Anaemia exacerbates underlying disease in IBD,3 and increases the risk of disease progression in CKD and CHF4,5
We can associate IDA with hospitalization of patients or prolongation of hospital stay1-3, 6-8
Pre-operative IDA can be associated with increased blood transfusions
All women of reproductive age are at risk of iron deficiency. It is estimated that 30% of women globally are anemic, with at least half of these cases arising from iron deficiency.
Among pregnant women, IDA has been associated with increased risks of low birth weight, prematurity, and maternal morbidity.
Iron deficiency and anemia reduce the work capacity of individuals and entire populations, bringing serious economic consequences and obstacles to national development.
Heavy menstrual bleeding is the leading cause of iron deficiency/iron deficiency anemia in women.
For clinical purposes, HMB should be defined as excessive menstrual blood loss which interferes with the woman’s physical, emotional, social and material quality of life, and which can occur alone or in combination with other symptoms. HMB should be recognized as having a major impact on a woman’s quality of life.
Any interventions should aim to improve quality-of-life measures.NICE guideline. Heavy menstrual bleeding. 2007. http://www.nice.org.uk/nicemedia/live/11002/30404/30404.pdf
It is well established that ID/IDA exerts various negative effects1,2. Specifically, ID/IDA has been shown to adversely influence physical and mental performance (exercise, physical activity, fatigue, mental and cognitive ability and performance)1,3,4 physiological processes (enzymatic activity such as the respiratory chain; thermoregulation)1 and immune (potential susceptibility to infections) and neurological function1. ID/IDA also affects the ability to tolerate heavy blood loss5
Anemia has a profound effect on the quality of life. Therefore, normalisation of the Hb level and iron status is a goal in the overall management of underlying diseases (Van Assche 2013, McMurray 2012).
Notably, a retrospective analysis of patients with inflammatory bowel disease who were treated for anemia and achieved normal Hb levels showed a 50% recurrence after 10 months (Kulnigg 2009). Iron deficiency, defined as ferritin <30 μg/L, recurred within a median time of 19 months, and iron deficiency recurred faster in patients with a post-treatment ferritin level <100 μg/L (median 4 months) than in patients with ferritin levels between 100-400 μg/L (median 11 months) and ferritin >400 μg/L (median 49 months; p<0.001).
Sufficient iron repletion (ferritin 100-400 μg/L) can prevent or delay anemia recurrence (Evstatiev 2013, Kulnigg 2009).
Since over 90% of ingested iron remains unabsorbed, oral iron preparations frequently lead to the occurrence of GI adverse effects, including nausea, flatulence, diarrhea and gastric erosion (Van Assche 2013).
Animal and human studies show that the generation of reactive oxygen species (Fenton reaction) by non-absorbed iron might lead to the exacerbation of IBD.
Several studies have shown that I.V. iron is at least as effective as oral iron, delivers faster response rates, and is safer in all but a very few patients who may experience side-effects.
Intravenous iron therapy is advisable in the following cases: for iron-deficient patients who are intolerant or unresponsive to oral iron supplementation (i.e., those showing an insufficient increase in serum iron parameters within the first 2 weeks of treatment); for patients with severe anemia (Hb <10 g/dL); for patients with pronounced disease activity; and for patients who are being treated with erythropoiesis-stimulating agents. Patients with mild anemia (Hb >10 g/dL) can be adequately treated with 100 mg/day iron sulphate.
·Accelerated erythropoiesis can increase demand for iron beyond the amount supplied orally
High oral iron doses can saturate the iron transport system if it rapidly released the iron, resulting in oxidative stress
Oral iron may not compensate for ongoing blood loss in IBD.1 Studies in animal models of inflammatory bowel disease (IBD) consistently show an increase in oxidative stress, disease activity, intestinal inflammation and colorectal cancer development through oral iron supplementation.2 This is not surprising, as approximately 90% of ingested iron is not absorbed, passes the sites of intestinal inflammation and induces local oxidative stress at sites of active inflammation (through the Fenton reaction).
Further studies show that nutritional iron may be one of the exogenous factors responsible for the onset of colitis.3,4 In patients with IBD, oral iron induces oxidative stress,5 increases local disease activity, particularly in patients with ulcerative colitis,6 and in patients with Crohn’s disease, the absorption of oral iron is inhibited, possibly through a hepcidin-mediated mechanism.7
If oral iron is used, there is limited data available to differentiate between products.
A study comparing iron polymaltose complex8 and ferrous sulphate showed that ferrous sulphate increased markers for lipid peroxidation more than iron polymaltose complex.