reactive arthritis
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Introduction
Joint inflammation alone without other features of Reiter's syndrome.
Etiology
- induced by a host response to an infectious agent
- etiologic infectious agents:
- associated disorders
- inflammatory bowel disease
- HIV1 associated with increased severity of reactive arthritis[2]
Epidemiology
- equal distribution between sexes
Pathology
- joint is aseptic
- disease is generally self-limited
- joint destruction is uncommon
- bacterial antigens are found in affected joints
Genetics
- HLA-B27 positive (80%)
Clinical manifestations
- may manifest 2-3 or 6 weeks after a GI infection or GU infection
- it is common for precipitating infection to have resolved prior to onset of reactive arthritis[2]
- sterile urethritis, prostatitis, cervicitis, salpingitis, balanitis
- classic triad of arthritis, conjunctivitis & urethritis/cervicitis in 1/3[2]
- monoarthritis or oligoarthritis (maybe not polyarthritis)[2]
- generally large joints, weight-bearing joints, especially knee, ankle
- distribution is asymmetric
- joint effusions may be massive
- usually non-erosive[2]
- popliteal (Baker's) cysts are common
- tenosynovitis
- dactylitis
- enthesopathy (enthesitis)
- arthritis generally self-limited & non-erosive[2]
- some patients have a relapsing, remitting course
- attacks are generally months in duration
- may be chronic
- symptoms of Reiter's syndrome, including sacroiliitis & spondylitis may develop[2]
- mucocutaneous manifestations
- psoriasis-like skin lesions
- mouth ulcers, red eyes
- keratoderma blennorrhagicum (psoriaform lesions on palms, soles & toes)[2]
- circinate balanitis (shallow, moist, serpinginous ulcers with raised borders)
- urethritis, cervicitis
- ocular manifestations:
- conjunctivitis more common than uveitis[2]
- photophobia
- may be more severe in patients with HIV1 infection, especially when HLA-B27 positive[2]
Laboratory
- GenProbe
- serology
- urethral cultures for Chlamydia
- throat cultures for Streptococcus
- urinalysis: urine protein, WBC, RBC
- synovial fluid analysis:
- rule out septic arthritis
- WBC: 15,000/uL with 70% monocytes (MKSAP17 case)
- gram stain negative, no crystals[2]
- HLA-B27 positive (80%)
Radiology
- radiographs may show localized osteopenia[2]
- radiograph of sacroiliac joint may show sacroiliitis[2]
Differential diagnosis
- coxitis (postinfectious arthritis)
- Chikungunya
- Dengue
- parvovirus B19
- Lyme disease
- Behcet syndrome: genital ulcers, not urethritis, not infectious
Management
- specific antibiotic if etiologic agent can be identified
- reactive arthritis due to Chlamydia
- doxycycline first line, azithromycin for pregnant women
- macrolides, fluoroquinolones, tetracyclines (doxycycline) active against Chlamydia trachomatis
- treatment of patient & sexual partner indicated
- long-term combination antibiotic treatment may be of benefit[2]
- doxycycline first line, azithromycin for pregnant women
- reactive arthritis due to enteric infection
- may be self-limited
- infection often resolved before patient diagnosed with reactive arthrtitis
- antibiotics not useful unless active infection is present[2]
- antibiotics usually not helpful if etiologic agent not identified[2]
- reactive arthritis due to Chlamydia
- NSAIDs (indomethacin first line)
- with caution in patients with inflammatory bowel disease
- intraarticular glucocorticoids may be effective after septic arthritis is ruled out
- disease-modifying anti-rheumatic drug (DMARD) if arthritis persists for 3-5 month
- sulfasalazine benefits some patients unresponsive to NSAIDs alone
- methotrexate, start with 7.5 mg PO QD
- TNF-alpha inhibitor
- tetracycline (doxycycline) for 3 months may diminish the duration & severity if secondary to Chlamydia trachomatis
- prognosis: resolution of symptoms generally within 6 months[2]
More general terms
More specific terms
Additional terms
References
- ↑ Mayo Internal Medicine Board Review, 1998-99, Prakash UBS (ed) Lippincott-Raven, Philadelphia, 1998, pg 865
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 Medical Knowledge Self Assessment Program (MKSAP) 11, 14, 15, 16, 17, 18, 19. American College of Physicians, Philadelphia 1998, 2006, 2009, 2012, 2015, 2018, 2022.
Medical Knowledge Self Assessment Program (MKSAP) 19 Board Basics. An Enhancement to MKSAP19. American College of Physicians, Philadelphia 2022 - ↑ Carter JD, Hudson AP. Reactive arthritis: clinical aspects and medical management. Rheum Dis Clin North Am. 2009 Feb;35(1):21-44. PMID: https://www.ncbi.nlm.nih.gov/pubmed/19480995
- ↑ Hannu T, Inman R, Granfors K, Leirisalo-Repo M. Reactive arthritis or post-infectious arthritis? Best Pract Res Clin Rheumatol. 2006 Jun;20(3):419-33. PMID: https://www.ncbi.nlm.nih.gov/pubmed/16777574
- ↑ Townes JM. Reactive arthritis after enteric infections in the United States: the problem of definition. Clin Infect Dis. 2010 Jan 15;50(2):247-54 PMID: https://www.ncbi.nlm.nih.gov/pubmed/20025528
- ↑ Carter JD, Inman RD. Chlamydia-induced reactive arthritis: hidden in plain sight? Best Pract Res Clin Rheumatol. 2011 Jun;25(3):359-74 PMID: https://www.ncbi.nlm.nih.gov/pubmed/22100286
- ↑ Morris D, Inman RD. Reactive arthritis: developments and challenges in diagnosis and treatment. Curr Rheumatol Rep. 2012 Oct;14(5):390-4 PMID: https://www.ncbi.nlm.nih.gov/pubmed/22821199
- ↑ Hannu T Reactive arthritis. Best Pract Res Clin Rheumatol. 2011 Jun;25(3):347-57. PMID: https://www.ncbi.nlm.nih.gov/pubmed/22100285
- ↑ Rohekar S, Pope J. Epidemiologic approaches to infection and immunity: the case of reactive arthritis. Curr Opin Rheumatol. 2009 Jul;21(4):386-90 PMID: https://www.ncbi.nlm.nih.gov/pubmed/19373091
- ↑ Carter JD, Hudson AP. Recent advances and future directions in understanding and treating Chlamydia-induced reactive arthritis. Expert Rev Clin Immunol. 2017 Mar;13(3):197-206. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/27627462