Iron supplement

Plant and Animal Nutrient. Copper is one of seven micronutrients that has been identified as essential to the proper growth of plants (87). Cereal crops are by far the most affected by copper deficiency (see Wheat and other cereal grains). Greenhouse studies have shown yield increases from 38% to over 500% for wheat, barley, and oats (88) using copper supplementation. A tenfold increase in the yield of oats was reported in France (89). Symptoms of copper deficiency vary depending on species, but often it is accompanied by withering or chlorosis in the leaves that is not ammenable to iron supplementation. In high concentrations, particularly in low pH sods, copper can be toxic to plants. 

Ferrous gluconate is the black dye used to color ripe olives. It is also used as an iron supplement to treat iron-deficiency anemia. 

Humans Hydrogen peroxide has been used as an enema or as a cleaning agent for endoscopes and may cause mucosal damage when applied to the surface of the gut wall. Hydrogen peroxide enteritis can mimic an acute ulcerative, ischaemic or pseudomembranous colitis, and ranges from a reversible, clinically inapparent process to an acute, toxic fulminant colitis associated with perforation and death (Bilotta and Waye, 1989). It is conceivable that anecdotal reports of exacerbation of IBD by iron supplementation (Kawai et al. 1992) are mediated by hydroxyl radical production by the Fenton reaction. 

Medications (analgesics, anticholinergerics, calcium channel blockers, clonidine, diuretics, phenothiazines, tricyclic antidepressants, iron supplements, calcium- and aluminum-containing antacids)... 

Generally, treatment requires a combination of ESA and iron supplementation. The goal of treatment for anemia of CKD is to increase Hgb levels greater than 11 g/dL (6.8 mmol/L). The goal for iron supplementation is to maintain serum ferritin... 

The first-line treatment for anemia of CKD involves replacement of erythropoietin with erythropoiesis-stimulating agents (ESAs). Use of ESAs increases the iron demand for RBC production and iron deficiency is common, requiring iron supplementation to correct and maintain adequate iron stores to promote RBC production. Androgens were used extensively... 

Iron Supplementation Use of ESAs can lead to iron deficiency if iron stores are not adequately maintained. If serum ferritin and TSAT fall below the goal levels, iron supplementation is required. Oral iron supplements are less costly than IV supplements and are generally the first-line treatment for iron supplementation. When administering iron by the oral route, 200 mg of elemental iron should be delivered daily to maintain adequate iron stores. 

Oral iron supplementation is generally not effective in maintaining adequate iron stores in patients receiving ESAs because of poor absorption and an increased need for iron with ESA therapy, making the IV route necessary for iron supplementation. The IV iron products currently available are iron dextran (distributed as INFeD by Watson Pharmaceuticals, Inc., Morristown, NJ, and Dexferrum by American Reagent, Inc.,... 

Shirley, NY) sodium ferric gluconate (Ferrlecit by Watson Pharmaceuticals, Inc., Corona, CA) and iron sucrose (Venofer by American Reagent, Inc., Shirley, NY). Initiation of IV iron should be based on evaluation of iron stores. A serum ferritin level less than 100 ng/mL in conjunction with a TSAT level less than 20% indicates absolute iron deficiency and is a clear indication for the need for iron replacement.31 When TSAT is less than 20% in conjunction with normal or elevated serum ferritin levels, treatment should be based on the clinical picture of the patient, as serum ferritin is an acute phase reactant, which may become elevated with inflammation and stress. Iron supplementation may be indicated if Hgb levels are below the goal level. 

When replacing iron stores in patients receiving ESA therapy, the general approach to treatment is to give a total of 1 g of IV iron, administered in smaller, sequential doses. Because iron stores deplete quickly in patients who do not receive iron supplementation, maintenance doses are often used, particularly in patients receiving hemodialysis. Maintenance doses consist of smaller doses of iron administered weekly or with each dialysis session (e.g., iron dextran or iron sucrose 20 to 100 mg per week sodium ferric gluconate 62.5 to 125 mg per week). 

Evaluate Hgb every 1 to 2 weeks when ESA therapy is initiated or the dose is adjusted until Hgb is greater than 11 g/dL (6.82 mmol/L). Once goal Hgb is attained, evaluate Hgb every 2 to 4 weeks thereafter. While the patient is receiving ESA therapy, monitor iron stores monthly in patients who are not receiving iron supplements or every 3 months in patients who are receiving iron supplements. When the goal Hgb is reached, monitor iron stores every 3 months. 

