BACKGROUND: C-reactive protein (CRP), an acutephase protein , is a sensitive systemic marker of inflammation and acute-phase reactions. Testing C-Reactive Protein CRP concentrations at hospital admission may provide information about disease risk and overall survival.
METHODS: All first-ever transmittals to the department of medical and chemical laboratory diagnostics for determination of low-sensitivity CRP (n = 274 515, 44.5% male, median age 51 years) between January 1991 and July 2003 were included [median follow-up time: 4.4 years (interquartile range, 2.3-7.4 years)]. The primary endpoint was all-cause mortality. Multivariate Cox regression adjusted for sex and age was applied for analysis.
RESULTS: Compared to individuals within the reference category (CRP <5 mg/L), hazard ratios (HR) for all-cause mortality increased from 1.4 (5-10 mg/L category) to 3.3 in the highest category (>80 mg/L, all P <0.001). CRP was associated with various causes of death. The relation of CRP to cancer death was stronger than to vascular death . Younger patients with increased CRP had relatively far worse outcome than older patients (maximal HR: 60 years: 1.7-3.7). Interestingly, both short- and long-term mortality were associated with increasing CRP concentrations (>80 mg/L: HR 22.8 vs 1.4).
CONCLUSION: Measurement of low-sensitivity CRP at hospital admission allowed for the identification of patients at increased risk of unfavorable outcome. Our findings indicate that close attention should be paid to hospitalized patients with high C-reactive protein not only because of very substantial short-term risk, but also long-term excess risk, the basis for which needs to be determined.
Marsik C, Kazemi-Shirazi L, Joukhadar C, Schickbauer T, Winkler S, Wagner OF, Endler G. Department of Medical and Chemical Laboratory Diagnostics. Clin Chem. 2007 Dec 21
Wednesday
Strawberry Intake, Lipids, C-Reactive Protein, and the Risk of Cardiovascular Disease in Women
Objective: There is indirect evidence suggesting that strawberries, containing several key nutrients, may be associated with the risk of cardiovascular disease (CVD). In the Women’s Health Study, we examined strawberry intake for both its prospective association with CVD risk in 38,176 women and its cross-sectional association with lipids and C-reactive protein (CRP) in a subset of 26,966 women.
Methods: Strawberry intake was assessed from a baseline semiquantitative food frequency questionnaire, along with other self-reported lifestyle, clinical and dietary factors. Participants returned baseline bloods which were assayed for lipids and CRP . We computed the relative risks (RRs) for total CVD (1,004 cases) (including confirmed myocardial infarction , stroke, revascularization , and cardiovascular death) occurring during 10.9 years of follow-up.
Results: At baseline, 25.6%, 41.9%, 24.8%, and 7.7% of women reported corresponding strawberry intake of none, 1–3 servings/month, 1 serving/week, and 2 servings/week. For total CVD, the multivariate RRs (95% confidence intervals) for increasing categories of strawberry intake were 1.00 (ref), 1.01 (0.85–1.19), 0.95 (0.77–1.17), and 1.27 (0.94–1.72) (P, trend = 0.06). We found a similar lack of an association for individual cardiovascular endpoints and comparing mean levels of lipids and C-reactive protein by category of strawberry intake. However, women consuming 2 servings/week versus none had a borderline significant, multivariate 14% lower likelihood of an elevated C-reactive protein of 3 mg/L.
Conclusions: Strawberry intake was unassociated with the risk of incident CVD, lipids , or CRP in middle-aged and older women, though higher strawberry intake may slightly reduce the likelihood of having elevated C-reactive protein levels. Additional epidemiologic data are needed to clarify any role of strawberries in CVD prevention.
Journal of the American College of Nutrition, Vol. 26, No. 4, 303-310 (2007)
Published by the American College of Nutrition
Divisions of Preventive Medicine and Aging, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School (H.D.S., J.M.G., J.E.B)
Department of Ambulatory Care and Prevention, Harvard Medical School (J.E.B)
Department of Epidemiology, Harvard School of Public Health (H.D.S., J.E.B.), Boston, MA
Clinical Nutrition and Risk Factor Modification Center, St Michael’s Hospital (D.J.A.J.), Toronto, Ontario, CANADA
Methods: Strawberry intake was assessed from a baseline semiquantitative food frequency questionnaire, along with other self-reported lifestyle, clinical and dietary factors. Participants returned baseline bloods which were assayed for lipids and CRP . We computed the relative risks (RRs) for total CVD (1,004 cases) (including confirmed myocardial infarction , stroke, revascularization , and cardiovascular death) occurring during 10.9 years of follow-up.
Results: At baseline, 25.6%, 41.9%, 24.8%, and 7.7% of women reported corresponding strawberry intake of none, 1–3 servings/month, 1 serving/week, and 2 servings/week. For total CVD, the multivariate RRs (95% confidence intervals) for increasing categories of strawberry intake were 1.00 (ref), 1.01 (0.85–1.19), 0.95 (0.77–1.17), and 1.27 (0.94–1.72) (P, trend = 0.06). We found a similar lack of an association for individual cardiovascular endpoints and comparing mean levels of lipids and C-reactive protein by category of strawberry intake. However, women consuming 2 servings/week versus none had a borderline significant, multivariate 14% lower likelihood of an elevated C-reactive protein of 3 mg/L.
Conclusions: Strawberry intake was unassociated with the risk of incident CVD, lipids , or CRP in middle-aged and older women, though higher strawberry intake may slightly reduce the likelihood of having elevated C-reactive protein levels. Additional epidemiologic data are needed to clarify any role of strawberries in CVD prevention.
