isanautoimmuneconditionthatdevelopsinresponsetoaninfection. • In 1916, HansReiterdescribedthetriadofnongonococcal urethritis, conjunctivitis, and arthritis inayoungGermanofficerwithbloodydysentery. • In 1916, FiessingerandLeroydescribed 4 patientswithwhattheycalledoculo-urethro-synovialsyndromeandassociatedthesyndromewithanoutbreakofShigelladysentery.

  3. Reactive arthritis hasbeenassociatedwithgastrointestinalinfectionswithShigella,Salmonella,andCampylobacterspeciesandothermicroorganisms, aswellaswithgenitourinaryinfections (especiallywithChlamydia trachomatis). Mycoplasma Reactive arthritis Chlamydia Yersinia Klebsiella Salmonella Shigella Chlamydia trachomatis, Mycoplasma hominis, Mycoplasma genitalium, Ureaplasma urealyticum, Salmonella enteritidis, Salmonella typhimurium, Shigella flexneri, Shigella dysenteriae, Campylobacter jejuni, Yersinia enterocolitica, Clostridia difficile

  4. Epidemiology • Dataontheincidenceandprevalenceofreactive arthritis arescarce, partlybecauseofalackofadiseasedefinitionanddiagnosiscriteria; thesefactorscomplicatedifferentiationofreactivearthritisfromotherarthritides. • Thereportedannualincidenceofreactive arthritis isapproximately 30-40 casesper 100,000 adults, withaprevalenceof 1%-7%, butthisvariesgreatlyamongdifferentgeographiclocations. • ReportsfromLatinAmerica, NorthAfrica, India, andThailandshowedlowprevalence, withminimaldifferencesbetweencountries. • Aswithotherspondyloarthropathies, HLA-B27 andreactive arthritis aremorecommoninwhitepeoplethaninblackpeople. • Reactive arthritis followingfoodborneentericinfectionsisequallycommoninmalesandfemales. Themale-to-femaleratioofdiseaseassociatedwithvenereallyacquiredinfectionsis 9:1. • Mostpatientswithreactive arthritis areaged 20-40 years.

  5. 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. • About 10% of patients do not have a preceding symptomatic infection.

  6. Pathophysiology • Inflammationofjoints, entheses, axialskeleton, skin, mucousmembranes, gastrointestinaltract, andeyesmayoccur. • Resultsfor HLA-B27 arepositivein 65%-96% ofpatients (average, 75%) withreactive arthritis. • Thelikelihoodofdevelopingreactive arthritis isincreased 50-fold inpatientswhoare HLA-B27–positive, butthissyndromecanalsooccurinpatientswhoare HLA-B27 negative.

  7. Pathophysiology • Patientswith HLA-B27, aswellasthosewithastrongfamilyclusteringofthedisease, tendtodevelopmoresevereandlong-termdisease. • Thefrequencyofreactive arthritis afterentericinfectionaverages 1%-4% butvariesgreatly, evenamongoutbreaksofthesameorganism. HLA-B27

  8. Pathophysiology • Themechanismoftheinteractionoftheincitingorganismwiththehost (often HLA-B27–positive) leadingtothedevelopmentofreactive arthritis isnotknown. • Itisunclearifmicrobialantigenscross-reactwithself-proteins, stimulating (molecularmimicry) andperpetuatinga Th2-cell–mediatedautoimmuneresponse. • Chronicityandjointdamagehavebeenassociatedwitha Th2 cytokineprofilethatleadstodecreasedbacterialclearance. • SynovialfluidculturesarenegativeforentericorganismsorChlamydiaspecies. However, asystemicandintrasynovialimmuneresponsetotheorganismshasbeenfoundwithintra-articularantibodyandbacterialreactive T cells. Furthermore, bacterialantigenhasbeenfoundinthejoints. Thus, theelementsforanimmune-mediatedsynovitisarepresent.

  9. Pathophysiology • Molecularevidenceofbacterial DNA (bypolymerasechainreaction [PCR]) insynovialfluidshasbeenfoundonlyinChlamydia -relatedreactive arthritis. • Thissuggeststhatpersistentinfectionmayplayarole, atleastinsomecasesofchlamydialreactive arthritis. • Theroleof HLA-B27 inthisscenarioremainstobedefinedbut, asdiscussedelsewhere (Ankylosing SpondylitisandUndifferentiatedSpondyloarthropathies), molecularmimicry, presentationofpathogenicpeptides, andanalteredhostresponsetothebacteriaareallpossible.

