Journal
AMERICAN JOURNAL OF MEDICINE
Volume 122, Issue 7, Pages 605-613Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.amjmed.2009.01.030
Keywords
Coagulation; Cytokines; D-dimer; Frailty; Inflammation; Interleukin-6; Sarcopenia; Tumor necrosis factor-alpha
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Funding
- Intramural Research Program, National Institute on Aging (National Institutes of Health)
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There are inevitable physiologic changes associated with advancing age, yet for some people these changes are exaggerated, and as a result a phenotype emerges recognized as frailty. Why some people become frail and others do not remains incompletely understood. Although chronic illnesses are common among frail elderly persons, some will develop all of the phenotypic features without a diagnosed underlying disease. It has been recognized that certain proinflammatory cytokines and coagulation factors are elevated to a greater extent in those who are frail than in age-matched nonfrail individuals. In this review, we provide an overview of current research in the biology of frailty with particular emphasis on the role of inflammatory pathways and disordered coagulation in its pathogenesis. Published by Elsevier Inc. The American Journal of Medicine (2009) 122, 605-613
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