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

Animals with hereditary abnormalities of hematopoiesis are quite useful in the study of regulatory pathways of megakaryocytopoiesis and platelet formation. Seven such animal models are analyzed here. The Wistar Furth rat has been recently discovered to have reduced platelet number, but large mean platelet volume, and is, therefore, a model of hereditary macrothrombocytopenia. Study of the Wistar Furth rat may help to elucidate the process of platelet formation. Two mouse mutants the S1/S1d and W/Wv, have macrocytic anemia with reduced megakaryocyte number, but normal platelet count. In these mice, the platelet count is maintained by increased platelet production per megakaryocyte. These models demonstrate that factors other than platelet level are monitored in the feedback regulation of megakaryocytopoiesis and platelet production, and further study should lead to a better understanding of the regulation of megakaryocyte size. The Belgrade rat has severe microcytic anemia with decreased megakaryocyte number. Megakaryocyte size is increased, but platelet count is moderately reduced and thus the megakaryocyte-platelet picture resembles that of severe iron deficiency anemia. A more in depth examination of this model should delineate the effects of iron deficiency and hypoxia on megakaryocytopoiesis. The grey collie dog has cyclic hematopoiesis with large asynchronous fluctuations in all blood cell counts at approximately 2-week intervals. Megakaryocytes have not been studied. This model should be a tool to define the relationships between hematopoietic growth factors and differentiation of the various hematopoietic cell lineages. The br/br rabbit has a transient disturbance in fetal megakaryocytopoiesis and brachydactyly due to spontaneous amputation. Further study of this model may provide a better understanding of fetal megakaryocyte development and establish whether an association exists between the abnormal megakaryocytes and the limb amputations. The nude mouse with its severe T-lymphocyte deficiency has been studied to ascertain whether T cells play a regulatory role in normal and acute thrombocytopenia-stimulated megakaryocytopoiesis. The question of whether T cells or their products are responsible for reactive thrombocytosis in chronic inflammation could be examined with this model. These animal mutants have provided and should continue to provide important models for understanding the regulation of megakaryocytopoiesis and platelet production.
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PMID:Animal models with inherited hematopoietic abnormalities as tools to study thrombopoiesis. 264 83

We describe our experience in creating a rule-based expert system for the interpretation of microcytic anemia using the expert system development tool, VP-Expert, running on an IBM personal computer. VP-Expert processes data (complete blood cell count results, age, and sex) according to a set of user-written logic rules (our program) to reach conclusions as to the following causes of microcytic anemia: alpha- and beta-thalassemia trait, iron deficiency, and anemia of chronic disease. Our expert system was tested using previously interpreted complete blood cell count data. In most instances, there was good agreement between the expert system and its pathologist-author, but many discrepancies were found in the interpretation of anemia of chronic disease. We conclude that VP-Expert has a useful level of power and flexibility, yet is simple enough that individuals with modest programming experience can create their own expert systems. Limitations of such expert systems are discussed.
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PMID:The diagnosis of microcytic anemia by a rule-based expert system using VP-Expert. 277 65

In order to predict a haemoglobin (Hb) rise, in response to treatment with iron from simple erythrocyte and serological parameters, we treated 28 anaemic RA patients with oral iron during 6 weeks. Iron deficiency, present in 57% of patients, was assessed by staining a bone marrow aspirate for iron. Response rate in this group was 81% and median Hb increase was 0.8 mmol/l. After 6 weeks 69% of iron deficient patients were still anaemic. Patients without iron deficiency, considered as having anaemia of chronic disease (ACD), showed no significant Hb rise. The finding of a hypochromic microcytic anaemia was associated with a significant Hb rise. MCV showed highest specificity and predictive value (90 and 88%) and ferritin was the most valid predictor of a Hb rise within 6 weeks. Combination of low MCV and low ferritin resulted in a 100% specificity and predictive value indicating that patients with values below cut off point of these variables will definitely respond to treatment. Disease activity tended to decrease after 6 weeks, but this was not correlated with a Hb rise. It was concluded that a Hb rise can be predicted accurately by blood parameters. Using certain combinations, bone marrow aspiration is rarely necessary. Iron treatment is only useful in iron deficient RA patients, although active RA limits maximal Hb rise. In contrast to earlier findings, iron treatment had no deleterious effects on disease activity.
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PMID:Prediction and evaluation of the effect of iron treatment in anaemic RA patients. 280 11

