Systematic Review of the Evidence of a Relationship Between Chronic Psychosocial Stress and C-Reactive Protein
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REVIEW ARTICLE
Systematic Review of the Evidence of a Relationship Between Chronic Psychosocial Stress and C-Reactive Protein Timothy V. Johnson • Ammara Abbasi Viraj A. Master
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Published online: 25 April 2013 Ó Springer International Publishing Switzerland 2013
Abstract Introduction C-reactive protein (CRP) is an acute-phase reactant with an increasing number of clinical functions. Studies in recent years have identified several social, economic, demographic, and psychological factors that contribute to baseline inflammation. Psychosocial stress represents a significant contributor to baseline inflammation. Given the importance of understanding background drivers of CRP levels, we conducted this review to assess the impact of chronic psychosocial stress on CRP levels. Methods Medline was searched through February 2013 for human studies examining CRP levels with respect to chronic psychosocial stress. Results The initial search identified 587 articles from which 129 potentially appropriate articles were reviewed. Of these 129 articles, 40 articles were included in the review. These studies were published between 2003 and 2013. Of these studies, 6 analyzed employment stress, 2 analyzed unemployment stress, 6 analyzed burnout and vital exhaustion, 6 analyzed caregiver stress, 3 analyzed interpersonal stress, 17 analyzed socioeconomic position, and 2 analyzed discrimination. T. V. Johnson Wills Eye Institute, Thomas Jefferson University, Philadelphia, PA, USA T. V. Johnson (&) 1365 Clifton Road NE, Atlanta, GA 30322, USA e-mail: [email protected] A. Abbasi V. A. Master Department of General Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA V. A. Master Winship Cancer Institute, Emory University, Atlanta, GA, USA
Conclusion We conclude that psychosocial stress significantly impacts CRP and should be considered when interpreting the meaning of CRP elevations.
1 Introduction C-reactive protein (CRP) is an acute-phase reactant produced primarily by the liver under the regulation of interleukin-6 (IL-6) [1, 2]. CRP binds microbial cell walls and cell membrane components, along with nuclear antigens, to facilitate phagocytosis through innate immunity [2]. CRP levels vary depending on genetic and environmental factors. In healthy individuals, CRP levels fluctuate between 0.1 and 10 mg/L [3, 4]. However, in response to many pathological states, CRP plasma levels can increase 1,000fold [2]. Consequently, CRP represents a potent marker of inflammation. CRP serves several clinical functions. For example, CRP levels in pediatric populations aid in the diagnosis of microbial infections [5, 6]. Preoperative and postoperative CRP levels also predict outcomes in malignancy and heart disease [7–9]. Finally, persistent elevations suggest treatment failure in malignancies and metastasis [7]. Important clinical decisions increasingly rely on individual and changes in CRP measurements. However, baseline inflammation responds to more than traditional pathological states. Studies in recent
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