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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The amount and effectiveness of erythropoiesis was measured using 59Fe in 10 patients with the anaemia of chronic disease and in 10 iron deficient patients with a comparable degree of anaemia. In both conditions the anaemia was the result of the failure of the marrow to compensate for a modest degree of peripheral haemolysis but ineffective erythropoiesis was significantly greater in iron deficiency than in chronic disease. The results suggest that although the peripheral blood picture is similar in both conditions the anaemia of chronic disease cannot be attributed simply to iron deficient erythropoiesis.
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PMID:Erythropoiesis in the anaemia of chronic disease. 30 42

Tests to evaluate body iron stores were compared in patients with iron deficiency and the anemia of chronic disease. The serum ferritin assay separated these disorders in 20 of 22 patients. One discrepancy was explained by the concomitant association of both disorders. From this study and review of literature a low serum ferritin level is a good indication for iron therapy. The serum ferritin assay is a clinically useful test in lieu of bone marrow estimation of body iron stores to detect patients with iron deficiency. Total iron binding capacity levels when high-normal or elevated are sometimes helpful as a screening test in separating iron deficiency from the anemia of chronic disorders. Free erythrocyte protoporphyrin values were elevated in both conditions but were higher in iron deficiency than in the anemia of chronic disorders with considerable overlap of values. Urinary iron excretion with deferoxamine was not helpful in separating these disorders but is a useful test to establish iron overload. An elevated serum ferritin level is usually found with disease of iron overload but serum iron levels, deferoxamine iron excretion tests, and liver biopsy for estimation of iron stores are still beneficial diagnostic aids.
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PMID:Serum ferritin, free erythrocyte protoporphyrin, and urinary iron excretion in patients with iron disorders. 86 19

We audited 281 consecutive orthopedic patients scheduled for surgery for whom blood type/cross-matching was requested over a 6-month period. One hundred and sixty-two patients predonated autologous blood at University Hospitals of Cleveland, and 34 (21%) of these were anemic [hematocrit (Hct) less than or equal to 39%] at initial donation. Twelve (35%) of these 34 anemic autologous blood donors subsequently received homologous blood. In contrast, 18 (15%) of 128 nonanemic autologous blood donors received homologous blood (p = 0.05). In 119 patients who did not donate autologous blood, 39 (33%) were anemic at admission. Of these, 22 (56%) received homologous blood. In the 80 remaining nonanemic patients, 33 (41%) received homologous blood (p = 0.119). Analysis of discharge Hct indicates that 31 (12%) of 263 evaluable patients were possibly transfused inappropriately. The anemias of a cohort of 30 autologous donors were analyzed: 5 had rheumatoid arthritis without iron deficiency. Nine (30%) others had evidence of iron deficiency. Sixteen (53%) had an unclassified anemia of chronic disease. We conclude: (1) the high rates of homologous blood exposure indicate a need for innovative blood conservation strategies in anemic autologous blood donors; (2) the prevalence of anemia and the high rates of homologous blood exposure in anemic patients who did not donate autologous blood demonstrate a need for early recognition and treatment in order to procure autologous blood and reduce homologous blood exposure; (3) the presence of inappropriate autologous and homologous transfusions demonstrates a need for more effective physician education programs that emphasize 'no blood transfusion' as an alternative to enhance blood conservation effectiveness.
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PMID:Prevalence and classification of anemia in elective orthopedic surgery patients: implications for blood conservation programs. 144 12

Iron deficiency occurs when the body's iron stores are exhausted. The source of blood loss leading to iron deficiency must be identified in all cases. Anemia of chronic disease generally results from an infectious, inflammatory, or malignant process. However, in some reported cases, no such process could be identified. Differentiating iron deficiency anemia from anemia of chronic disease may be difficult because of similarities in presentation. Physicians need to be aware of special clinical considerations when these two types of anemia coexist. Ferrous sulfate therapy is the ideal form of iron replacement.
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PMID:Iron deficiency and anemia of chronic disease. Clues to differentiating these conditions. 152 10