A method for measuring erythrocyte aluminum content was developed. Erythrocyte aluminum levels correlated with plasma aluminum concentrations in normal controls and in patients undergoing dialysis (r = 0.90, p less than 0.001). In vitro studies showed that erythrocyte aluminum concentrations were not altered by contamination of blood samples, which is a common problem with plasma determinations. The need for anticoagulation and rapid processing were disadvantages of this assay. In the dialysis population studied, the correlative data between mean cell volume and both plasma and erythrocyte aluminum levels (r = -0.50, p less than 0.001; and r = -0.69, p less than 0.001) and lack of correlation with serum ferritin suggested that aluminum overload and not iron deficiency was the cause of microcytic anemia. Patients undergoing continuous ambulatory peritoneal dialysis had lower plasma and erythrocyte aluminum levels and absence of microcytic anemia compared with patients undergoing hemodialysis. Therapy with deferoxamine in 13 patients with aluminum-related microcytic anemia resulted in a decrease in erythrocyte and plasma aluminum content in all patients (265.5 +/- 69.2 micrograms/L to 22.6 +/- 9.7 micrograms/L and 196 +/- 30 micrograms/L to 129 +/- 13.8 micrograms/L). The relatively smaller decrease in plasma aluminum levels suggested mobilization of aluminum from tissues other than erythrocytes. Aluminum chelation most probably occurred from premature erythrocytes, because in vitro studies showed that deferoxamine was unable to chelate aluminum from mature erythrocytes. Hemoglobin level, hematocrit measurement, and mean cell volume showed significant improvement (p less than 0.001). Ten patients showed normalized mean cell volume after 6.2 +/- 2 months of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Application of an erythrocyte aluminum assay in the diagnosis of aluminum-associated microcytic anemia in patients undergoing dialysis and response to deferoxamine therapy. 290 50

In 114 patients (52 males and 62 females) with long-standing pernicious anaemia, hypoferritinaemia was found in 27 (23.7%) and hypochromic microcytic anaemia in 19 (16.6%). Our findings indicate that iron deficiency is a common yet neglected complication of long-standing pernicious anaemia and warrants greater diagnostic and therapeutic attention.
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PMID:Iron deficiency in pernicious anaemia: a neglected diagnosis. 221 45

Neonatal rats from dams receiving 2 or 3 g NaNO2/liter in the drinking water through -gestation and lactation suffered severe microcytic anemia as well as growth retardation and high mortality. Lipemia, fatty liver damage, decreased erythropoiesis of spleen and bone marrow, and reduced plasma and tissue iron levels were noted in affected pups. These effects were all consistent with and characteristic of iron deficiency. Experiments presented here were designed to show that the maternally mediated toxicity of nitrite is actually an iron deficiency syndrome in the pups caused by inadequate iron transfer from dam to pup. It was found that administration of exogenous iron supplement to pups of treated mothers reversed the anemia and other effects of nitrite toxicity noted both in previous studies and in unsupplemented littermates. Mothers of affected pups were themselves anemic. Finally, we fully documented severe iron deficiency in pups of nitrite-treated mothers and showed that these mothers produced milk of reduced iron content. It appears then that nitrite-consuming dams have a reduced capacity to transfer iron to their pups. The nitrite-associated toxicities in the pups are actually a result of an iron deficiency.
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PMID:Nitrite-induced iron deficiency in the neonatal rat. 318 25

