Expression of C-Reactive Protein and Serum Amyloid A in Early to Late Manifestations of Lyme Disease.
Expression of C-Reactive Protein and Serum Amyloid A in Early to Late Manifestations of Lyme Disease.
复制标题
莱姆病早期到晚期表现中 C 反应蛋白和血清淀粉样蛋白 A 的表达。
DOI:
10.1093/cid/ciw599
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发表时间:
2016
期刊:
影响因子:
--
通讯作者:
Alaedini,Armin
中科院分区:
文献类型:
--
作者:
Uhde,Melanie;Ajamian,Mary;Li,Xueting;Wormser,GaryP;Marques,Adriana;Alaedini,Armin
BackgroundInfection withBorrelia 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 toB. burgdorferihas 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.MethodsCirculating 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.ResultsCRP 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 antibiotic-refractory Lyme arthritis and in those with post-treatment Lyme disease syndrome.ConclusionsThese 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.