Iron deficiency effects

Thus, our attention should shift from the concern of potential adverse effects to the health benefits imparted by hormonal contraceptives. The use of oral contraceptives for at least 12 months reduces the risk of developing endometrial cancer by 50%. Furthermore, the risk of epithelial ovarian cancer in users of oral contraceptives is reduced by 40% compared with that on nonusers. This kind of protection is already seen after as little as 3-6 months of use. Oral contraceptives also decrease the incidence of ovarian cysts and fibrocystic breast disease. They reduce menstrual blood loss and thus the incidence of iron-deficiency anemia. A decreased incidence of pelvic inflammatory disease and ectopic pregnancies has been reported as well as an ameliorating effect on the clinical course of endometriosis. 

Inorganic iron is absorbed only in the (reduced) state, and for that reason the presence of reducing agents will enhance absorption. The most effective compound is vitamin C, and while intakes of 40-60 mg of vitamin C per day are more than adequate to meet requirements, an intake of 25-50 mg per meal will enhance iron absorption, especially when iron salts are used to treat iron deficiency anemia. Ethanol and fructose also enhance iron absorption. Heme iron from meat is absorbed separately and is considerably more available than inorganic iron. However, the absorption of both inorganic and heme iron is impaired by calcium—a glass of milk with a meal significantly reduces availabiUty. 

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. 

Parenteral iron therapy currently is available in three different formulations, which are listed in Table 63-3. Iron dex-tran was the first parenteral iron formulation to be approved, followed by ferric gluconate, and then iron sucrose. Although these newer agents are only approved by the Food and Drug Administration (FDA) to treat anemia associated with CKD in patients receiving erythropoietin products, they are effective in treating iron-deficiency anemia as well. Iron dextran is FDA approved for treating documented iron deficiency in patients who are unable to tolerate the oral formulation. 

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. 

Absorption of americium is greater in iron deficient animals than in iron replete adult animals (Sullivan and Ruemmler 1988 Sullivan et al. 1986) (see Section 3.4.1.2). Concurrent oral exposure to Fe3+ and americium also appears to increase the absorption of ingested americium the latter effect may result from redox reactions in the gastrointestinal tract catalyzed by Fe3+ (Sullivan et al. 1986). These differences are accounted for in the discussions and dosimetric/metabolic models of the ICRP (1989, 1993) and the NEA (1988). 

Iron Mouse Lead retention Iron deficiency has no effect on lead retention Hamilton 1978... 

Pollitt E Univ of California, Administration, Davis, CA The effects of lead and iron interaction on behavioral development the effects of iron treatment on iron status, blood lead level, and behavioral development in children with elevated lead levels and iron deficiency U. S. Department of Agriculture, Competitive Research... 

Iron is an extremely important element present in all living organisms correspondingly, iron metabolism is well studied. Both iron deficiency and iron excess are origins of serious pathologies (iron-deficit anemias, hereditary hemochromatosis, thalassemia, etc.) associated with the overproduction of oxygen radicals. Free radical-mediated processes, characteristic of these pathologies, are considered in Chapter 31 here we will look at some mechanisms of toxic effects of iron. 

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. 

Some other examples of free radical formation in various pathologies are discussed below. (Of course, they are only few examples among many others, which can be found in literature.) Mitochondrial diseases are associated with superoxide overproduction [428] and cytochrome c release [429], For example, mitochondrial superoxide production apparently contributes to hippocampal pathology produced by kainate [430]. It has been found that erythrocytes from iron deficiency anemia are more susceptible to oxidative stress than normal cells but have a good capacity for recovery [431]. The beneficial effects of treatment of iron deficiency anemia with iron dextran and iron polymaltose complexes have been shown [432,433]. 

Sublethal effects in birds are similar to those in other species and include growth retardation, anemia, renal effects, and testicular damage (Hammons et al. 1978 Di Giulio et al. 1984 Blus et al. 1993). However, harmful damage effects were observed at higher concentrations when compared to aquatic biota. For example, Japanese quail (Coturnix japonica) fed 75 mg Cd/kg diet developed bone marrow hypoplasia, anemia, and hypertrophy of both heart ventricles at 6 weeks (Richardson et al. 1974). In zinc-deficient diets, effects were especially pronounced and included all of the signs mentioned plus testicular hypoplasia. A similar pattern was evident in cadmium-stressed quail on an iron-deficient diet. In all tests, 1% ascorbic acid in the diet prevented cadmium-induced effects in Japanese quail (Richardson et al. 1974). In studies with Japanese quail at environmentally relevant concentrations of 10 pg Cd/kg B W daily (for 4 days, administered per os), absorbed cadmium was transported in blood in a form that enhanced deposition in the kidney less than 0.7% of the total administered dose was recovered from liver plus kidneys plus duodenum (Scheuhammer 1988). 

Iron deficiency may develop, especially in children and in menstruating women. This may be caused by diet. If necessary, give iron in short courses. A period of 2 hours should elapse between administration of penicillamine and iron, because orally administered iron reduces the effects of penicillamine. 

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