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      Anemia in the Elderly

      review-article
      Author(s):   1 , 1 , 2
      Publication date (Electronic):
      Journal: HemaSphere
      Publisher: Wolters Kluwer Health

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          Abstract

          Anemia affects a substantial fraction of the elderly population, representing a public health problem that is predicted to further increase in coming years because of the demographic drive. Being typically mild, it is falsely perceived as a minor problem, particularly in the elderly with multimorbidity, so that it often remains unrecognized and untreated. Indeed, mounting evidence indicates that anemia in the elderly (AE) is independently associated with disability and other major negative outcomes, including mortality. AE is generally multifactorial, but initial studies suggested that etiology remains unexplained in near one-third of cases. This proportion is consistently declining due to recent advances highlighting the role of several conditions including clonal hematopoiesis, “inflammaging,” correctable androgen deficiency in men, and under-recognized iron deficiency. Starting from a real-world case vignette illustrating a paradigmatic example of anemia in an elderly patient with multimorbidity, we review the main clinical and pathophysiological aspect of AE, giving some practical insights into how to manage similar cases.

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          Inflamm-aging. An evolutionary perspective on immunosenescence.

          C Franceschi, M BonaFe, S Valensin … (2000)
          In this paper we extend the "network theory of aging," and we argue that a global reduction in the capacity to cope with a variety of stressors and a concomitant progressive increase in proinflammatory status are major characteristics of the aging process. This phenomenon, which we will refer to as "inflamm-aging," is provoked by a continuous antigenic load and stress. On the basis of evolutionary studies, we also argue that the immune and the stress responses are equivalent and that antigens are nothing other than particular types of stressors. We also propose to return macrophage to its rightful place as central actor not only in the inflammatory response and immunity, but also in the stress response. The rate of reaching the threshold of proinflammatory status over which diseases/disabilities ensue and the individual capacity to cope with and adapt to stressors are assumed to be complex traits with a genetic component. Finally, we argue that the persistence of inflammatory stimuli over time represents the biologic background (first hit) favoring the susceptibility to age-related diseases/disabilities. A second hit (absence of robust gene variants and/or presence of frail gene variants) is likely necessary to develop overt organ-specific age-related diseases having an inflammatory pathogenesis, such as atherosclerosis, Alzheimer's disease, osteoporosis, and diabetes. Following this perspective, several paradoxes of healthy centenarians (increase of plasma levels of inflammatory cytokines, acute phase proteins, and coagulation factors) are illustrated and explained. In conclusion, the beneficial effects of inflammation devoted to the neutralization of dangerous/harmful agents early in life and in adulthood become detrimental late in life in a period largely not foreseen by evolution, according to the antagonistic pleiotropy theory of aging.
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            Clinical effect of point mutations in myelodysplastic syndromes.

            Rafael Bejar, Kristen Stevenson, Omar Abdel-Wahab … (2011)
            Myelodysplastic syndromes are clinically heterogeneous disorders characterized by clonal hematopoiesis, impaired differentiation, peripheral-blood cytopenias, and a risk of progression to acute myeloid leukemia. Somatic mutations may influence the clinical phenotype but are not included in current prognostic scoring systems. We used a combination of genomic approaches, including next-generation sequencing and mass spectrometry-based genotyping, to identify mutations in samples of bone marrow aspirate from 439 patients with myelodysplastic syndromes. We then examined whether the mutation status for each gene was associated with clinical variables, including specific cytopenias, the proportion of blasts, and overall survival. We identified somatic mutations in 18 genes, including two, ETV6 and GNAS, that have not been reported to be mutated in patients with myelodysplastic syndromes. A total of 51% of all patients had at least one point mutation, including 52% of the patients with normal cytogenetics. Mutations in RUNX1, TP53, and NRAS were most strongly associated with severe thrombocytopenia (P<0.001 for all comparisons) and an increased proportion of bone marrow blasts (P<0.006 for all comparisons). In a multivariable Cox regression model, the presence of mutations in five genes retained independent prognostic significance: TP53 (hazard ratio for death from any cause, 2.48; 95% confidence interval [CI], 1.60 to 3.84), EZH2 (hazard ratio, 2.13; 95% CI, 1.36 to 3.33), ETV6 (hazard ratio, 2.04; 95% CI, 1.08 to 3.86), RUNX1 (hazard ratio, 1.47; 95% CI, 1.01 to 2.15), and ASXL1 (hazard ratio, 1.38; 95% CI, 1.00 to 1.89). Somatic point mutations are common in myelodysplastic syndromes and are associated with specific clinical features. Mutations in TP53, EZH2, ETV6, RUNX1, and ASXL1 are predictors of poor overall survival in patients with myelodysplastic syndromes, independently of established risk factors. (Funded by the National Institutes of Health and others.).
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              Inflammaging and 'Garb-aging'.

              Claudio Franceschi, Paolo Garagnani, Giovanni Vitale … (2017)
              'Inflammaging' refers to the chronic, low-grade inflammation that characterizes aging. Inflammaging is macrophage centered, involves several tissues and organs, including the gut microbiota, and is characterized by a complex balance between pro- and anti-inflammatory responses. Based on literature data, we argue that the major source of inflammatory stimuli is represented by endogenous/self, misplaced, or altered molecules resulting from damaged and/or dead cells and organelles (cell debris), recognized by receptors of the innate immune system. While their production is physiological and increases with age, their disposal by the proteasome via autophagy and/or mitophagy progressively declines. This 'autoreactive/autoimmune' process fuels the onset or progression of chronic diseases that can accelerate and propagate the aging process locally and systemically. Consequently, inflammaging can be considered a major target for antiaging strategies.
              Article 0 comments Cited 340 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Hemasphere
                Journal ID (iso-abbrev): Hemasphere
                Journal ID (publisher-id): HS9
                Title: HemaSphere
                Publisher: Wolters Kluwer Health
                ISSN (Electronic): 2572-9241
                Publication date (Electronic): 17 April 2018
                Publication date Collection: June 2018
                Volume: 2
                Issue: 3
                Electronic Location Identifier: e40
                Affiliations
                [1 ]Department of Medicine, Section of Internal Medicine, University of Verona, Verona, Italy
                [2 ]Division of Genetics and Cell Biology, San Raffaele Scientific Institute, Milan, Italy.
                Author notes
                Correspondence: Domenico Girelli (e-mail: domenico.girelli@ 123456univr.it ).
                Article
                Publisher ID: HEMASPHERE-2018-0020 Accession ID: 006
                DOI: 10.1097/HS9.0000000000000040
                PMC ID: 6745992
                PubMed ID: 31723768
                SO-VID: 506c6f63-52f9-429d-bf8d-2c6ccb501e07
                Copyright © Copyright © 2018 the Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the European Hematology Association.
                License:

                This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0

                History
                Date received : 30 January 2018
                Date revision received : 19 March 2018
                Date accepted : 19 March 2018
                Categories
                Subject: Reviews
                Custom metadata
                OPEN-ACCESS TRUE

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