Journal of the American College of Nutrition, Vol. 26, No. 4, 303-310 (2007)
Published by the American College of Nutrition
Divisions of Preventive Medicine and Aging, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School (H.D.S., J.M.G., J.E.B)
Department of Ambulatory Care and Prevention, Harvard Medical School (J.E.B)
Department of Epidemiology, Harvard School of Public Health (H.D.S., J.E.B.), Boston, MA
Clinical Nutrition and Risk Factor Modification Center, St Michael’s Hospital (D.J.A.J.), Toronto, Ontario, CANADA
Friday
Serum C-reactive protein response to percutaneous coronary intervention in patients with unstable or stable angina pectoris is associated with the ris
Abstract
Inflammation plays a pivotal role in the pathogenesis of atherosclerosis. Previous reports have used vaccination as a model to stimulate inflammation. The aim of the present study was to investigate the role of C-reactive protein response to PCI in the risk of clinical restenosis or new coronary stenosis, considering PCI as a model to stimulate inflammation.
Material and methods
Eight hundred and ninety-one patients with stable or unstable angina pectoris and with normal serum troponin T ≤ 0.03 μg/L before PCI were investigated. The survivors after a follow-up period of 2.6 years (850 patients) were included. Serum C-reactive Protein CRP and troponin T concentration were measured before and the day after PCI. Restenosis and new coronary stenosis, detected by coronary angiography due to symptomatic coronary heart disease, were determined.
Results
C-reactive Protein response to PCI, unstable angina pectoris, the number of vessels dilated and lack of stent implantation were associated with restenosis or new coronary stenosis. In multivariate analysis, patients in the highest tertile of CRP, induced by PCI, had an increased risk (risk ratio 1.7 [95% CI 1.1–2.9]) for restenosis or new coronary stenosis. Furthermore, patients with restenosis had an increased CRP response to PCI compared with those with new coronary stenosis.
Conclusion
The C-reactive Protein response to PCI, as a model to stimulate inflammation, is associated with an increased risk of clinical restenosis. The results emphasize the role of CRP in the pathogenesis of coronary artery disease progression and in particular restenosis.
Atherosclerosis
Volume 195, Issue 2, December 2007, Pages 374-378
i:10.1016/j.atherosclerosis.2006.10.026
aKarolinska University Hospital, Karolinska Institute, Stockholm, Sweden
Inflammation plays a pivotal role in the pathogenesis of atherosclerosis. Previous reports have used vaccination as a model to stimulate inflammation. The aim of the present study was to investigate the role of C-reactive protein response to PCI in the risk of clinical restenosis or new coronary stenosis, considering PCI as a model to stimulate inflammation.
Material and methods
Eight hundred and ninety-one patients with stable or unstable angina pectoris and with normal serum troponin T ≤ 0.03 μg/L before PCI were investigated. The survivors after a follow-up period of 2.6 years (850 patients) were included. Serum C-reactive Protein CRP and troponin T concentration were measured before and the day after PCI. Restenosis and new coronary stenosis, detected by coronary angiography due to symptomatic coronary heart disease, were determined.
Results
C-reactive Protein response to PCI, unstable angina pectoris, the number of vessels dilated and lack of stent implantation were associated with restenosis or new coronary stenosis. In multivariate analysis, patients in the highest tertile of CRP, induced by PCI, had an increased risk (risk ratio 1.7 [95% CI 1.1–2.9]) for restenosis or new coronary stenosis. Furthermore, patients with restenosis had an increased CRP response to PCI compared with those with new coronary stenosis.
Conclusion
The C-reactive Protein response to PCI, as a model to stimulate inflammation, is associated with an increased risk of clinical restenosis. The results emphasize the role of CRP in the pathogenesis of coronary artery disease progression and in particular restenosis.
Atherosclerosis
Volume 195, Issue 2, December 2007, Pages 374-378
i:10.1016/j.atherosclerosis.2006.10.026
aKarolinska University Hospital, Karolinska Institute, Stockholm, Sweden
Thursday
Human C-Reactive Protein Latest Research
THE LATEST IN Human C-Reactive Protein (CRP) Research:
Transgenic expression of human C-Reactive Protein suppresses endothelial nitric oxide synthase expression and bioactivity after vascular injury .These in vivo observations support the hypothesis that C-reactive Protein modulates NO metabolism and may have implications regarding the mechanisms by which CRP modulates vascular disease. Source: Am J Physiol Heart Circ Physiol 293: H489-H495, 2007
human C-Reactive Protein Binds Activating Fcγ Receptors and Protects Myeloma Tumor Cells from Apoptosis. human C-Reactive Protein also enhanced myeloma cell secretion of IL-6 and synergized with IL-6 to protect myeloma cells from chemotherapy drug-induced apoptosis. Thus, our results implicate CRP as a potential target for cancer treatment.Source: Cancer Cell, Vol 12, 252-265, 11 September 2007
Transgenic expression of human C-Reactive Protein suppresses endothelial nitric oxide synthase expression and bioactivity after vascular injury .These in vivo observations support the hypothesis that C-reactive Protein modulates NO metabolism and may have implications regarding the mechanisms by which CRP modulates vascular disease. Source: Am J Physiol Heart Circ Physiol 293: H489-H495, 2007
human C-Reactive Protein Binds Activating Fcγ Receptors and Protects Myeloma Tumor Cells from Apoptosis. human C-Reactive Protein also enhanced myeloma cell secretion of IL-6 and synergized with IL-6 to protect myeloma cells from chemotherapy drug-induced apoptosis. Thus, our results implicate CRP as a potential target for cancer treatment.Source: Cancer Cell, Vol 12, 252-265, 11 September 2007
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