How do you solve a problem like anaemia?
3 July 2014
Anaemia is a condition where sufferers have a reduced number of functional red blood cells. It is a global problem which affects over 270 million pre-school children worldwide, the majority of whom are from low and middle-income countries in regions such as sub-Saharan Africa. There is an evident need to continue research of this disease and here Raffaella Facchini describes recent work from Hal Drakesmith’s lab at the WIMM that could help to develop more targeted prevention strategies for children in the developing world.
Anaemia is often treated by iron supplementation, which is effective if the cause of the disease is due to a lack of iron. Leaders in global health often recommend that iron should be given to all young children in populations where anaemia is highly prevalent.
However, contrary to popular belief, iron deficiency is not the only cause of anaemia. It can also be caused by nutrient deficiencies such as vitamin B12, inherited genetic disorders (such as defects in the genes that produce haemoglobin, the protein that carries oxygen in red blood cells) and also by infections such as malaria.
Indeed, there is evidence that giving iron to everybody, including those who don’t need it, may increase the risk of infections such as malaria. This is because pathogens like the malaria parasite also require iron to grow. The problem of ‘mis-treating’ anaemia is greater in locations where the prevalence of malaria and other infections is higher – a problem recognised by leaders in global health.
The task of preventing anaemia effectively is therefore quite tricky, but work done jointly by Hal Drakesmith’s group within the MRC Human Immunology Group at the WIMM, the Department of Paediatrics, MRC groups in The Gambia and KEMRI-Wellcome Trust in Kenya has started to address this by investigating the most appropriate time of year for giving iron to such populations, and to also develop a method to quickly detect iron deficiency so that children who would truly benefit from iron supplementation could be identified within a population.
To do this, the researchers investigated the hormone hepcidin, which is produced to help the body to control how iron is used. When levels are high, it prevents the body absorbing iron and when it is low, dietary iron can be taken up freely. By looking at the level of hepcidin in two groups of children, one in the Gambia and one in Tanzania, they were able to determine three things: if the children were iron deficient; if their anaemia was due to iron deficiency or due to inflammation; and also if their red blood cells were able to take up iron.
The researchers also undertook another study, where they evaluated samples from over 800 children in The Gambia and Kenya before and after a malaria season. They found that at the end of the season, the children showed reduced hepcidin levels and there was a greater prevalence of iron deficiency. This indicated that iron supplementation would likely be more successful at the end of the malaria season, as at this time specifically there would be a greater requirement for iron that would be more effectively absorbed.
These results have helped make positive steps forwards in the correct treatment of anaemia. Using hepcidin to guide iron supplementation holds the potential to not only ensure that individuals in need of additional iron get the supplements they need, but critically could protect those to whom iron supplementation would be harmful.
Post edited by Bryony Graham, Sarah Atkinson, Andrew Armitage and Alexander Drakesmith.