European society of clinical microbiology and infectious diseases edition:2006, pages:abstract: r2072
ESCMID edition:16the location:Nice, France date:1-4 april 2006
Measurements of C-reactive protein (CRP) are commonly used in clinic to differentiate inflammatory from non-inflammatory conditions. We sought to delineate the clinical significance of extremely elevated CRP levels.
From the 2004 lab files of a university hospital we extracted all patients with at least one CRP value >500 mg/L. We reviewed the electronic records and assessed the clinical diagnosis of the inflammatory event, comorbid conditions and mortality. Infections were differentiated from non-infectious inflammatory conditions.
CRP surpassed 500 mg/L in 212 samples from 130 patients, representing 0.065% of all samples. Median age was 62 years (range, 2–94). In 80% of patients, maximal CRP was reached within the first week of admission. A wide variety of infections caused the CRP elevation in 114 of the 130 patients (88%), with the lower respiratory tract and the abdomen as prevailing foci. In the minority without readily identifiable infection, sterile necrosis, ischaemia or heavy tumour burden were responsible for the excessive acute-phase response. In 88 of 114 (77%) of patients with infection, a causative pathogen could be identified. Apart from 5 mycotic infections, all were bacterial. Blood cultures were positive in 44 of 109 patients (40%), demonstrating gram-negative bacteraemia in 22, gram-positive bacteraemia in 20 and candidaemia in 2. Overall, 47 of the 130 patients (36%) died, mostly within the first month. Mortality was especially high in patients with active cancer (28/46, 61%) and with neutropaenia (11/15, 73%). Of 38 patients without debilitating conditions, 5 died (13%).
A wide variety of mostly bacterial infections, that are generally readily identified, accounts for the majority of cases of extremely elevated CRP. Mortality is high, especially in patients with active malignancies, underscoring the importance of prompt identification and control of the source of inflammation.