Malabsorption of iron

Iron supplements are often used to treat iron-deficient anaemia. This might occur through severe haemorrhage, dietary deficiency or malabsorption of iron and in pregnancy. Supplements are usually salts of iron. Iron supplements may be administered orally, or sometimes by injection, in the form of ferrous fumarate, ferrous gluconate, ferrous glycine sulphate and ferrous sulphate. 

Which of the clinical conditions listed below can be associated with the malabsorption of iron ... 

Anemia may be present in some patients due to impaired erythropoietin regulation, nutritional factors (vitamin E and iron malabsorption), or chronic inflammation. With chronic pulmonary disease, increased cytokine production can lead to shortened red blood cell survival, reduced erythropoietin response, and impaired mobilization of iron stores. 

Formation of strictures, abscesses, fistulae, and obstructions in patients with CD is possible. Patients with CD may develop significant weight loss or nutritional deficiencies secondary to malabsorption of nutrients in the small intestine, or as a consequence of multiple small- or large-bowel resections. Common nutritional deficiencies encountered in IBD include vitamin B12, fat-soluble vitamins, zinc, folate, and iron. Malabsorption in children with CD may contribute to significant reductions in growth and development. 

Drugs continue to be absorbed after even the most major resections of the stomach - C ax may be higher and Tmax earlier if gastric contents move more rapidly into the upper small intestine. The intestine itself has enormous redundancy - i.e., there is far more than is acmally needed - and disease, including moderate forms of malabsorption, such as coeliac disease, make relatively little impact although salts of iron and folic acid are often transported poorly and deticiencies may occur. 

After confirmation of iron deficiency iron therapy can be given by oral or parenteral route. Generally oral iron therapy is given unless the patient is suffering from severe anaemia, malabsorption syndrome, gastrectomy or patient is showing adverse effects to oral iron therapy. 

A 47-year-old woman weighing 59 kg took acarbose 50 mg tds. Her blood glucose improved but she lost about 1 kg/month. She had a sore tongue without oral ulcers and no evidence of malabsorption. Later she developed general weakness and iron deficiency anemia but no other evidence of malabsorption. After she had lost 7 kg in 5 months, acarbose was withdrawn. Her complaints disappeared, her weight normalized, and she had no signs of iron deficiency anemia, even without iron therapy. 

Patients with iron deficiency anemia present with fatigue, weakness, and pallor, and possibly also with glossitis, headache, dysphagia, fingernail changes, gastric atrophy, and paresthesias. Inadequate intake of iron, malabsorption, and blood loss from any origin are the principal causes of iron deficiency anemia. 

Diet plays a significant role because iron is poorly absorbed from vegetables, grain products, dairy products, and eggs iron is best absorbed fi om meat, fish, and poultry. Administration of iron therapy with a meal decreases absorption hy more than 50% but may be needed to improve tolerabiUty. Parenteral iron may be required for patients with iron malabsorption, intolerance of oral iron therapy, or noncompliance. Parenteral administra-... 

Prolonged heavy excess of iron intake overwhelms the mechanism described and results in haemo-siderosis, as there is no physiological mechanism to increase iron excretion in the face of increased absorption. Iron-deficient subjects absorb up to 20 times as much administered iron as those with normal stores. Abnormalities of the small intestine may interfere with either the absorption of iron, as in coeliac disease and other malabsorption syndromes, or possibly with the conversion of iron into a soluble and reduced form, e.g. following loss of acid secretion after a partial gastrectomy. 

Dietary. Cp deficiency is due to nutritional copper deficiency, with secondarily low levels of Cp, and is associated with neutropenia, thrombocytopenia, low serum iron, and hypochromic, normocytic, or macrocytic anemia unresponsive to iron therapy. The deficiency may be due to inadequate dietary intake, long-term parenteral nutrition without copper supplementation, malabsorption of any cause, penicillamine therapy, or combinations of these. Therapy includes dietary change or copper supplementation, plus treatment of the primary cause of malabsorption if present. 

Anemia occurs when there is significant blood loss from the GI tract. If the patient can consume oral medication, ferrous sulfate should be administered. If the patient is unable to take oral medication and the patient s hematocrit is sufficiently low, blood transfusions or intravenous iron infusions may be required. Anemia may also be related to malabsorption of vitamin B12 or fohc acid, so these may also be required. 

Iron deficiency anaemia is the commonest of all single-nutrient deficiences.. Millions of people worldwide are affected, with. seriously impaired quality of life and work efficiency. The principal causes arc chronic blood loss and poor dietary intake of bioavailable iron, e.g. the uptake of iron from the diet can be decreased by a number of dietary constituents such as phytic acid and fibre. Iron deficiency can also occur in ctK liac di.sease and other intestinal disorders where malabsorption is a feature. 

Lynch SR (1984) Iron. In Solomons NW and Rosenberg UH, eds. Absorption and malabsorption of mineral nutrients, pp. 89-124. Alan R Liss Inc, New York. 

In general, pancreatic enzyme preparations are well tolerated by patients. For patients with hypersensitivity to pork protein, bovine enzymes are available. Hyperuricosuria in patients with cystic fibrosis can occur, and malabsorption of folate and iron has been reported. 

Iron deficiency is the most common nutritional cause of anemia in humans. It can result from inadequate iron intake, malabsorption, blood loss, or an increased requirement, as with pregnancy. When severe, it results in a characteristic microcytic, hypochromic anemia. Iron is an essential component of myoglobin heme enzymes such as the cytochromes, catalase, and peroxidase and the metalloflavoprotein enzymes, including xanthine oxidase and the mitochondrial enzyme a-glycerophosphate oxidase. Iron deficiency can affect metabohsm in muscle independent of the effect of anemia on delivery, possibly due to a reduction in the activity of iron-dependent mitochondrial enzymes. Iron deficiency also has been associated with behavioral and learning problems in children, abnormahties in catecholamine metabolism, and impaired heat production. 

Iron-deficiency anemia results from dietary intake of iron that is inadequate to meet normal requirements (nutritional iron deficiency), blood loss, or interference with iron absorption. Most nutritional iron deficiency in the U.S. is mild. More severe iron deficiency is usually the result of blood loss, either from the GI tract, or in women, from the uterus. Impaired absorption of iron from food results most often from partial gastrectomy or malabsorption in the small intestine. Finally, erythropoietin therapy can result in a functional iron deficiency. 

Stewart CA, Termanini B, Sutliff VE, Serrano J, Yu F, Gibril F, Jensen RT (1998) Assessment of the risk of iron malabsorption in patients with Zollinger-Ellison syndrome treated with long-term gastric acid antisecretory therapy. Aliment Pharmacol Ther 12 83-98... 

Reports of human copper deficiency are limited and suggest that severe nutrient deficiency coupled with malabsorption is required for this disease state to occur. Infants fed an exclusive cows milk diet are at risk for copper deficiency. Cows milk not only has substantially less copper than human milk but the bioavailability is also reduced. High oral intake of iron or zinc decrease copper absorption and may predispose an individual to copper deficiency. Other infants at risk include those with (1) prematurity secondary to a lack of hepatic copper stores (2) prolonged diarrhea and (3) intestinal malabsorption syndromes. Even the premature liver is capable of impressive copper storage. By 26 weeks gestational age the liver already has 3 mg of copper stored. By 40 weeks gestational age, the hepatic liver has 10-12 mg copper stored with the majority being deposited in the third trimester. Iron and zinc... 

Parenteral iron may be required for patients with iron malabsorption, intolerance of oral iron therapy, or noncompliance. Parenteral administra-... 

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