There are many diseases where failure to adequately absorb iron contributes to iron deficiency and iron deficiency anaemia. The treatment will depend on the<unk>  levels that are present, as oral treatment will be unlikely to be effective if<unk>  is blocking enteral absorption, in which cases parenteral iron treatment would be appropriate. Studies have found that measuring<unk>  would be of benefit to establish optimal treatment, although as this is not widely available, C-reactive protein (CRP) is used as a surrogate marker. β-thalassemia, one of the most common congenital anemias, arises from partial or complete lack of β-globin synthesis. Excessive iron absorption is one of the main features of β-thalassemia and can lead to severe morbidity and mortality. The serial analyses of β-thalassemic mice indicate hemoglobin levels decreases over time, while the concentration of iron in the liver, spleen, and kidneys markedly increases. The overload of iron is associated with low levels of<unk> . Patients with β-thalassemia also have low<unk>  levels. The observations led researchers to hypothesize that more iron is absorbed in β-thalassemia than is required for erythropoiesis. Increasing expression of<unk>  in β-thalassemic mice limits iron overload, and also decreases formation of insoluble membrane-bound globins and reactive oxygen species, and improves anemia. Mice with increased<unk>  expression also demonstrated an increase in the lifespan of their red cells, reversal of ineffective erythropoiesis and splenomegaly, and an increase in total hemoglobin levels. From these data, researchers suggested that therapeutics to increase<unk>  levels or act as<unk>  agonists could help treat the abnormal iron absorption in individuals with β-thalassemia and related disorders. In later studies in mice, erythroferrone has been suggested to be the factor that is responsible for the<unk>  suppression. Correcting<unk>  and iron levels in these mice did not improve their anemia.
Hepcidin
Ferritin
Ovoferrin
Beta-2 transferrin
Thyroglobulin
Gamma globulin
Alpha-1 antitrypsin
Toxidrome