Microcytic anemia, long considered an effect of lead poisoning, may in fact result from coexisting iron deficiency. In this study, how RBC size, hemoglobin, and zinc protoporphyrin vary as a function of iron status in a group of children with high lead levels was examined. Charts of all children (N = 51) admitted to Cook County Hospital for treatment of lead poisoning in 1981 to 1983 were reviewed for data on age, blood lead level, hemoglobin concentration, MCV, transferrin saturation and zinc protoporphyrin level. The mean lead level was 86 micrograms/dL and the range was 63 to 190 micrograms/dL. Children with transferrin saturation values less than 7% had a mean MCV of 56 microL, hemoglobin of 8.9 g/dL, and zinc protoporphyrin of 693 micrograms/dL; for those with saturations of 7% to 16%, the values were 61 microL, 10.1 g/dL, and 581 micrograms/dL, respectively; the children with saturations greater than 16% had normal mean MCVs and hemoglobin concentrations (74 microL and 11.4 g/dL) and a mean zinc protoporphyrin value of 240 micrograms/dL (P less than .0005). Multiple linear regression was used to correct for effect of age, and transferrin saturation remained the most important predictor of MCV, hemoglobin, and zinc protoporphyrin levels; the addition of lead did not improve the models. Results of this study suggest that iron deficiency is strongly associated with some of the observed toxicities of lead. Also, lead poisoning can exist without producing microcytosis or anemia, and zinc protoporphyrin concentration may not be a sensitive indicator of lead level in the absence of iron deficiency.
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PMID:Interaction of iron deficiency and lead and the hematologic findings in children with severe lead poisoning. 327 57

Copper deficiency was found in an adult patient who had received excessive daily oral zinc for 10 mo. The deficiency was characterized by hypochromic-microcytic anemia, leukopenia, and neutropenia. Although initially thought to be caused by iron deficiency, the anemia did not respond to oral or intravenous iron. Cessation of zinc tablets and ingestion of an oral copper preparation daily for 2 mo failed to correct the anemia or leukopenia. It was not until shortly after intravenous administration of a cupric chloride solution during a 5-day period, at a total dose of 10 mg, that serum copper and ceruloplasmin levels increased and the anemia, leukopenia, and neutropenia resolved. These data suggest that the elimination of excess zinc is slow and that, until such elimination occurs, the intestinal absorption of copper is blocked.
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PMID:Zinc-induced copper deficiency. 333 23

Documented differences exist in red blood cell (RBC) and granulocyte counts between black and white people. However, little comparative information is available on differences in platelet counts in the two racial groups. Therefore, this study was performed to compare platelet counts in healthy white (94), black (92), and Latin-American (63) persons. Black women had significantly higher platelet counts than did white women (P less than 0.025). Latin-American women were between the other two groups. No differences were noted among men. Black women also had a significantly higher prevalence of iron deficiency and microcytosis of RBCs than did white women. After exclusion of women with either microcytosis or iron deficiency, racial differences in platelet counts were no longer evident. The authors conclude that the differences in the platelet counts between black and white women were secondary to common RBC differences (such as iron deficiency and other causes of microcytic anemia) and were not intrinsic to the platelets. These and other factors that can affect platelet counts should be excluded before determining the reference ranges for proper interpretation of the platelet counts.
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PMID:Platelet counts in three racial groups. 360 82

The RBC distribution width has been reported to be of value in the discrimination of iron deficiency anemia from other microcytic anemias, but studies in pediatric populations are lacking. A population of 734 normal children was studied to establish age-appropriate normal values for RBC distribution width. The RBC distribution width of 47 patients with microcytic anemia was then evaluated. RBC distribution width was elevated in 19 of 22 patients with iron deficiency but was also increased in six of 14 patients with thalassemia trait and two of 11 patients with anemia secondary to inflammatory disease. The resulting discrimination was better than that obtained by using Mentzer's index or the discriminant function in the patients studied. The RBC distribution width, albeit a less then perfect tool, can be of value in evaluating pediatric patients with microcytic anemia.
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PMID:Red blood cell distribution width in pediatric microcytic anemias. 361 97


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