Prevalence and Causes of Anemia in Elderly Hospitalized Patients

Matzner, Yaacov; Levy, S M; Grossowicz, N.; Izak, G.; Hershko, C

doi:10.1159/000212328

Cited by 36 publications

(34 citation statements)

References 8 publications

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“…However, it has limited utility in the context AI when iron is sequestered from iron-dependent host tissues. [30][31][32][33][34] In malaria-endemic areas such as western Kenya, there is growing concern that iron therapy or iron replete state may increase the risk of malaria morbidity, which further supports weighing the costs and benefits of iron provision, particularly in the presence of AI. 35,36 The current therapeutic recommendation for AI is treatment of the underlying infection or condition.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Anemia in Schistosoma mansoni–Infected School Children in Western Kenya

Butler¹,

Muok²,

Montgomery³

et al. 2012

The American Society of Tropical Medicine and Hygiene

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Abstract. A better understanding of the mechanism of anemia associated with Schistosoma mansoni infection might provide useful information on how treatment programs are implemented to minimize schistosomiasis-associated morbidity and maximize treatment impact. We used a cross-sectional study with serum samples from 206 Kenyan school children to determine the mechanisms in S. mansoni-associated anemia. Serum ferritin and soluble transferrin receptor levels were measured by using an enzyme-linked immunosorbent assay. Results suggest that S. mansoni-infected persons are more likely (odds ratio = 3.68, 95% confidence interval = 1.33-10.1) to have levels of serum ferritin ( 100 ng/mL) that are associated with anemia of inflammation (AI) than S. mansoni-uninfected children. Our results suggest that AI is the most common form of anemia in S. mansoni infections. In contrast, the mechanism of anemia in S. mansoni-uninfected children was iron deficiency. Moreover, the prevalence of AI in the study participants demonstrated a significant trend with S. mansoni infection intensity (P 0.001). Our results are consistent with those observed in S. japonicum-associated anemia.

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Section: Discussionmentioning

confidence: 99%

Mechanism of Anemia in Schistosoma mansoni–Infected School Children in Western Kenya

Butler¹,

Muok²,

Montgomery³

et al. 2012

The American Society of Tropical Medicine and Hygiene

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“…1,2 ACD develops in subjects with diseases involving acute or chronic immune activation, such as patients with infections, malignancies, or autoimmune disorders. At least 3 major immunitydriven mechanisms contribute to the anemia of ACD.…”

Section: Introductionmentioning

confidence: 99%

Regulation of iron homeostasis in anemia of chronic disease and iron deficiency anemia: diagnostic and therapeutic implications

Theurl

Aigner

Theurl

et al. 2009

Blood

356

352

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The anemia of chronic disease (ACD) is characterized by macrophage iron retention induced by cytokines and the master regulator hepcidin. Hepcidin controls cellular iron efflux on binding to the iron export protein ferroportin. Many patients, however, present with both ACD and iron deficiency anemia (ACD/IDA), the latter resulting from chronic blood loss. We used a rat model of ACD resulting from chronic arthritis and mimicked ACD/IDA by additional phlebotomy to define differing iron-regulatory pathways. Iron retention during inflammation occurs in macrophages and the spleen, but not in the liver. In rats and humans with ACD, serum hepcidin concentrations are elevated, which is paralleled by reduced duodenal and macrophage expression of ferroportin. Individuals with ACD/IDA have significantly lower hepcidin levels than ACD subjects, and ACD/IDA persons, in contrast to ACD subjects, were able to absorb dietary iron from the gut and to mobilize iron from macrophages. Circulating hepcidin levels affect iron traffic in ACD and ACD/IDA and are more responsive to the erythropoietic demands for iron than to inflammation. Hepcidin determination may aid to differentiate between ACD and ACD/IDA and in selecting appropriate therapy for these patients. IntroductionThe anemia of chronic disease (ACD), also termed the "anemia of inflammation," is the most prevalent anemia in hospitalized patients. 1,2 ACD develops in subjects with diseases involving acute or chronic immune activation, such as patients with infections, malignancies, or autoimmune disorders. At least 3 major immunitydriven mechanisms contribute to the anemia of ACD.First, the retention of iron within the mononuclear phagocytic system leads to hypoferremia and subnormal saturation of transferrin, resulting in a limited availability of iron for erythroid progenitor cells or "functional iron deficiency." 1,3,4 Second, cytokines, such as tumor necrosis factor-␣, interferon-␥, and interleukin-1 (IL-1), exert a negative impact on the proliferation and differentiation of erythroid progenitor cells and can induce apoptosis. 5 Third, patients with ACD display an impaired response to erythropoietin (EPO). 6 The functional iron deficiency present in patients with ACD can be complicated by true iron deficiency resulting from chronic blood loss. 7 Differentiation between ACD and ACD/iron deficiency anemia (IDA) is clinically important because iron supplementation is beneficial for ACD/IDA patients but may be deleterious for ACD patients, especially if these subjects have underlying infections or malignancies. 1 In clinical practice, however, differentiating between ACD and ACD/IDA is difficult, as both diseases present with decreased serum iron concentration and transferrin saturation. In addition, ferritin levels are difficult to interpret during inflammation because ferritin expression is induced by both iron overload and inflammatory cytokines. 8 A ratio of soluble transferrin receptor (sTfR)/log ferritin may be useful in distinguishing ACD from ACD/IDA, but the ratio h...