  10. Pathophysiology • Reactive arthritis, includingclassicReitersyndrome, canoccurinpatientsinfectedwith HIV orwhohave AIDS. • Thisislikelybecausebothconditionscanbesexuallyacquiredratherthanbeingtriggeredby HIV. • Thecourseofreactive arthritis inthesepatientstendstobesevere, withageneralizedrashthatresembles psoriasis, profound arthritis, andfrank AIDS. • Thefrequencyof HLA-B27 isthesameofthatassociatedwithnon–AIDS-relatedreactive arthritis inasimilardemographicgroup. • Thisassociationpointsoutthelikelyimportanceof CD8+ cytotoxic T cellscomparedto CD4+ helper T cellsinthepathogenesisofreactive arthritis.

  11. Classification • Reactive arthritis belongs to seronegative spondiloarthritis, with two major forms: • uro-genital form; • entero-colitis form. • After onset of illness: • Acute <6 months; • Trenant (dragged on) 6-12 months, • Chronic> 12 months;

  12. Clinical manifestations • Reactive arthritis usuallydevelops 2-4 weeksafteragenitourinaryorgastrointestinalinfection. • About 10% ofpatientsdonothaveaprecedingsymptomaticinfection. • Bothpostvenerealandpostentericformsofreactive arthritis maymanifestinitiallyasnongonococcal urethritis. • Milddysuria, mucopurulentdischarge, prostatitis and epididymitis inmen, andvaginaldischargeand/or cervicitis inwomenareotherpossiblemanifestations.

  13. Clinical manifestations • Theonsetofreactive arthritis isusuallyacuteandcharacterizedbymalaise, fatigue, andfever. • Anasymmetrical, predominatelylower-extremity, oligoarthritisisthemajorpresentingsymptom. • Low-backpainoccursin 50% ofpatients. • HeelpainiscommonbecauseofenthesopathiesattheAchillesorplantaraponeurosisinsertiononthecalcaneus. • ThecompleteReitertriadof urethritis, conjunctivitis, and arthritis mayoccur.

  14. Clinical manifestations • Joints, axialskeleton, entheses • Peripheraljointinvolvementassociatedwithreactive arthritis istypicallyasymmetricandusuallyaffectstheweight-bearingjoints (ie, knees, ankles, hips), buttheshoulders, wrists, andelbowsmayalsobeaffected. • Inmorechronicandseverecases, thesmalljointsofthehandsandfeetmayalsobeinvolved. Asinotherspondyloarthropathies, dactylitis (ie, sausagedigits) maydevelop.

  15. Clinical manifestations • Joints, axial skeleton, entheses • 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.

  16. Clinical manifestations • Joints, axialskeleton, entheses • Aswithotherspondyloarthropathies, theenthesopathyofreactive arthritis maybeassociatedwithfindingsofinflammation (ie, pain, tenderness, swelling) attheAchillesinsertion. Othersitesincludetheplantarfascialinsertiononthecalcaneus, ischialtuberosities, iliaccrests, tibialtuberosities, andribs.

  17. Clinical manifestations

  18. Clinical manifestations • Skin and nails • Keratoderma blennorrhagica on the palms and soles is indistinguishable from pustular psoriasis and is highly suggestive of chronic reactive arthritis.

  19. Clinical manifestations • Skinandnails • Erythema nodosum maydevelopbutisuncommon. • Nailscanbecomethickenedandcrumble, resemblingmycoticinfectionorpsoriaticonychodystrophy, butnailpittingisnotobserved. • Circinatebalanitismayalsodevelop.

  20. Clinical manifestations • Other mucosal signs and symptoms: Painless shiny patches in the palate, tongue, and mucosa of the cheeks and lips have been described.

  21. Clinical manifestations • Ocularfindings • Conjunctivitis ispartoftheclassictriadofReitersyndromeandcanoccurbeforeorattheonsetof arthritis. • Otherocularlesionsincludeacuteuveitis (20% ofpatients), episcleritis, keratitis, andcornealulcerations. Thelesionstendtorecur.

  22. Clinical manifestations • Entericinfections • Entericinfectionsmaytriggerreactive arthritis. • PathogensincludeSalmonella, Shigella, Yersinia,andCampylobacterspecies. • Thefrequencyofreactive arthritis aftertheseentericinfectionsisabout 1%-4%. • Otherentericbacteriathathavebeenassociatedwithreactive arthritis includeClostridiumdifficile,Escherichiacoli,andHelicobacterpylori. • Somepatientswithreactive arthritis continuewithintermittentboutsofdiarrheaandabdominalpain. Lesionsresembling ulcerative colitisor Crohn diseasehavebeendescribedwhenileocolonoscopyisperformedinpatientswithestablishedreactive arthritis.

