The American Journal of Medicine
Volume 122, Issue 7 , Pages 605-613, July 2009

Inflammation, Coagulation, and the Pathway to Frailty

  • Bindu Kanapuru, MD
    • ,
  • William B. Ershler, MD

      Affiliations

    • Corresponding Author InformationRequests for reprints should be addressed to William B. Ershler, MD, National Institute on Aging, Harbor Hospital, 3001 S. Hanover St, Baltimore, MD 212225

Clinical Research Branch, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD

Abstract 

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.

Keywords: Coagulation, Cytokines, D-dimer, Frailty, Inflammation, Interleukin-6, Sarcopenia, Tumor necrosis factor-α

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 Funding: This work was supported by the Intramural Research Program, National Institute on Aging (National Institutes of Health).

 Conflict of Interest: None.

 Authorship: All authors had access to the data and played a role in writing this manuscript.

PII: S0002-9343(09)00288-5

doi:10.1016/j.amjmed.2009.01.030

The American Journal of Medicine
Volume 122, Issue 7 , Pages 605-613, July 2009

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