Authors' reply

Patel, Praful; Mendall, Michael A.; Carrington, David; Strachan, D. P.; Leatham, E; Molineaux, N.; Levy, J.; Blakeston, C; Seymour, Carol A.; Camm, A. John; Northfield, T. C.

doi:10.1136/bmj.312.7025.252

Cited by 1 publication

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“…The prospective data of Ridker et al (Physician Health First, chronic infections that cause a rise in circulating CRP also yield a higher risk for cardiovascular disease Study) provide convincing evidence that the baseline plasma concentrations of CRP in apparently healthy men [46][47][48]. Second, CRP is a cardiovascular risk factor even after correction for other risk factors [41].…”

Section: Structure and Function Of C-reactive Proteinmentioning

confidence: 99%

The link of biocompatibility to cytokine production

Panichi¹,

Migliori²,

Pietro³

et al. 2000

Kidney International

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The link of biocompatibility to cytokine production. Recent reactants (APRs), and the magnitude and rapidity of studies suggest that chronic inflammation plays a role in the their induction following an acute phase response, topathogenesis of cardiovascular disease. Cytokines released from gether with their short half-life, suggest a particularly critijeopardized tissues stimulate the liver to synthesize acute phase cal requirement in the establishment of host defense [2, 3]. proteins, including C-reactive protein (CRP). Baseline levels of More recently, the acute phase response has been CRP in apparently healthy persons or in persons with unstable angina constitute an independent risk factor for cardiovascular more narrowly defined as the change in concentrations events. More recently, it has been suggested that CRP is useful of a number of plasma protein that results largely from not only as a marker of the acute phase response, but is also a rearrangement of plasma protein synthesis in hepatoinvolved in the pathogenesis of the disease. CRP may, in fact, cytes. The proteins that manifest substantial change in directly interact with the atherosclerotic vessels or ischemic myocardium by activation of the complement system, thereby concentrations are referred to as the APRs (Fig. 1) [4, 5]. promoting inflammation and thrombosis. Several studies in Ceruloplasmin and the complement component C3 uremic patients have implicated CRP as a marker of malnutriand C4 typically display only a modest acute phase retion, resistance to erythropoietin, and chronic stimulation in sponse, while aptoglobin and fibrinogen may increase twohemodialysis. An increased cytokine production secondary to fold to fivefold. blood interaction with bioincompatible dialysis components has been reported by several studies; interleukin-1 (IL-1), tumor

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Section: Structure and Function Of C-reactive Proteinmentioning

confidence: 99%