Iron also deficiency

Since there is no true excretion of iron from the body, iron-deficiency anemia occurs mostly because of inadequate absorption of iron or excess blood loss. Inadequate absorption may occur in patients who have congenital or acquired intestinal diseases, such as inflammatory bowel disease, celiac disease, or bowel resection. Achlorhydria and diets poor in iron also may contribute to poor absorption of iron. In contrast, iron deficiency also may occur in patients who exhibit a higher rate of iron loss from the body. This is manifested in... 

Adsorption of aniline on minerals, such as kaolinite, montmorillonite and vermiculite as well as on a-alumina and iron powders, has been studied in order to better understand the interaction of the adsorbate with natural adsorbents154-157. However, the results, similarly to those obtained on a smooth polycrystalline platinum electrode158, are not useful for the removal of aniline from waste water. The commonly used activated charcoal is also deficient owing to slow kinetics of the removal of dissolved pollutants. In this situation, activated carbon fibers, woven as a C-cloth, seem to be the ideal adsorbents for removal of aniline from waste streams. The reports of Niu and Conway159,160 explained the adsorptive and electrosorptive behavior of aniline on C-cloth electrodes and suggested a methodology for clean-up of industrial waste waters. 

Ionic forms of iron (referred to hereafter as iron) also participate in a variety of enzymatic reactions as nonheme irons, which are present as iron-sulfur clusters (e.g., mitochondrial electron transport). There are also both storage and transportable forms of iron that are bound to proteins. Under normal physiological conditions only trace amounts of free iron exist. In the body, if iron exceeds the sequestration capacity of the iron-binding proteins present in different physiological compartments, the free iron can cause tissue damage. Cellular injury is caused by reactive oxygen species that are produced from H2O2 in a reaction catalyzed by iron. Thus, iron homeostasis in the body is in a delicate balance. Either the deficiency or the excess results in abnormalities and presents as a common cause of human diseases. 

Ferrous sulfate (feosol, others) is the hydrated salt, FeSO 7Hff), which contains 20% iron. Ferrous fumarate (feostat, others) contains 33% iron and is moderately soluble in water, stable, and almost tasteless. Ferrous gluconate (fergon, others), which contains 12% iron, also is used in the therapy of iron-deficiency anemia. Polysaccharide—iron complex (niferex, others), a compound of ferrihydrite and carbohydrate, has comparable absorption. The effective dose of these preparations is based on iron content. 

Colorless belite, according to Lee (1983), can occur as very small inclusions in alite and contains very little impurity. Large-crystal, ringlike belite nests (from coarse alkali feldspar) are also colorless because of iron-oxide deficiency. These occurrences of belite, therefore, do not reflect the cooling rate. Consequently, Ono (1978) recommends color observation of roughly 20 pm belite crystals in order to judge the cooling rate. 

Vitamins, minerals, and electrolytes— Studies have shown that during moderate to severe stresses, more zinc, copper, magnesium, and calcium are lost in the urine. Furthermore, stress results in altered blood levels of vitamins A and C, and of zinc and iron. Also, part of the response to stress includes water and sodium retention, via veisopressin and aldosterone secretion. As for the water-soluble vitamins—thiamin, riboflavin, niacin, pyridoxine (B-6), pantothenic acid, folic acid, and vitamin C stress increases their requirement. However, no dietary recommendations are made for these nutrients for individuals under stressful situations. Still, it seems wise to supply some supplementation before deficiency symptoms appear. 

The realization that selenium (Se) may be an essential micronutrient for human diets has arisen only recently, in the second half of the twentieth century. Selenium deficiency, attributable to low soil selenium levels in farm animals, especially sheep that are afflicted by selenium-responsive white muscle disease, has been recognized for at least half a century. However, the more recent identification of Keshan and Kashin-Beck diseases as endemic selenium-responsive conditions, occurring in a central 4000-1— km-wide belt of central China and in areas of Russia, demonstrated conclusively that not only is selenium an essential element for man but also deficiencies occur naturally and require public health measures to alleviate them. Selenium incorporation into plants is affected by the acidity of the soil and by the concentrations of iron and aluminum present so that selenium content of human diets is modulated by these components of the environment. The very recent discovery that these diseases probably arise through the interaction of selenium deficiency with enhanced viral virulence has added a further layer of complexity, but it does not alter the fact that selenium is an essential dietary component that cannot be substituted by any other element. Another complicating factor is that moderately increased soil selenium concentrations result in the opposite condition of seleno-sis, or selenium overload, with equally debilitating consequences. Of all elements, selenium has a very narrow safe intake range, and unlike some other potentially toxic elements, it is absorbed efficiently by the intestine over a wide range of concentrations and across a variety of different molecular forms. 

