Abstract:Lyme arthritis shares features with both septic and nonseptic non-Lyme arthritis. This overlap prevents the creation of a clinically useful predictive model for Lyme arthritis. In endemic areas, Lyme testing should be performed on all patients presenting with acute monoarticular arthritis.
“…All three pointed to a lack of substantially enhanced systemic CRP response in most patients with Lyme arthritis [21][22][23], in agreement with our results. A serum analysis in 20 patients with early neurologic Lyme disease reported a lack of increased CRP concentration in most [24], while a study of 44 Lyme disease patients with EM found both CRP and SAA to be significantly elevated in comparison to 23 healthy controls [25].…”
Section: Discussionsupporting
confidence: 92%
“…non-Lyme arthritis, without incorporating healthy controls [21,22], and one study examined CRP levels in 20 Lyme arthritis patients and 10 healthy volunteers [23]. All three pointed to a lack of substantially enhanced systemic CRP response in most patients with Lyme arthritis [21][22][23], in agreement with our results.…”
Background. Infection with Borrelia burgdorferi, the causative agent of Lyme disease, triggers host immune responses that affect the clinical outcome and are a source of biomarkers with diagnostic utility. Although adaptive immunity to B. burgdorferi has been extensively characterized, considerably less information is available about the development of innate acute-phase responses in Lyme disease. Our aim in this study was to evaluate the expression of C-reactive protein (CRP) and serum amyloid A (SAA), the prototype acute-phase response proteins, in the context of the varying manifestations associated with Lyme borreliosis.Methods. Circulating concentrations of CRP and SAA in patients with a range of early to late objective manifestations of Lyme disease and in individuals with post-treatment Lyme disease syndrome were compared with those in healthy control groups.Results. CRP and SAA levels were significantly elevated in early localized and early disseminated Lyme disease but not in the later stages of active infection. Levels of CRP, but not SAA, were also found to be significantly increased in patients with antibioticrefractory Lyme arthritis and in those with post-treatment Lyme disease syndrome.Conclusions. These findings indicate that circulating CRP and SAA levels are highest when the concentration of spirochetes is greatest in skin and/or blood and that levels decline after the dissemination of the organism to extracutaneous sites in subsequent stages of infection. The data also suggest that antibiotic-refractory Lyme arthritis and post-treatment Lyme disease syndrome are associated with elevated CRP responses that are driven by inflammatory mechanisms distinct from those in active infection.
“…All three pointed to a lack of substantially enhanced systemic CRP response in most patients with Lyme arthritis [21][22][23], in agreement with our results. A serum analysis in 20 patients with early neurologic Lyme disease reported a lack of increased CRP concentration in most [24], while a study of 44 Lyme disease patients with EM found both CRP and SAA to be significantly elevated in comparison to 23 healthy controls [25].…”
Section: Discussionsupporting
confidence: 92%
“…non-Lyme arthritis, without incorporating healthy controls [21,22], and one study examined CRP levels in 20 Lyme arthritis patients and 10 healthy volunteers [23]. All three pointed to a lack of substantially enhanced systemic CRP response in most patients with Lyme arthritis [21][22][23], in agreement with our results.…”
Background. Infection with Borrelia burgdorferi, the causative agent of Lyme disease, triggers host immune responses that affect the clinical outcome and are a source of biomarkers with diagnostic utility. Although adaptive immunity to B. burgdorferi has been extensively characterized, considerably less information is available about the development of innate acute-phase responses in Lyme disease. Our aim in this study was to evaluate the expression of C-reactive protein (CRP) and serum amyloid A (SAA), the prototype acute-phase response proteins, in the context of the varying manifestations associated with Lyme borreliosis.Methods. Circulating concentrations of CRP and SAA in patients with a range of early to late objective manifestations of Lyme disease and in individuals with post-treatment Lyme disease syndrome were compared with those in healthy control groups.Results. CRP and SAA levels were significantly elevated in early localized and early disseminated Lyme disease but not in the later stages of active infection. Levels of CRP, but not SAA, were also found to be significantly increased in patients with antibioticrefractory Lyme arthritis and in those with post-treatment Lyme disease syndrome.Conclusions. These findings indicate that circulating CRP and SAA levels are highest when the concentration of spirochetes is greatest in skin and/or blood and that levels decline after the dissemination of the organism to extracutaneous sites in subsequent stages of infection. The data also suggest that antibiotic-refractory Lyme arthritis and post-treatment Lyme disease syndrome are associated with elevated CRP responses that are driven by inflammatory mechanisms distinct from those in active infection.
“…In contrast to septic arthritis, Lyme arthritis is not commonly associated with a hot, erythematous, extremely painful joint, or with high fever. In a recent study of acute monarthritis, fever was a negative predictor for Lyme versus septic arthritis and knee involvement was a positive predictor (Thompson et al, 2009).…”
“…The diagnostic yield of synovial fluid white cell count remains controversial, with a few studies suggesting levels >50,000 cells/μL as a threshold for consideration of septic arthritis [37,38]. However, similar results can also be seen in patients with an acute episode of crystal arthropathy [39][40][41] or acute Lyme arthritis [42].…”
Septic arthritis is a common rheumatological emergency requiring prompt diagnosis and treatment, since delays in management can lead to high morbidity and mortality. In this review article, we discuss the epidemiology and recent advances in knowledge of the pathogenesis of septic arthritis, with a special emphasis on various bacterial and host factors involved in mediating the inflammatory process and the potential for targeted therapy to modulate the immune response. Recent advances in laboratory and imaging techniques are reviewed along with treatment and potential new therapies.
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