Microcytic anemia is defined as the presence of small, often hypochromic, red blood cells in a peripheral blood smear and is usually characterized by a low MCV (less than 83 micron 3). Iron deficiency is the most common cause of microcytic anemia. The absence of iron stores in the bone marrow remains the most definitive test for differentiating iron deficiency from the other microcytic states, ie, anemia of chronic disease, thalassemia, and sideroblastic anemia. However, measurement of serum ferritin, iron concentration, transferrin saturation and iron-binding capacity, and, more recently, serum transferrin receptors may obviate proceeding to bone marrow evaluation. The human body maintains iron homeostasis by recycling the majority of its stores. Disruptions in this balance are commonly seen during menstruation, pregnancy, and gastrointestinal bleeding. Although the iron-absorptive capacity is able to increase upon feedback regarding total body iron stores or erythropoietic activity, this physiologic response is minimal. Significant iron loss requires replacement with iron supplements. The vast majority of patients respond effectively to inexpensive and usually well-tolerated oral iron preparations. In the rare circumstances of malabsorption, losses exceeding maximal oral replacement, or true intolerance, parenteral iron dextran is effective. In either form of treatment, it is necessary to replete iron stores in addition to correcting the anemia.
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PMID:Microcytic anemia. Differential diagnosis and management of iron deficiency anemia. 157 56

Recent studies have shown that the serum transferrin receptor is a sensitive, quantitative measure of tissue iron deficiency. This study was undertaken to determine the serum transferrin receptor's ability to distinguish iron-deficiency anemia from the anemia of chronic inflammation and to identify iron deficiency in patients with liver disease. The mean transferrin receptor level in 17 normal controls was 5.36 +/- 0.82 mg/L compared with 13.91 +/- 4.63 mg/L in 17 patients with iron-deficiency anemia (p less than 0.001). The mean serum receptor level was normal in all 20 patients with acute infection, including five with acute hepatitis, and was also normal in 8 of 10 anemic patients with chronic liver disease. Receptor levels were in the normal range in all but 4 of 41 patients with anemia of chronic disease. We conclude that unlike serum ferritin levels, which are disproportionately elevated in relation to iron stores in patients with inflammation or liver disease, the serum transferrin receptor level is not affected by these disorders and is therefore a reliable laboratory index of iron deficiency anemia.
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PMID:Serum transferrin receptor distinguishes the anemia of chronic disease from iron deficiency anemia. 158 89

Anaemia in rheumatoid arthritis (RA) is a common and debilitating complication. The most common causes of this anaemia are iron deficiency and anaemia of chronic disease. Investigations have suggested that interleukin 1 (IL-1) or tumour necrosis factor (TNF), or both, from monocytes associated with chronic inflammation are responsible for the anaemia of chronic disease. On bone marrow examination anaemia of chronic disease is characterised by the diversion of iron from the erythropoietic compartment into marrow macrophages. This phenomenon is termed failure of iron utilisation. In this study, CFU-E (colony forming unit erythroid; late red cell precursors) and BFU-E (burst forming unit erythroid; early red cell precursors) stem cells were cultured from 10 normal marrow samples and 12 marrow samples from patients with RA with iron deficiency anaemia and 10 samples from patients with RA with failure of iron utilisation. All patients with RA were anaemic (haemoglobin less than 100 g/l), Potential accessory or inhibitory cells of erythropoiesis (CD4, CD8, or CD14 positive cells) were removed before culture. Control marrow samples were studied in a similar manner. Normal marrow samples yielded 377 (17) CFU-E and 133 (6) BFU-E (mean (SD)) colonies for each 2 x 10(5) light density cells plated. CD4 ablation caused reductions of 62 and 100% in CFU-E and BFU-E colonies respectively. CD14 removal resulted in considerable but lesser reductions of 46% for CFU-E and 25% for BFU-E. In both groups of patients with RA, CFU-E colony numbers were significantly lower than those seen in normal control subjects, 293 (17) for patients with iron deficiency anaemia and 242 (35) for patients with failure of iron utilisation. BFU-E colony numbers were 102 (13) and 108 (20) respectively. In patients with RA, CD4 removal caused a significantly greater loss of CFU-E colonies compared with normal control subjects. Cytolysis of CD14 positive cells caused a reduction in CFU-E colonies in the two RA groups which was similar to that seen in normal subjects. In conclusion, patients with RA seem to have fewer CFU-E progenitors but essentially normal numbers of BFU-E stem cells. Our data suggest a stimulatory role for marrow CD4 and CD14 cells in erythropoiesis in patients with RA. Monocytes-macrophages (CD14 positive) are known to be producers of IL-1 or TNF, or both, however, the predicted increase in the CFU-E colonies on removal of CD14 cells is not seen. Therefore, if IL-1 or TNF, or both, are responsible for the impairment of erythropoiesis in patients with RA, marrow macrophages are unlikely to be the source. Moreover, these results indicate the probability of erythropoietin resistance on the basis of diminished CFU-E colony formation in patients with RA.
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PMID:Anaemia of chronic disease in rheumatoid arthritis: effect of the blunted response to erythropoietin and of interleukin 1 production by marrow macrophages. 161 58

