Iron deficiency causes

Iron-deficiency anaemia results from a discrepancy between iron availability and the amount required for production of red blood cells. The causes of acquired iron deficiency in so-called underdeveloped and developed countries must be differentiated. In underdeveloped countries, the main causes of iron deficiency are (a) the poor availability of iron in the diet due to low haem and high fibre and phytate content (D Souza et ah, 1987), and (b) chronic blood loss due to hookworm, schistosomiasis and malaria (Stoltzfus et ah, 1997 Olsen et ah, 1998 Dreyfuss et ah, 2000). Inflammation and vitamin A deficiency often interfere with the above causes of iron deficiency, causing a mixed type of anaemia. In underdeveloped countries diet improvement, iron fortification of natural foods and eradication of parasites will have a much higher impact than will refinement of diagnostic procedures and therapy of iron-deficiency anaemia. 

There are numerous in vitro and in vivo studies, in which the damaging free radical-mediated effects of iron have been demonstrated. Many such examples are cited in the following chapters. However, recent studies [170,171] showed that not only iron excess but also iron deficiency may induce free radical-mediated damage. It has been shown that iron deficiency causes the uncoupling of mitochondria that can be the origin of an increase in mitochondria superoxide release. Furthermore, a decrease in iron apparently results in the reduction of the activity of iron-containing enzymes. Thus, any disturbance in iron metabolism may lead to the initiation of free radical overproduction. 

Iron is used to regenerate hemoglobin. Iron is absorbed in the intestine and enters plasma as heme. Iron is stored as ferritin in the liver, spleen, and bone marrow. Five to twenty milligrams of iron are required daily. Iron deficiency causes anemia. Iron is found in liver, lean meats, egg yolks, dried beans, green vegetables (i.e., spinach), and fruit. Women who are pregnant should increase their iron intake as specified by the healthcare provider. Large doses of iron are prescribed in the second and third trimesters. The patient must adhere to the... 

Iron (ferrous sulfate, gluconate, or fumarate) is used for the regeneration of hemoglobin. Iron deficiency causes anemia. The patient requires 5 to 20 mg of iron each day from eating liver, lean meats, egg yolks, dried beans, green vegetables (such as spinach), and fruit. 

In male, weanling Sprague-Dawley rats iron deficiency caused a loss in intestinal xanthine oxidase activity, but also caused an increase in hepatic xanthine oxidase activity (Kelley and Amy 1984). 

Anemia is a decrease in the number of red blood cells (RBCs), a decrease in die amount of hemoglobin in RBCs, or bodi a decrease in die number of RBCs and hemoglobin. When diere is an insufficient amount of hemoglobin to deliver oxygen to die tissues, anemia exists. There are various types and causes of anemia For example, anemia can be die result of blood loss, excessive destruction of RBCs, inadequate production of RBCs, and deficits in various nutrients, such as in iron deficiency anemia Once the type and cause have been identified, die primary health care provider selects a method of treatment. 

Avoid tiie indiscriminate use of advertised iron products. If a true iron deficiency occurs, the cause must be determined and therapy should be under the care of a health care provider. 

Yoshiji, H., Nakae, D., Mizumoto, Y., Horiguchi, K., Tamura, K., Denda, A., Tsujii, T. and Konishi, Y. (1992). Inhibitory effect of dietary iron deficiency on inductions of putative preneoplastic lesions as well as 8-hydroxydeoxyguanosine in DNA and lipid peroxidation in the livers of rats caused by exposure to a choline-deficient L-amino acid defined diet. Carcinogenesis 13, 1227-1233. 

Figure 3 Root fingerprints of Pseudomimets sp. associated with barley seedlings showing the production of siderophore by actively growing bacteria located in the zone of elongation behind the root tips. Root.s were pressed on to an iron-deficient minimal medium selective for Pseudomonas. After growth of the colonies, the production of siderophore was visualized by exposure of the agar plate to ultraviolet light, which causes the siderophore to Huoresce.

Although EPO deficiency is the primary cause of CKD anemia, iron deficiency is often present, and it is essential to assess and monitor the CKD patient s iron status (NKF-K/DOQI guidelines). Iron stores in patients with CKD should be maintained so that transferrin saturation (TSAT) is greater than 20% and serum ferritin is greater than 100 ng/mL (100 mcg/L or 225 pmol/L). If iron stores are not maintained appropriately, epoetin or darbepoetin will not be effective, and most CKD patients will require iron supplementation. Oral iron therapy can be used, but it is often ineffective, particularly in CKD patients on dialysis. Therefore, intravenous iron therapy is used extensively in these patients. Details of the pharmacology, pharmacokinetics, adverse effects, interactions, dose, and administration of erythropoietin and iron products have been discussed previously. 

Iron-deficiency anemia in chronic PN patients may be due to underlying clinical conditions and the lack of iron supplementation in PN. Parenteral iron therapy becomes necessary in iron-deficient patients who cannot absorb or tolerate oral iron. Parenteral iron should be used with caution owing to infusion-related adverse effects. A test dose of 25 mg of iron dextran should be administered first, and the patient should be monitored for adverse effects for at least 60 minutes. Intravenous iron dextran then may be added to lipid-free PN at a daily dose of 100 mg until the total iron dose is given. Iron dextran is not compatible with intravenous lipid emulsions at therapeutic doses and can cause oiling out of the emulsion. Other parenteral iron formulations (e.g., iron sucrose and ferric gluconate) have not been evaluated for compounding in PN and should not be added to PN formulations. 

Anemia of chronic kidney disease A decline in red blood cell production caused by a decrease in erythropoietin production by the progenitor cells of the kidney. As kidney function declines in chronic kidney disease, erythropoietin production also declines, resulting in decreased red blood cell production. Other contributing factors include iron deficiency and decreased red blood cell lifespan, caused by uremia. 

An impressive number of proteins that are involved in iron transport have been identified in recent years (Andrews, 1999 Griffiths et al., 1999). Most of them can either be up-regulated or down-regulated in situations of iron deficiency and different forms of iron overload, in order to maintain a safe iron balance. However, variations in the absolute levels or genetic defects of these proteins may cause iron overload or iron deficiency. In many forms of iron-related pathology detailed information can be obtained using appropriate animal models. 

Inhibition of synthesis of the aromatic matrix by inhibitors of phenylalanine ammonia lyase causes the inhibition of deposition of aliphatic components and prevents development of diffusion resistance. Inhibition of synthesis of peroxidase, the enzyme involved in the deposition of the polymeric phenolic matrix, caused by iron deficiency, prevents deposition of aliphatic components of suberin. 

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