Revisiting Iron Metabolism, Iron Homeostasis and Iron Deficiency Anemia.

BACKGROUND: Iron deficiency anemia (IDA) is one of the commonest clinical scenarios especially in children, women of childbearing age, and elders. The crux of this review was revisiting iron homeostasis, mechanism of iron absorption, causes, laboratory diagnosis, and management of IDA. METHODS: This narrative review is compiled after a relevant literature search from electronic databases including, but not limited to, Google, Google Scholar, PMC, PubMed, Science Direct, and Scopus. The key words used for searching relevant literature include iron, iron deficiency, iron deficiency anemia, iron metabolism, hepcidin, transferrin, causes of iron deficiency anemia, and laboratory diagnosis of iron deficiency anemia. Reference hema-tology books were also consulted. RESULTS: According to the published literature, about one mg of iron is required daily which equals its loss, although the iron requirement increases in pregnancy and lactating mothers. Dietary non heme iron (oxidized Fe3+) is reduced to the ferrous (Fe2+) form by ferrireductase present in the brush border of duodenal enterocytes. Ferrous iron is absorbed in the brush border of duodenal enterocytes through a carrier protein, divalent metal transporter 1 (DMT1). Heme iron is absorbed by the duodenal enterocytes through a mechanism that is not well understood or a receptor yet to be discovered. Transferrin receptor helps in the internalization of iron in the cells. Hepcidin acts as a gatekeeper and controls iron absorption by enterocytes and macrophages. IDA may be caused by decreased intake of iron, increased iron requirements or loss of iron from the body. CONCLUSIONS: Iron deficiency anemia is the most common nutritional anemia that affects large numbers of people in developed as well as in developing countries. It is estimated that approximately 2 billion people around the world have IDA. Microcytosis with marked reduction in serum iron, decreased % saturation of transferrin, low ferritin, and reduced or even undetectable hepcidin are the laboratory features of IDA. In addition, total iron binding capacity and soluble transferrin receptors increase significantly in IDA. Management of IDA is incomplete if the underlying cause is not ruled out and left untreated.

Disorders associated with malabsorption of iron: A critical review.

Malabsorption is a disorder of the gastrointestinal tract that leads to defective digestion, absorption and transport of important nutrients across the intestinal wall. Small intestine is the major site where most of the nutrients are absorbed. There are three main mechanisms of malabsorption; premucosal, mucosal and postmucosal. Premucosal malabsorption is the inadequate digestion due to improper mixing of gastrointestinal enzymes and bile with chyme. This could be because of surgical resection of the small intestine or a congenital deficiency of the enzymes and bile responsible for digestion e.g. postgastrectomy, chronic pancreatitis, pancreatic cancer, cystic fibrosis, gallstones, cholangitis etc. Mucosal malabsorption occurs in celiac disease, tropical sprue, Crohn's disease etc. Postmucosal condition arises due to impaired nutrients transport e.g. intestinal lymphangiectasia, macroglobulinemia etc. Disorders of malabsorption lead to decreased iron absorption and produce iron deficiency anemia. Using the index terms malabsorption, postgastrectomy, chronic pancreatitis, pancreatic cancer, cystic fibrosis, gallstones, cholangitis, celiac disease, tropical sprue, Crohn's disease intestinal lymphangiectasia, macroglobulinemia and iron deficiency anemia the MEDLINE and EMBASE databases were searched. Additional data sources included bibliographies and references of identified articles.

Prevalence of A2 and A2B Subgroups and Anti-A1 Antibody in Blood Donors in Jazan, Saudi Arabia.

PURPOSE: A2 and A2B are rare phenotypes of the ABO blood group system. Some individuals with A2 and A2B may have anti-A1 antibodies that may be clinically significant or insignificant. The aim of this study was to determine the frequency of A2, A2B phenotypes and anti-A1 antibodies in blood donors in Jazan, Saudi Arabia. This study also evaluated the reactivity potential of anti-A1 antibodies. MATERIALS AND METHODS: Blood samples collected from 446 blood donors were typed for ABO (cell and serum grouping) and Rh D. Individuals with blood group A and AB were further subtyped by testing with anti-A1 lectin. In addition to the serum grouping using A1 red cells, A2 and A2B individuals were screened for the presence of anti-A1 in their sera against A1 red cells at 4°C, 22°C and 37°C to determine the thermal amplitude of the reacting anti-A1 antibody (if present). RESULTS: Among A and AB, A1 was the commonest phenotype (20.2%, n=90 out of 446) while A1B was found to be 1.8% (n=8) among AB phenotype. A2 and A2B were found to be 2.2% (n=10) and 0.9% (n=4), respectively. Only one individual with A2B blood type showed cold reactive anti-A1 antibody, the strength of which was 32. CONCLUSION: A2 and A2B were the rarest among ABO phenotypes in the studied population. Although rare, anti-A1 antibody is not so uncommon. Care shall be taken during routine ABO grouping especially in cases of mix-field or weak positive reactions in A and AB phenotypes.

Effect of Intravenous Iron Supplementation on Hepcidin Levels in Iron Deficient Pregnant Females in Second and Third Trimester.

Objective of the study was to assess effect of iron therapy on serum hepcidin levels in iron deficient pregnant women and its correlation with hemoglobin, serum iron profile and C-reactive protein (CRP). A total of 100 pregnant women were enrolled in the study; 25 were included in the "control group" having normal hematological and biochemical parameters while 75 iron deficient pregnant women were enrolled in the "patient group" with low hematological and biochemical parameters. CRP was done to rule out inflammation and to observe its association with hepcidin. Intravenous iron was administered to the patient group. Post treatment CBC, serum iron, serum ferritin and serum hepcidin were determined. Difference between pre and post treatment hemoglobin, serum iron, serum ferritin and serum hepcidin levels were determined and correlation among them was calculated. Post treatment serum hepcidin levels were significantly higher than pretreatment level (p = 0.001). However, no correlation was seen between serum hepcidin, serum iron, serum ferritin and hemoglobin. Hepcidin levels remain low during pregnancy as there is increased demand for iron in pregnancy. Iron supplementation results in increased hepcidin levels; however no mathematical correlation was found between serum hepcidin level and serum iron profile.