Levodopa, a dopamine precursor, is the most effective agent for PD. Patients experience a 40% to 50% improvement in motor function. It is absorbed in the small intestine and peaks in the plasma in 30 to 120 minutes. A stomach with excess acid, food, or anticholinergic medications will delay gastric emptying time and decrease the amount of levodopa absorbed. Antacids decrease stomach acidity and improve levodopa absorption. Levodopa requires active transport by a large, neutral amino acid transporter protein from the small intestine into the plasma and from the plasma across the blood-brain barrier into the brain (Fig. 29-2). Levodopa competes with other amino acids, such as those contained in food, for this transport mechanism. Thus, in advanced disease, adjusting the timing of protein-rich meals in relationship to levodopa doses may be helpful. Levodopa also binds to iron supplements and administration of these should be spaced by at least 2 hours from the levodopa dose.1,8,16,25... 

A number of factors can alter LT4 dose requirements (Table 41—4). The most common cause of increased dose requirement is the co-administration of LT4 with calcium or iron supplements. Counsel patients that they should take the LT4 dose at least 2 hours before or 6 hours after the calcium or iron dose. 

Iron supplementation resolves anemia by replacing iron stores in the body that are necessary for red blood cell production and maturation. If treated properly, a response (via the presence of reticulocytosis) should be seen in 7 to 10 days, and hemoglobin values should rise by about 1 g/dL (10 g/L or 0.62 mmol/L) per week. Patients should be reassessed if hemoglobin does not increase by 2 g/dL (20 g/L or 1.24 mmol/L) in 3 weeks. 

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. 

Wasserman GA, Graziano JH, Factor-Litvack P, et al. 1994. Consequences of lead exposure and iron supplementation on childhood development at age 4 years. Neurotoxicol Teratol 16 233-240. 

The mitochondrial dysfunctionality seen in manganese neurotoxicity might be related to the accumulation of reactive oxygen species (Verity, 1999). Mitochondrial Mn superoxide dismutase (MnSOD) is found to be low or absent in tumour cells and may act as a tumour suppressor. It is induced by inflammatory cytokines like TNF, presumably to protect host cells. In a rat model, iron-rich diets were found to decrease MnSOD activity, although a recent study reported that in rat epithelial cell cultures iron supplementation increased MnSOD protein levels and activity, but did not compromise the ability of inflammatory mediators like TNF to further increase the enzyme activity (Kuratko, 1999). 

Recently, Carr and Frei reviewed studies on the antioxidant and prooxidant effects of ascorbic acid [8]. These authors pointed out that a highly controversial work by Podmore and coworkers [71] who found that the prooxidant effect of ascorbic acid supplementation to healthy volunteers is much questionable. These authors demonstrated that of the 44 in vivo studies, 38 showed the antioxidant effect of ascorbic acid, 14 showed no change, and only six showed the enhancement of oxidative damage after ascorbate supplementation. It was concluded that ascorbic acid is an antioxidant in biological fluids, animals, and humans, both with and without iron supplementation. 

Iron supplementation is necessary to replete iron stores (Fig. 76-5). Parenteral iron therapy improves response to erythropoietic therapy and reduces the dose required to achieve and maintain target indices. In contrast, oral therapy is often inadequate. 

Consider holding IV iron if receiving iron supplementation... 

For the second level, the correction of modest iron deficiency, various iron salts have been recommended or prescribed as iron supplements. These salts have included iron(II) succinate, fumarate, gluconate, and lactate, and iron(III) citrate - or, better (335), ammonium iron(III) citrate as iron(III) citrate seems to be a poorly characterized compound (337). There are two main problems. The first is the ease of oxidation of the iron(II) salts, particularly the lactate. The second is that absorption of iron from these sources is very inefficient (57), as species such as Fe (aq), Fe (aq), and simple hydrolysed entities such as FeOH (aq) cross membranes such as those that constitute the wall of... 

The use of iron(II) sulfate as a detoxicant for mimosine-affected sheep is an unusual example of iron supplementation (7). It provides an interesting complement and link to the following paragraphs on the use of hydroxypyridinones as detoxicants for iron-burdened humans. 

Amenorrhoea, which refers to the absence of menstruation, is managed by the administration of progestogen components such as dydrogesterone. Nonsteroidal anti-inflammatory drugs are indicated in premenstrual tension. Iron supplements are indicated in menorrhagia (abnormal heavy menstruation). 

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