  23. Clinical manifestations • Othermanifestations • Othermanifestationsofreactive arthritis includemildrenalpathologywithproteinuriaandmicrohematuria. • Inseverechroniccases, amyloiddepositsandimmunoglobulin A (IgA) nephropathyhavebeenreported. • Cardiacconductionabnormalitiesmaydevelop, and aortitis with aortic regurgitationoccursin 1%-2% ofreactive arthritis cases.

  24. LaboratoryStudies • Thevaluesofacute-phasereactants, includingerythrocytesedimentationrate (ESR) andC-reactiveprotein (CRP), areusuallyelevatedmarkedlybutlaterreturntothereferencerangewhentheinflammationsubsides. • Otherlaboratoryfindingsincludeanormocyticnormochromicanemiaalongwithmildleukocytosisandthrombocytosisduringtheacutephase. • IgA antibodiestospecificbacterialantigenshavebeenreported. • Urinalysismayrevealasepticpyuria.

  25. LaboratoryStudies • Synovialfluidanalysisrevealsahigh WBC count, mostoftenwithelevatedpolymorphonuclearleukocytesacutely. • Gramstainandcultureresultsarenegativeandarenecessarytoexcludeseptic arthritis. • Microbialcomponentsandantigenshavebeenidentifiedinjointfluidusingsophisticatedlaboratorytechniques.

  26. LaboratoryStudies • 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.

  27. ImagingStudies • Radiography • Earlyinthediseaseprocess, radiographyrevealsnoabnormalities. • Inmoreadvancedorlong-termreactive arthritis, periostealreactionandproliferationatsitesoftendoninsertionarevisible. • Exuberantplantarspursareacommonsigninlong-termreactive arthritis.

  28. ImagingStudies • Radiography • Inthehandsandfeet, marginalerosionswithadjacentboneproliferationoccur. • Spinalradiographicfindingsincludesacroiliitisandsyndesmophytes. Sacroiliitisoccursinlessthan 10% ofacutecasesbutdevelopsinhalfofpatientswithchronicseveredisease. • Syndesmophytesareusuallyasymmetricalandarefoundmostcommonlyinthethoracolumbarregion. • Severeankylosingspondylitisoccursinlessthan 5% ofcases.

  29. ImagingStudies • MRI: MRI of the sacroiliac joints may reveal disease earlier than conventional radiography.

  30. OtherTests • ECG shouldbeperformedinpatientswithaprolongedcourseofreactive arthritis toevaluateforconductiondisturbances. • HLA-B27 testingresultsarepositivein 65%-96% ofcases. HLA-B27 testingisnotnecessaryinclassicReitersyndromebutmaybehelpfultosupportthediagnosisofreactive arthritis inpatientswithjoint-restrictedsymptoms. • Needleaspirationofajointmaybenecessarytoruleoutsepticorcrystal-induced arthritis.

  31. Criteria of Amor et al for Spondylarthropathy • Amor et al developed a scoring system for the diagnosis of spondylarthropathy based on clinical, radiologic, genetic and therapeutic criteria. The authors are from Paris, France. • Parameters (12 items): • (1) clinical symptoms, current or past history of: 9 items • (2) radiological findings: 1 item • (3) genetic background: 1 item • (4) response to treatment: 1 item

  32. Criteria of Amor et al for Spondylarthropathy

  33. Criteria of Amor et al for Spondylarthropathy

  34. Criteria of Amor et al for Spondylarthropathy score = SUM(points for all 12 parameters) Interpretation:  minimum score: 0  maximum score: 21   A score >= 6 indicates that the patient has a spondylarthropathy.

  35. Criteria of Sieper and Braun for Reactive Arthritis Features of reactive arthritis - all of the following: • (1) asymmetrical arthritis • (2) predominantly of the lower limbs • (3) evidence of a preceding infection - one or more of the following: • (3a) diarrhea within the 4 weeks preceding onset • (3b) urethritis within the 4 weeks preceding onset • (3c) stool culture positive for Salmonella, Shigella, Yersinia • (3d) detection of Chlamydia trachomatis • (3e) serologic evidence of Salmonella or Shigella infection (antibodies to lipopolysaccharide or specific antigen) • (3f) antibodies to Chlamydia trachomatis • (3g) detection of chlamydial DNA in a joint by PCR • (4) exclusion of other rheumatic diseases

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

  37. Treatment • Antibiotics • Thecurrentconceptsonthepathogenesisofreactive arthritis indicatethataninfectiousagentisthetriggerofthedisease, butantibiotictreatmentdoesnotchangethecourseofthedisease, evenwhenamicroorganismisisolated. • Inthesecases, antibioticsareusedtotreattheunderlyinginfection, butspecifictreatmentguidelinesforreactive arthritis arelacking. • However, inchlamydia-inducedreactive arthritis, studieshavesuggestedthattheappropriatetreatmentoftheacuteurogenitalinfectioncanpreventreactive arthritis andthattreatmentofacutereactivearthritiswitha 3-month courseoftetracyclinereducesthedurationofillness.

