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Reactive arthritis

description of reactive arthritis

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Reactive arthritis

  1. 1. Presented By: Dr Bushu Harna Fellow OrthoRheumatology
  2. 2.  36 y/o gentleman admitted to the hospital with 2 days of acute onset of arthritis in his right knee that progressed to the left knee. The patient was investigated and discharged on Paracetamol + Ibroprofen TDS. But not responded well.  Patient had red eyes for past 7 days
  3. 3.  Past History: 3 weeks previous to admission he had an episode of diarrhea that lasted for 10 days and improved after treatment with Ciprofloxacin.  Family History: Sister had a similar episode 2 years back
  4. 4. General Examination: fever 1010 F. Otherwise within normal limits. Joint exam: tenderness, redness and effusions in both knees. Labs: Normal CBC, ESR 60, CRP 32. Synovial fluid showed no crystals and Gram stain revealed no organisms. RA Factor: Negative. HLA B-27 positive. Eye Examination: Anterior Uvetitis Patient was started on indomethacin 50 mg PO QID with significant improvement of his symptoms.
  5. 5.  “Reactive Arthritis (ReA) is an infectious induced systemic illness characterized by an ASEPTIC inflammatory joint involvement occurring in a genetically predisposed patient with a bacterial infection localized in a distant organ/system”.
  6. 6.  First described by Hans Reiter in 1916. Also known as Reiter Syndrome  Triad: Arthritis, Urethritis, Conjunctivitis  Name changed to Reactive Arthritis What’s So Reactive??  Aberrant autoimmune response to infection Postinfectious arthritis nongonococcal urethritis conjunctivitis
  7. 7. EPIDEMIOLOGY  Occurs in 20-40 years.  Begins with an enteric, urogenital or upper respiratory tract infections.  M:F::3:1  Arthritis occurs few days to 6 weeks after infection  30-70% positive for HLA-B27.  Incidence more in urethritis, cervicitis and infectious diarrhea.  Incidence varies widely (1% to 20%).  Frequency varies after infection with Salmonella, Shigella, Campylobacter or Yersinia.
  8. 8.  1. Microbes-host interaction. Components of triggering bacteria includes protein and nucleic acid. These can be found in the synovium and circulatory monocytes.
  9. 9.  2. Role of immune system In patients with ReA, they have an elevated production of Th2 cytokines, such us IL-10 and a possible decrease production in Th1 cytokines. Macrophages, CD4+ and CD8+ lymphocytes are activated in the joints of the patients. Some bacterial antigens like heat shock protein 60 present in Chlamydia and Yersinia. Molecular cross reactive has been also associated  All these factors cause a decrease in the effective clearance of bacteria.
  10. 10. 3. Immunogenetics HLA-B27 probably works as an antigen presenting molecule. Some arthritogenic peptide from chlamydia and yersinia can be presented by HLA-B27 leading to stimulation of CD8+ T cells.  IFN-gamma: low level  IL-10: High level
  11. 11.  Causative organisms  Chlamydial trachomatis  Ureaplasma urealyticum Urethritis  Salmonella enteritidis  Salmonella typhimurium  Shigella flexneri  Shigella dysenteriae Enteritis  Campylobacter jejuni  Yersinia enterocolitica  Streptococcus SP
  12. 12.  Less common association:  Chlamydia pneumoniae  Neisseria meningitidis serogroup B  Bacillus cereus  Pseudomonas  Clostridium difficile  Borrelia burgdorferi  Escherichia coli  Helicobacter pillory  Lactobacillus  Brucella abortus  Hafnia alvei
  13. 13. Clinical Manifestations:  Infection: History: diarrhea, urethritis, cervicitis, STDs  Postenteric ReA is described equally in men an women.  The episode of diarrhea is usually prolonged.  Postchlamydial is most common in men.  In females episodes of cervicitis, vaginitis can precede.
  14. 14.  In patients with postchlamydial disease, urethritis is usually mild, painless and nonpurulent.  Conjunctivitis is usually observed very early, before the onset of arthritis. Uveitis is less common but occurs in 15% of patients with chronic persistent disease.  Skin manifestations include: Keratoderma blenorrhagica, Circinate balanitis and oral ulcers.  Less common patients can develop valvulitis, rhythm disturbances.
  15. 15. Arthritis pattern  Asymmetric mono or oligo arthritis often of lower limbs including knees, ankles and feet.  Musculoskeletal: peripheral arthritis, inflammatory pain in cervical, thoracic, and lumbar spine  Sacroilitis  Enthesitis: plantar facisitis, heel pain, patellar tendon insertion pain, GT hip pain, base 5th MT, MT head pain  Sausage digits: IP joints with digital tendonitis and multiple entheseal lesion
