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Iron deficiency stages

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. [Pg.383]

Restless-legs syndrome occurs in 5% to 15% of the population, making it a common sleep disorder.11,12 The prevalence of RLS increases with age and in various medical conditions such as end-stage renal disease (ESRD), pregnancy, and iron deficiency.13 RLS appears to be more common in women than in men and has a genetic link. The majority of RLS patients (63% to 92%) report a positive family history.14... [Pg.622]

The earliest and most sensitive laboratory change for iron-deficiency anemia is decreased serum ferritin (storage iron), which should be interpreted in conjunction with decreased transferrin saturation and increased total iron-binding capacity (TIBC). Hb, hematocrit, and RBC indices usually remain normal until later stages of iron-deficiency anemia. [Pg.379]

The answer is d. (Hardman, pp 1331-1333.) Iron-deficiency anemia usually occurs in infants undergoing rapid growth. In adults in a late stage, it may result in a bowel syndrome associated with gastritis and hypochlo-rhydria (Plummer-Vinson syndrome). Characteristically, all iron-deficiency anemias are associated with a hypochromic microcytic blood profile. Infestation with the tapeworm D. latum is accompanied by a hyperchromic macrocytic anemia, which is treatable with vitamin B12. Bleeding syndromes are treated with iron. [Pg.116]

Iron deficiency is a serious problem in crop production in certain regions of the world ami some nutritionists consider iron deficiency anemia to be one of the most frequently observed mineral element deficiency conditions in humans. Bui iron ferlilizalion of soils is not likely to be effective in decreasing the incidence of this deficiency. The reasons for this apparent contradiction arc based upon the behavior of iron at several stages in the food chain. [Pg.874]

Erythropoietin [ery throw PO eetin] is a glycoprotein, normally made by the kidney, that regulates red cell proliferation and differentiation in bone marrow. Human erythropoietin, produced by recombinant DNA technology, is effective in the treatment of anemia caused by end-stage renal disease, anemia associated with HIV-infected patients, and anemia in some cancer patients. Supplementation with iron may be required to assure an adequate response. The protein is usually administered intravenously in renal dialysis patients, but in others the subcutaneous route is preferred. Side effects such as iron deficiency and an elevation in blood pressure occur. [Note The latter may be due to increases in peripheral vascular resistance and/or blood viscosity.]... [Pg.217]

In times of iron deficiency, many bacteria and fungi release low molecular weight chelators called siderophores (see Iron Transport Siderophores). These molecules bind ferric iron tightly and the ferric-siderophore complexes are then transported into the cell by a system of uptake proteins. The first stage in the uptake process involves an outer membrane receptor specific to each siderophore. One of the best characterized of these receptors is FhuA, the ferrichrome uptake receptor of E. coli, and we will describe this in detail. However, though other ferric-siderophore complexes are taken up by cells, and their iron released by systems similar to those of ferrichrome, their mechanisms may vary from those of ferrichrome in some respects. FepA and FecA" are two of the outer membrane ferric-siderophore receptors that have recently been structurally characterized. [Pg.2266]

In the later stages of IDA, the Hgb and Hct fall below normal values, and a microcytic, hypochromic anemia develops. Microcytosis may precede hypochromia, as erythropoiesis is programmed to maintain normal Hgb concentration in deference to ceU size. As a consequence, even slightly abnormal Hgb and Hct levels may indicate significant depletion of iron stores and should not be ignored. In terms of RBC indices, MCV reduction occurs earlier in iron-deficient hematopoiesis than reduction in Hgb concentration. [Pg.1814]

Most patients tolerate EPO therapy well. Iron deficiency can occur in patients treated with EPO and close monitoring of iron levels is necessary. Oral iron supplementation should be given if transferrin saturation drops to 20% or the serum ferritin level drops below 100 ng/mL. Some patients develop functional iron deficiency, in which the iron stores are normal, but the supply of iron to the erythroid marrow is less than that necessary to support the demand for RBC production. Therefore many practitioners routinely supplement EPO therapy with oral iron therapy. The hypertension commonly seen in end-stage renal disease patients on EPO is far less common in AIDS patients. More common toxicities of EPO administration include nausea, headache, fever, bone pain, and fatigue. Other adverse effects to monitor include seizures, thrombotic events, and allergic reactions such as rash or local reactions at the injection site. [Pg.1823]

Gleason G. Iron deficiency anemia finally reaches the global stage of public health. Nutt Clin Care 2002 5 217-219. [Pg.1829]

Iron deficiency anaemia develops in three stages ... [Pg.22]

Iron deficiency amicmia. There is low hacmoglohin resulting in a microcytic hypochromic anaemia (Fig. 3). Low stainahle iron is seen in bone marrow. Only in the late stages of iron deficiency anaemia arc low concentrations of senim iron observed. [Pg.23]

FIGURE 53-5 Sequential changes (from left to right) in the development of iron deficiency in the adult. Rectangles enclose abnormal test results that identify the stage of Fe-deficiency. RE marrow Fe, reticuloendothelial hemosiderin RBC, red blood cells. [Pg.936]

Iron-deficiency anaemia is one result of the advanced-stage of iron deficiency. For food fortification with iron, many compounds of iron and elemental iron are used. In the evaluation of the biological value of the individual compounds, the increased level of haemoglobin (which cannot be formed in iron deficiency) in experimental animals on an iron dose is used as a criterion. Ferrous sulfate is used as a reference compound. Compared with ferrous sulfate, the usable forms of iron can be divided into three groups ... [Pg.436]

Iron deficiency and iron deficiency anemia have been associated with impaired cognitive development and functioning. These effects of iron deficiency may be mediated in part by the deprivation of functional iron in brain tissue, and the impact of iron deprivation may vary depending on its timing in relation to critical stages of brain development. Iron interventions in anemic school-age children generally result in improved school performance. The results of iron interventions in infants and... [Pg.16]

Severe hypochromic microcytic anemia, responding only to vitamin B6 and not to iron, a typical symptom of B6 deficiency in many species of animals, is related to the dependence of porphyrin biosynthesis on vitamin Be, preceding the 8-aminolevulinic acid stage, at the condensation of glycine with succinate to yield a-amino- 3-ketoadipate, the immediate precursor of 8-aminolevulinic acid. [Pg.212]


See other pages where Iron deficiency stages is mentioned: [Pg.236]    [Pg.260]    [Pg.260]    [Pg.125]    [Pg.147]    [Pg.167]    [Pg.183]    [Pg.251]    [Pg.756]    [Pg.756]    [Pg.116]    [Pg.823]    [Pg.826]    [Pg.826]    [Pg.829]    [Pg.1814]    [Pg.1814]    [Pg.2392]    [Pg.500]    [Pg.191]    [Pg.17]    [Pg.436]    [Pg.174]    [Pg.572]    [Pg.12]    [Pg.15]    [Pg.3]    [Pg.101]    [Pg.300]    [Pg.590]   
See also in sourсe #XX -- [ Pg.936 ]




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Iron deficiency

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