We determined serum ferritin, C-reactive protein (CRP), fibrinogen, and the erythrocyte sedimentation rate (ESR) in 73 patients with anemia of chronic disease. Nomograms of CRP, ESR, or fibrinogen vs ferritin concentrations were constructed and used to estimate the iron store in bone marrow. Iron stores estimated from the nomograms were compared with the results of staining cytological bone marrow smears for iron, the reference method for evaluating iron in bone marrow. In contrast to the results of Witte et al. (Clin Chem 1985;31:1011; Am J Clin Pathol 1986;85:202-6 and 1988;90:85-7), we observed that nomograms of CRP, fibrinogen, or ESR (i.e., acute-phase reactants not influenced by changes in iron metabolism) vs ferritin are not suitable to correct for the acute-phase component of changes in ferritin concentrations. For ferritin concentrations less than 70 micrograms/L, we found that iron deficiency, as judged from bone marrow iron stain, apparently was always present.
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PMID:Measurements of serum ferritin used to predict concentrations of iron in bone marrow in anemia of chronic disease. 190 71

In the vast majority of cases, the cause of microcytic hypochromic anemia is clearly suggested by the patient history, physical examination results, red cell indexes, and peripheral blood smear. Thus, further diagnostic testing, if necessary, can be very selective. When the underlying cause of anemia is obscure, the serum ferritin concentration should be measured first. If it is normal or increased, serum iron and free erythrocyte protoporphyrin levels can be determined. The serum iron level is low in anemias caused by iron deficiency and chronic disease but normal or elevated in those resulting from the thalassemias, hemoglobin E disorders, and lead toxicity. The free erythrocyte protoporphyrin level is elevated with iron deficiency, the anemia of chronic disease, and lead toxicity but normal with thalassemias and hemoglobin E disorders. Results of these two test indicate which of the more specific tests is most likely to yield the correct diagnosis.
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PMID:Determining the cause of anemia. General approach, with emphasis on microcytic hypochromic anemias. 202 Jun 45

We investigated the serum erythropoietin (Epo) response in 11 rheumatoid arthritis (RA) patients without anaemia, 7 with RA and iron deficiency (ID) and 12 with RA and anaemia of chronic disease (ACD). In all patients the serum Epo was higher than in healthy subjects. Apparently this increase was insufficient to prevent anaemia in ID and ACD. Serum Epo correlated negatively with serum ferritin. Ten RA patients with ACD were treated with the oral iron chelator 1,2-dimethyl-3-hydroxypyrid-4-one (L1). No obvious toxicity signs occurred after one week of treatment. It effectively released iron from iron stores. The Hb rise (in 70% of the patients) was correlated positively with an Epo increase and negatively with a serum ferritin decrease. We conclude that a serum Epo increase does not overcome ACD. Epo response might correlate inversely with iron stores. L1 treatment effectively chelates iron from iron stores. The effects of L1 on erythropoiesis and serum Epo and its safety need further substantiation after prolonged treatment in more RA patients.
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PMID:Impaired erythropoietin responsiveness to the anaemia in rheumatoid arthritis. A possible inverse relationship with iron stores and effects of the oral iron chelator 1,2-dimethyl-3-hydroxypyrid-4-one. 205 65


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