8 - Spondyloarthropathies - Treatment Flashcards
Reactive arthritis (reiter’s syndrome)
Inflammatory arthritis preceded by infection with enteric pathogens:
Salmonella Yersinia Shigella Campylobacter The Oculogenital pathogens (Chlamydia trachomatis)
Things that classify it as a spondyloarthritis spectrum condition:
HLA-B*27 association
Pattern of joint involvement
Absence of autoantibodies
Post-Chalmydia-Induced ReA
Viable organisms can be detected in the joints
Post-Enteric ReA
Viable organisms can NOT be detected in the joints
ReA - 2 clinically different forms
Triad of explosive, severe arthritis, conjunctivitis and urethritis along with enthesitis and keratodermic skin and nail lesions
OR
More common, somewhat milder and more self-limited post infectious arthritis without evidence of skin or eye involvement or urethritis
Typically self limited course (~70%) resolving over one or two months.
~30% have a chronic or recurrent course
ReA Features
Arthritis is severe and often develops over a few hours
Accompanied by malaise, fatigue, fever
One or both knees or other lower extremity joints
Joint fluid leukocytes > 20,000 (mostly PMNs, with activated macrophages)
ReA ddx
Gonococcal or other septic arthritis, especially to be considered if monoarticular
Enthesitis may be prominent (Lover’s heel post-chlamydia)
Dactylitis and sacroiliitis may be present, erosions may develop.
ReA - Urethritis
Culture negative Appears at the time of arthritis Dysuria Frequency Urgency Urethral discharge
Cervicitis & Cystitis in females
Conjunctivitis with marked erythema, pain and tearing
Less common:
Diarrhea
Abdominal pain
Findings of IBD on endoscopy
Uncommon:
Cardiac involvement
Kidney involvement
Severe eye involvement
ReA - Specific Infections (Enteric)
Develops 7 - 30 days after enteric infection with certain Gram negative rods:
Salmonella typhimurium Salmonella paratyphi Salmonella heidelbergii Shigella flexneri 2a and 2b, but not Shigella sonnei Yersinia enterocolitica Campylobacter jejuni Campylobacter fetus
They invade intestinal and other cells, likely resulting in the expression of arthritogenic peptides in class I MHC molecules, at the time of ReA, they’re usually culture negative
ReA - Specific Infections (Venereal)
Develops 7 - 30 days after venereal infection with:
Chlamydia trachomatis
Chlamydia psittaci
Reactive Arthritis in the setting of AIDS
Keratodermia Blenorrhagicum:
Pustular psoriasis-like lesions of palms and soles
Psoriasis-like Lesions: T Cell infiltration Keratinocytes HLA-DR+ with delayed differentiation Parakeratosis Sterile microabscesses
The psoriatic arthritis gets worse as you move further distally
What does ReA in the setting of AIDS suggest?
Residual CD8 T cells are central to the disease pathogenesis.
Common to all cases of ReA
7 - 30 day delay in development (perhaps clonal expansion of memory/effector CD8s?)
IL-17 is a major cytokine in the joint fluids and Th17 T cells are likely the effector population.
HLA-B*27 Epi
70% of northern european caucasions, alaskan inuit and northern asians (frequency more like 25 - 40%) who develop reactive arthritis
0% in central africa, where ReA in the setting of advanced HIV is a major health problem
Major non-B*27 allele associated with susceptibility in northern european caucasoids
HLA-B*07
HLA-B*51 associated with susceptibility in some populations
B*27 penetrance
Up to 50% of HLA-B*27 individuals develop ReA during major epidemics of dysentery by arthritogenic organisms
ReA - Therapy
NSAIDs are sufficient if the ReA features rapidly resolve
Steroids not effective
Sometimes use RA drugs like Methotrexate, sulfasalazine, TNF inhibitors if persistent inflammation
Antibiotic therapy usually not indicated for enteric form unless there is evidence of microbial persistence
Use tetracycline for chlamydia
Psoriasis
Skin disease with retardation in keratinocyte differentiation
Induced by cytokines released from activated T cells
Onset - 15 - 30 years
Prevalence ~3% - Common
10 - 20% progress to PsA within 20 years