Tin. The widespread use of caimed foods results in a daily intake of tin that is ca 1—17 mg for an adult male (154). At this level it has not been shown to be toxic. Some grains also contain tin. Too much tin can adversely affect 2inc balance and iron metaboHsm. EssentiaUty has not been confirmed for humans. It has been shown for the rat. An enhanced growth rate results from tin supplementation of low tin diets (85). Animals on deficient diets exhibit poor growth and decreased feed efficiency (155). 

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. 

Iron dextran is a parenteral iron that is also used for die treatment of iron deficiency anemia It is primarily used when the patient cannot take oral drugs or when the patient experiences gastrointestinal intolerance to oral iron administration. Other iron preparations, both oral and parenteral, used in the treatment of iron deficiency anemia can be found in the Summary Drug Table Dragp Used in the Treatment of Anemia... 

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

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. 

Nutrient availability also plays a major role in exudation, with deficiencies in N, P, or K often increasing the rate of exudation (218). It is believed that nutrient deficiency may trigger the release of substances such as organic acids or nonproteinogenic amino acids (phytosiderophores), which may enhance the acquisition of the limiting nutrient (219,220). An example here might be the release of phenolic acids such as caffeic acid in response to iron deficiency, which results in an increase in uptake of the cation (221). 

The magnetic properties of the new solid solution series SrFe Rui 3 3, (0 < X < 0.5) with distorted perovskite structure, where iron substitutes exclusively as Fe(in) thereby causing oxygen deficiency, has also been studied by Greenwood s group [147] using both u and Fe Mossbauer spectroscopy. Iron substitution was found to have little effect on the magnetic behavior of Ru(IV) provided that X remains small (x < 0.2). 

Several other factors also contribute to the development of anemia in patients with CKD. Uremia, a result of declining renal function, decreases the lifespan of RBCs from a normal of 120 days to as low as 60 days in patients with stage 5 CKD. Iron deficiency and blood loss from regular laboratory testing and hemodialysis also contribute to the development of anemia in patients with CKD. 

Mean cell hemoglobin concentration (MCHC) Iron Studies Serum iron 33.4-35.5 g/dL (334-355 g/L) Hemoglobin divided by the hematocrit also low in iron-deficiency anemia. 

The patient is diagnosed with iron-deficiency anemia and is started on ferrous sulfate 325 mg orally three times daily to be taken on an empty stomach. Follow-up CBC 1 month later reveals a Hgb of 10 g/dL (100 g/L or 6.2 mmol/L), previously 9.3 g/dL (93 g/L or 5.77 mmol/L). The patient complains of shortness of breath on exertion and constipation. She also admits to taking only one tablet a day because of nausea. 

Cancer patients also may have concurrent iron deficiency secondary to erythropoietin use ( functional iron deficiency) or to cancer. Therefore, it is imperative that these patients have iron studies done to assess adequate iron stores needed to drive hematopoiesis. If the patient is determined to have sub-optimal iron stores or is iron deficient, then replacement either orally or intravenously may be necessary, in addition to the use of erythropoietin products. The use of iron in these patients is the same as discussed previously under Iron-Deficiency Anemia. ... 

Besides anemia associated with cancer and CKD, anemia of chronic disease can result from inflammatory processes and occurs commonly in autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus. In treating these types of anemia of chronic disease, the most important principle is treating the underlying disease. These patients also may have iron deficiency and should be treated in the manner already discussed. Erythropoietin therapy such as epoetin-alfa therapy at a dose of 150 units/kg three times a week also may be used in these patients. 

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. 

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