  38. Treatment • Tetracycline group • Doxycycline - 200 mg / day • Macrolide group: • Clarithromycin - 1 g / day • Azithromycin - 500 mg - first day, after THEN 250 mg / day - 6 days • Roxithromycin - 300 mg / day • Quinolones: • Ciprofloxacin – 1 g/ day • Ofloxacin – 400 mg/ day • Lomefloxacin – 400 mg/ day • Perfloxacin – 800 mg/ day

  39. Treatment • Nonsteroidalanti-inflammatorydrugs • NSAIDsarethefoundationoftherapy. Theseagentsshouldbeusedregularlytoachieveagoodanti-inflammatoryeffect. • Thechoiceofaspecificagentdependsontheindividualresponsetotreatment. • Diclofenac(75-150 mg)or • Meloxicam(7,5-15 mg) or • Nimesulid (100-200 mg) or • Ibuprofen (800 – 1600 mg) or • Flurbiprofen (100 – 200 mg)

  40. Treatment • Corticosteroids • Theseagentscanbeusedaseitherintra-articularinjectionorsystemictherapy. • Jointinjectionscanproducelong-lastingsymptomaticimprovementandhelpavoidtheuseofothersystemictherapy. Sacroiliacjointscanbeinjected, usuallyunderfluoroscopicguidance. • Systemiccorticosteroidscanbeused, particularlyinpatientsinwhomNSAIDselicitapoorresponseorinthosewhodevelopadverseeffectsrelatedtotheiruse. • Thestartingdoseisguidedbyapatient'ssymptomsandobjectiveevidenceofinflammation. • Prednisone 0.5-1 mg/kg/dcanbeusedinitiallyandtaperedaccordingtoresponse.

  41. Treatment • Disease-modifyingantirheumaticdrugs • Inpatientswithchronicsymptomsorinpatientswithpersistentinflammationdespitetheuseoftheagentsmentionedabove, othersecond-linedrugsmaybeused. • Clinicalexperiencewiththeseso-calleddisease-modifyingantirheumaticdrugs (DMARDs) hasbeenmostlyin rheumatoid arthritis andinpsoriaticarthritis. • DMARDshavealsobeenusedinreactive arthritis, althoughtheirdisease-modifyingeffectsinthereactive arthritis settingareuncertain.

  42. Treatment • Disease-modifying antirheumatic drugs • 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 (2-3 gr per day) is widely used in all seronegative spondylitis.

  43. Treatment • Disease-modifying antirheumatic drugs • Methotrexate (7.5 – 15.0 mg per week) can be used in patients who present with rheumatoidlike disease. • Several reports have shown good response. Reports also describe the use of azathioprine. • Patients with reactive arthritis and HIV/AIDS should not receive methotrexate or other immunosuppressive agents.

  44. Treatment • Disease-modifyingantirheumaticdrugs • AlthoughbiologicagentssuchasTNF-blockershavebeendemonstratedtobebeneficialandformallyapprovedforthetreatmentofpsoriatic arthritis andankylosingspondylitis, double-blind, randomizedtrialshavenotbeenperformedtoproveclinicalbenefitinreactivearthritisorinundifferentiatedspondyloarthropathy. • Casereportsusingthechimericmonoclonalantibodyinfliximabhaveshownpotentialefficacyinsymptomreliefinpatientsinwhomothertherapiesfailed.

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

  46. Prognosis • Reactive arthritis typicallyfollowsaself-limitedcourse, withresolutionofsymptomsby 3-12 months, eveninpatientswhoareacutelyincapacitated. • However, reactive arthritis hasahightendencytorecur, particularlywithocularandurogenitalinflammation. • Individualswhoare HLA-B27–positiveareatahigherriskofrecurrence. • A newinfectionorotherstressfactorcouldcausereactivationofthedisease.

  47. Prognosis • About 15% ofpatientswithreactive arthritis developalong-term, sometimesdestructive, arthritisorenthesitisorspondylitis. InastudybyAmoretal (1994), 7 factorswereanalyzedaspredictorsoflong-termoutcomeinspondyloarthropathies. • Thenumberofpatientswithreactive arthritis inthisstudywaslow, andavalidsubgroupanalysiswasimpossible. • Thepresenceofhip-jointinvolvement, anerythrocytesedimentationrate (ESR) higherthan 30, andunresponsivenesstononsteroidalanti-inflammatorydrugs (NSAIDs) probablyportendasevereoutcomeorchronicityinreactive arthritis.

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