High-Sensitivity C-Reactive Protein Levels and Cancer Mortality

Abstract

Background: High-sensitivity C-reactive protein (hs-CRP) is an important inflammatory marker, and inflammation is known to be involved in the initiation and progression of cancer. We investigated the association between serum hs-CRP levels and all-cause mortality, cancer mortality, and site-specific cancer mortality in apparently cancer-free Koreans.Methods: A total of 33,567 participants who underwent routine check-ups at a single tertiary hospital healthscreening center between May 1995 and December 2006, and whose serum hs-CRP level data were available, were included in the study. Baseline serum hs-CRP levels were obtained and subjects were followed up for mortality from baseline examination until December 31, 2008.Results: During an average follow-up of 9.4 years, 1,054 deaths, including 506 cancer deaths, were recorded. The adjusted HRs (aHR; 95% confidence interval [CI]) of subjects with hs-CRP !3 mg/L for all-cause and cancer-related mortality were 1.38 (1.15-1.66) and 1.61 (1.25-2.07) in men, and 1.29 (0.94-1.77) and 1.24 (0.75-2.06) in women, respectively, compared with subjects with hs-CRP 1 mg/L. Elevated hs-CRP was also associated with an increased risk of site-specific mortality from lung cancer for sexes combined (2.53 [1.57- 4.06]).Conclusions: This study suggests that elevated levels of hs-CRP in apparently cancer-free individuals may be associated with increased mortality from all-causes and cancer, in particular, lung cancer in men, but not in women.Impact: As a marker for chronic inflammation, hs-CRP assists in the identification of subjects with an increased risk of cancer death. Cancer Epidemiol Biomarkers Prev; 21(11); 2076-86. Ó2012 AACR.

Self-rated health and C-reactive protein in young adults

“…Indeed, one study reported that among individuals with less than “very good” self-rated health, men were more likely to die from cancer and also heart disease than women (Benjamins et al, 2004)—and both of these conditions are also associated with elevated hs-CRP (e.g., Ko et al, 2012; Ridker, 2007; Shah et al, 2009). …”

A review of the Hispanic paradox: time to spill the beans?

“…In several prospective studies, elevated markers of systemic inflammation have been repeatedly associated with a decline in lung function in young adults [17][18][19] and COPD in adults [20][21][22]. Similarly, in numerous prospective studies of cancer, elevated systemic markers have been associated with the development of lung cancer 5-15 years later [23][24][25][26][27]. Further evidence supporting a role for systemic inflammation in COPD and lung cancer comes from animal studies showing overexpression of IL-6 is linked to the development of COPD and that systemic inflammation in a nonsmoking murine model is linked to innate immune response-mediated DNA damage in the bronchial epithelium [28][29][30][31].…”

“…This increase in systemic inflammation may result from either an overactive bronchial epithelial response to smoking or an underlying primary hyper-immune response of the innate immune system, or both [28][29][30][31]. Support for the latter comes from studies showing systemic inflammation is linked to many cancers, where smoking (or obesity) are known risk factors, although the link is strongest for lung cancer [23][24][25][26][27]. Systemic inflammation, to varying degrees, affects between 50% and 70% of those with COPD and lung cancer [20,22,26].…”

“…4) [15][16][17][18][19][20][21][22][23][24][25][26][27]. Moreover, a reduction in IL-6-mediated systemic inflammation, through the use of HMGCoA reductase inhibitors (statins), has been closely linked to improved outcomes and reduced mortality in COPD, and to reduced mortality and prevalence of lung cancer [16,32].…”

The 2014 National Nursing Research Roundtable: The science of caregiving

“…He noted that there are more than 10 million dementia caregivers, and they have a 63% higher mortality risk than noncaregivers (Schulz & Beach, 1999), with some of this increased risk associated with increased inflammation (Frasure-Smith et al, 2007; Ko et al, 2012; Ridker, Hennekens, Buring, & Rifai, 2000). …”