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“…Anemia of chronic disease (ACD), also termed anemia of chronic inflammation, is the most prevalent anemia among hospitalized patients 1,2 and is primarily found in subjects suffering from diseases with associated chronic immune activation, such as cancer, auto-immune diseases, chronic infection or dialysis-dependent renal failure. [1][2][3][4][5] A central mechanism by which chronic immune activation causes anemia is the retention of iron in the reticuloendothelial system, [6][7][8][9] causing a "functional iron deficiency" and consequently an insufficient iron supply for erythropoiesis.…”

Section: Introductionmentioning

confidence: 99%

“…[1][2][3][4][5] A central mechanism by which chronic immune activation causes anemia is the retention of iron in the reticuloendothelial system, [6][7][8][9] causing a "functional iron deficiency" and consequently an insufficient iron supply for erythropoiesis. 10 In addition, cytokine-mediated effects on erythropoietin functionality and erythrocyte half-life, along with antiproliferative effects of cytokines and radicals on the proliferation and differentiation of erythroid progenitors, further contribute to the pathogenesis of ACD/anemia of chronic inflammation.…”

Section: Introductionmentioning

confidence: 99%

“…29,30 treatment of anemia with erythropoiesis-stimulating agents (ESA; epoetin or darbepoetin alfa) was introduced into clinical practice. This therapy can significantly improve patients' quality of life 29,30 but can also result in undesirable side effects, such as thrombophilia, stroke and death, as observed in cancer patients or subjects Hepcidin as a predictive factor and therapeutic target in erythropoiesisstimulating agent treatment for anemia of chronic disease in rats Milan Theurl, 1,2 Manfred Nairz, 1 Andrea Schroll, 1 Thomas Sonnweber, 1 Malte Asshoff, 1 David Haschka, 1 Markus Seifert, Furthermore, ESA treatment is ineffective in some patients suffering from ACD/anemia of chronic inflammation, 2,4 even if true iron deficiency has been ruled out. 34 Clinically useful biomarkers which predict the efficacy of ESA treatment are desirable, but have not been identified thus far.…”

Section: Introductionmentioning

confidence: 99%

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Hepcidin as a predictive factor and therapeutic target in erythropoiesis-stimulating agent treatment for anemia of chronic disease in rats

et al. 2014

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Prevalence and Causes of Anemia in Elderly Hospitalized Patients

Cited by 36 publications

References 8 publications

Mechanism of Anemia in Schistosoma mansoni–Infected School Children in Western Kenya

Mechanism of Anemia in Schistosoma mansoni–Infected School Children in Western Kenya

Regulation of iron homeostasis in anemia of chronic disease and iron deficiency anemia: diagnostic and therapeutic implications

Hepcidin as a predictive factor and therapeutic target in erythropoiesis-stimulating agent treatment for anemia of chronic disease in rats

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