Iron deficiency anaemia: pathophysiology, assessment, practical management

Abstract

The WHO has recognised iron deficiency anaemia (IDA) as the most common nutritional deficiency in the world, with 30% of the population being affected with this condition. Although the most common causes of IDA are gastrointestinal bleeding and menstruation in women, decreased dietary iron and decreased iron absorption are also culpable causes. Patients with IDA should be treated with the aim of replenishing iron stores and returning the haemoglobin to a normal level. This has shown to improve quality of life, morbidity, prognosis in chronic disease and outcomes in pregnancy. Iron deficiency occurs in many chronic inflammatory conditions, including congestive cardiac failure, chronic kidney disease and inflammatory bowel disease. This article will provide an updated overview on diagnosis and management of IDA in patients with chronic conditions, preoperative and in pregnancy. We will discuss the benefits and limitations of oral versus intravenous iron replacement in each cohort, with an overview on cost analysis between the different iron formulations currently on the market.

Keywords: inflammatory bowel disease; iron absorption; iron deficiency; iron metabolism.

Figure 1

The two different iron absorption pathways. Non-haem absorption pathway (left): insoluble ferric iron (Fe³⁺) is reduced to absorbable ferrous iron (Fe²⁺), which is carried out by the enzyme duodenal cytochrome B (DcytB). The divalent metal transporter 1 (DMT1) imports Fe²⁺ across the apical surface and into the cell, which can then be either stored as ferritin or exported into circulation through ferroportin. Prior to exiting the enterocyte, Fe²⁺ must be oxidised back to Fe³⁺ by hephaestin or ceruloplasmin. Haem absorption pathway (right): the haem carrier protein (HCP1) transports haem iron directly into the enterocyte. Once inside the enterocyte, haem iron can either be released into plasma via the haem exporter FLVCR1 or be converted back into Fe²⁺ via the haem oxidase (HO) enzyme. The ferroportin receptor then releases Fe²⁺ into the plasma. Hepcidin, a hepatic peptide hormone, controls ferroportin, the sole iron exporter, by promoting its endocytosis. Hepcidin production and circulation are regulated by plasma iron concentration and iron stores. Hepcidin is increased in the presence of inflammation, which then promotes the degradation of ferroportin and subsequently impairs the exportation of cellular iron into plasma. Figure taken with permission from Kumar and Brookes.

Figure 2

Iron deficiency treatment pathway in patients with IBD patients as followed by the South East London Clinical Commissioning Group. Hb, haemoglobin; IBD, inflammatory bowel disease.