Anemia in frailty

Abstract

Although anemia is regarded as a relatively common occurrence in older adults, the vigor with which the medical community should intervene to correct this common problem is disputed. Epidemiologic data clearly correlate anemia with functional decline, disability, and mortality. Anemia may contribute to functional decline by restricting oxygen delivery to muscle, or to cognitive decline by restricting oxygen delivery to the brain. On the other hand, the erythron may be a separate target of the same biologic mediators that influence deterioration of physiologic systems that contribute to weakness, functional and cognitive decline, and mortality. Clinical trials aimed at treating anemia in older adults could assess whether physical performance is improved or whether mortality risk declines with improved hemoglobin, but sufficient evidence from such trials is currently lacking. With few guidelines regarding treatment of older adults and significant risk for adverse events associated with transfusion and erythroid stimulating agents, anemia often goes untreated or ignored in geriatric clinics. This article reviews the problem of anemia in older adults, with a particular emphasis on the frail elderly. The gaps in the evidence base for the treatment of anemia in older adults are reviewed and the options for advancing the field are assessed.

Figure 1. Overview of NFkB and Chronic Inflammation

Type I acute phase cytokines, tumor necrosis factor α (TNFα), interleukin-1 (IL-1); signaling through the toll like receptors (TLR); and reactive oxygen species (ROS) all induce translocation of NFkB (p65/p50) to the nucleus where it induces transcription of the chemokines IL-8 and Monocyte Chemoattractant Protein 1 (MCP1) as well as the proinflammatory cytokine IL-6. Increased circulating neutrophils, increased circulating monocytes and increased IL-6 are all markers of aging and a central piece of the frailty phenotype (Courtesy of Cindy N. Roy, PhD, Baltimore, MD)