Iron and anemia in human biology: a review of mechanisms

Abstract

The biology of iron in relation to anemia is best understood by a review of the iron cycle, since the majority of iron for erythropoiesis is provided by iron recovered from senescent erythrocytes. In iron-deficiency anemia, storage iron declines until iron delivery to the bone marrow is insufficient for erythropoiesis. This can be monitored with clinical indicators, beginning with low plasma ferritin, followed by decreased plasma iron and transferrin saturation, and culminating in red blood cells with low-Hb content. When adequate dietary iron is provided, these markers show return to normal, indicating a response to the dietary supplement. Anemia of inflammation (also known as anemia of chronic disease, or ACD) follows a different course, because in this form of anemia storage iron is often abundant but not available for erythropoiesis. The diagnosis of ACD is more difficult than the diagnosis of iron-deficiency anemia, and often the first identified symptom is the failure to show a response to a dietary iron supplement. Confirmation of ACD is best obtained from elevated markers of inflammation. The treatment of ACD, which typically employs erythropoietin (EPO) supplements and intravenous iron (i.v.-iron), is empirical and often falls shorts of therapeutic goals. Dialysis patients show a complex pattern of anemia, which results from inadequate EPO production by the kidney, inflammation, changes in nutrition, and blood losses during treatment. EPO and i.v.-iron are the mainstays of treatment. Patients with heart failure can be anemic, with incidence as high as 50%. The causes are multifactorial; inflammation now appears to be the primary cause of this form of anemia, with contributions from increased plasma volume, effects of drug therapy, and other complications of heart disease. Discerning the mechanisms of anemia for the heart failure patient may aid rational therapy in each case.

Evaluation of the Debye temperature for iron cores in human liver ferritin and its pharmaceutical analogue, Ferrum Lek, using Mössbauer spectroscopy

“…However, iron concentrations in body tissues must be strictly regulated because excessive iron leads to tissue damage, as a result of formation of free radicals and iron overload. Disorders of iron metabolism are among the most common diseases of humans and encompass a broad spectrum of diseases with diverse clinical manifestations, ranging from iron deficiency anemia to iron overload and, likely, to neurodegenerative diseases [1][2][3]. In healthy organism the problem of the regulation of the iron concentration has been solved by storing iron in the iron storage protein ferritin that consists of 24 protein subunits shell and nanosized ferrihydrite (5Fe 2 O 3 9H 2 O) core [4].…”

“…In healthy organism the problem of the regulation of the iron concentration has been solved by storing iron in the iron storage protein ferritin that consists of 24 protein subunits shell and nanosized ferrihydrite (5Fe 2 O 3 9H 2 O) core [4]. The iron deficiency is a serious disease leading to anemia [1,2]. In the case of the latter iron containing medicaments are used for treatment the iron deficiency.…”

Haematopoietic effects of Angelica sinensis root cap polysaccharides against lisinopril-induced anaemia in albino rats

“…This reduction in the EPO level increases the hepicidin (antimicrobial peptide produced by hepatocytes) expression which causes systemic iron deficiency and anaemia (Handelman & Levin, 2008). Another action of ACEI is the pharmacological inhibition of the renin-angiotensin system in clinical trials, which is correlated with minute but statistically significant reduction in Hb levels (Tang & Katz 2006).…”

“…This effect on haematological parameters might be due to the depression of renin-angiotensin system by ACEIs, as this system is involved in the regulation of haematopoiesis (Cole et al 2000). This depression of renin-angiotensin system down regulates EPO which might affect the hepcidin expression and cause iron deficiency with anaemia (Handelman & Levin 2008;Liu et al 2012). In our study, the EPO-treated group showed improvement in the haematological parameters and anaemia induced by lisinopril (ACEI).…”

Atención Integrada a las Enfermedades Prevalentes de la Infancia-AIEPI, para ferropenia en niños

“…El progreso en la depleción de las reservas de este mineral se expresa como anemia, estadío final de esta carencia (9)(10)(11). Ambos estadíos, tienen similares implicaciones en el deterioro de la capacidad intelectual, desarrollo motor y la capacidad laboral (2,9,(12)(13)(14)(15).…”