  16. 16.  Predictors of more severe disease: hip arthritis, ESR>30, poor response to NSAIDS, Lumbar spine stiffness, dactylitis, oligoarthritis, <16 years.  In HLA-B27 positive patients: more severity and increased markers like ESR and CRP.
  17. 17.  Eye: conjunctivitis, anterior uveitis, episcleritis and keratitis  Genitourinary: urethritis, cervicitis, prostatitis, cystitis, circinate balanitis, salpingo-oophoritis  Mucosal and skin: mucosal ulcers, keratoderma blenorrhagica, erythema nodosum  Cardiac  Nail changes: onycholysis, subungual keratosis, nail pits
  18. 18.  Mono or oligo arthropathy: RA, AS, Ps arthritis  Gonococcal arthritis  Gouty arthritis  Septic arthritis  Rheumatic fever  Tubercular arthritis  Secondary syphilis  Rare: IBD, celiac, whipple disease and behcet disease, immunotherapy related arthropathy
  19. 19. Bases on observational data from Germany and Scandinavia *  Mono or oligo arthritis  Exclusion of other diagnosis Both criteria present: probability is 40%.  Evidence of previous infection Then chances are 60%.  If the bacteria can be culture, then 70%  If there is history of symptomatic preceding infection with Chlamdydia trachomatis, then 90% *Sieper J, Rudwaleit M, Braun J, et al. Diagnosing reactive arthritis: Role of clinical
  20. 20. Definitive: Both Major criteria + 1 Minor Criteria Probable: Both Major criteria
  21. 21.  Lab: raised ESR and CRP  Neutrophilic leukocytosis  HLA-B27  Rule out: RF, ANA, Gram staining and culture of the joint fluid, HIV  Radiographs: Not required to diagnose. A large bulky paravertebral area of ossification "floating osteophyte" is often seen. Early juxta-articular osteoporosis, uniform joint space loss and fusiform soft tissue swelling.  Ultrasound  Scintigraphy  MRI
  22. 22.  Others: ECG, ophthalmological examination, urine and stool examination, Nucleic acid amplification tests  Histopathological dermal features similar to psoriasis.  Synovial fluid reveals large macrophages, reiter cell that have phagocytosed neutrophils, lymphocytes and plasma cells. Extensive pannus formation is rare.
  23. 23.  Goal 1. Decrease pain and inflammation 2. Minimize disability 3. Prevent relapse or progression to chronic disease  Team effort  Patient education  Early diagnosis and treatment
  24. 24.  Acute: RICE, NSAIDs, orthotics  Intra-articular glucocorticoid injection  Systemic corticosteroids and Topical Steroids  Antibiotics  DMARDs: Methotrexate, SSZ  Anti-TNF agents: Etanercept, Infliximab
  25. 25.  It can be self limiting, recurrent or chronic  Depends on triggering pathogen and genetic background of the host.  Chronic arthritis (>6months) occurs in 4-19% patients. (arthritis caused by salmonella or shigella).  Chronic relapsing arthritis is seen in 6-8% patients (induced by salmonella, shigella or chlamydia).
  26. 26. Good history taking: Past history and family history Good General Physical Examination: EYE, NAIL, SKIN Exclude other Spondyloarthropathy Involve Physician & Rheumatologist NSAIDs, Steroids and DMARDs form the main basis of treatment.
  27. 27.  Kim PS, Klausmeier TL, Orr DP. Reactive arthritis: a review. Journal of Adolescent Health. 2009 Apr 1;44(4):309-15.  Cheeti A, Chakraborty RK, Ramphul K. Reactive Arthritis (Reiter Syndrome). InStatPearls [Internet] 2020 Mar 13. StatPearls Publishing.  Stavropoulos PG, Soura E, Kanelleas A, Katsambas A, Antoniou C. Reactive arthritis. Journal of the European Academy of Dermatology and Venereology. 2015 Mar;29(3):415-24.  García-Kutzbach A, Chacón-Súchite J, García-Ferrer H, Iraheta I. Reactive arthritis: update 2018. Clinical Rheumatology. 2018 Apr 1;37(4):869-74.  Colmegna I, Cuchacovich R, Espinoza LR. HLA-B27-associated reactive arthritis: pathogenetic and clinical considerations. Clinical microbiology reviews. 2004 Apr 1;17(2):348-69.  Carter JD. Treating reactive arthritis: insights for the clinician. Therapeutic advances in musculoskeletal disease. 2010 Feb;2(1):45-54.  Mukherjee S, Kar M. Reactive arthritis: current perspectives. J Ind Acad Clin Med. 2000 Oct;1:233-8.  Selmi C, Gershwin ME. Diagnosis and classification of reactive arthritis. Autoimmunity reviews. 2014 Apr 1;13(4-5):546-9.  HARRISON B, SILMAN A, SYMMONS D. Diagnostic evaluation of classification criteria for RA and reactive arthritis. Annals of the Rheumatic Diseases. 2000 May 1;59(5):397-8.

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description of reactive arthritis

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