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At least 19 recordsLinked to original sources
PubMed1975

Intestinal iron absorption under the influence of available storage iron and erythroblastic hyperplasia. Comparative studies in children with hereditary spherocytosis, nonspherocytic enzymopenic hemolytic anemia, acquired hemolytic anemia, vitamin B12 deficiency induced megaloblastic anemia, erythroblastic hypoplasia and aplastic anemia.

A high negative correlation (coefficient similar to 0.9) between increased 59Fe absorption from a diagnostic 0.56 mg 59Fe2+ dose and the depletion of available storage iron was observed in menstruating and pregnant women, fullterm and premature infants, blood donors, patients with infections, inflammations, tumors, hepatic cirrhosis, gastric surgery, increased urogenital or gastrointestinal blood loss. The increased diagnostic 59Fe2+ absorption is a reliable and sensitive indicator of at least depleted iron stores or prelatent iron deficiency as caused by iron malnutrition or maldigestion, increased iron requirement in pregnancy, infancy, urogenital or gastrointestinal blood loss. Although the messenger system which signalyzes the depletion of iron stores to the iron absorbing enterocytes of the duodenal and jejunal mucosa is not yet known available storage iron seems to control intestinal iron absorption under normal and the great majority o pathological condition in humans. Anemia per se or high erythropoietin levels in blood do not influence iron absorption since patients with even severe erythroblastic hypoplasia, aplastic anemia and megaloblastic anemia due to vitamin B12 deficiency absorb iron according to their iron stores. An only mild hyperplasia of the erythropoietic system in the bone marrow does also not effect iron absorption which was still under the control of available storage iron in patients with hereditary spherocytosis, nonspherocytic congenital hemolytic anemia due to glucose-6-phosphate dehydrogenase deficiency, acquired hemolytic anemia and vitamin B12 deficiency induced megaloblastic anemia..

Adolescent↗
PubMed1987

Factors influencing nonleukemic death in refractory anemia, refractory anemia with ring sideroblasts, and refractory anemia with excess of blasts.

The association between nonleukemic death and various features recorded at presentation in patients with refractory anemia (RA), RA with ring sideroblasts, and RA with excess of blasts was analyzed in 251 patients using the proportional hazards model. Features associated with higher nonleukemic death rates were: 1% or more metamyelocytes in peripheral blood (PB); lower 59Fe incorporation rate; 1% or more blasts in PB; lower hematocrit or hemoglobin; presence of giant platelets; 1 microgram/liter or higher serum vitamin B12 levels; higher periodic acid-Schiff positive erythroblasts; and 1% or higher promyelocytes in PB. Multivariate analysis was also performed using the following predictor variables: metamyelocytes in PB, micromegakaryocytes, hemoglobin, giant platelets, presence or absence of RA with excess of blasts, and mononuclear large megakaryocytes. Patients were divided arbitrarily into low (hazard ratio, less than 0.55), intermediate (hazard ratio, 0.55-1.5), and high (hazard ratio, greater than 1.5) risk groups. The cumulative nonleukemic death rates in the high and intermediate risk groups reached a median at 602 and 1984 days from presentation, respectively, while the rate reached a plateau level of 49.4% after 2644 days in the low risk group. The risk factors for leukemic transformation and nonleukemic death were found to be different and to need separate consideration.

Anemia, Refractory↗
PubMed1988

Regulation of erythropoietin and burst-promoting activity production in patients with aplastic anemia and iron deficiency anemia.

To clarify the control mechanism of production of erythropoietic growth factors in anemic states, we compared erythropoietin (Epo) and burst-promoting activity (BPA) in patients with aplastic anemia and iron deficiency anemia, using in vitro erythroid progenitor assays. Although serum levels of Epo activity increased in the presence of anemia, the rise was more marked in patients with aplastic anemia. BPA was high only in the sera of aplastic anemia patients. Serum levels of BPA of patients with aplastic anemia negatively correlated with hemoglobin concentrations, while those of patients with iron deficiency anemia did not correlate. In 2 patients with aplastic anemia who responded well to androgen therapy, serum levels of Epo activity and BPA decreased after the hemopoiesis had recovered. These results suggest that serum levels of BPA do not rise in response to anemia only. The elevated BPA levels in sera in cases of aplastic anemia are probably related to a reduction in the number of hemopoietic stem cells. Moreover, we observed that BPA in bone-marrow-conditioned medium (BMCM) from patients with severe aplastic anemia increased more than in the BMCM from patients with severe iron deficiency anemia. Therefore, our findings suggest that the enhanced BPA production depends on a decrease in hemopoietic precursors rather than the anemic state.

Adolescent↗
PubMed1988

Pernicious anemia. The expected findings of very low serum cobalamin levels, anemia, and macrocytosis are often lacking.

When patients are examined for possible cobalamin deficiency, great stress is often placed on the presence or absence of macrocytosis and anemia and on how low the serum cobalamin level is. The present study, however, shows that only 45 (64%) of 70 consecutively diagnosed patients with pernicious anemia, the most common cause of cobalamin deficiency, had very low cobalamin levels (less than 74 pmol/L [or less than 100 ng/L]). Anemia was absent in 13 (19%) of the patients, and macrocytosis was absent in 23 (33%) of the patients; such absence was particularly common when cobalamin levels were only slightly or moderately low (74 to 184 pmol/L). Coexisting iron deficiency was responsible for the absence of macrocytosis in nine patients. Of the ten patients with neither anemia nor macrocytosis, neurological disturbance was prominent in six, including four whose only noticeable abnormality was cerebral. These observations indicate that macrocytosis and anemia, two classic features of pernicious anemia, may be overstressed in our diagnostic approach. All subnormal serum cobalamin results are best viewed as pathological until proved otherwise. Emphasis on only very low cobalamin levels risks delaying the diagnosis of pernicious anemia in a substantial proportion of cases, particularly in those without anemia or macrocytosis.

Adult↗
PubMed1979

Macrocytosis, mild anemia, and delay in the diagnosis of pernicious anemia.

Various factors led to delays of several months to several years in the diagnosis of pernicious anemia in 11 patients, occasionally with serious consequences. These cases illustrate that earlier diagnosis is possible with closer attention to abnormal results of common tests. Macrocytosis, detected by high mean corpuscular volume, often preceded anemia but was not investigated, especially when anemia was only slight. Several cases demonstrated that vitamin B12 deficiency may initially produce only a mild macrocytic anemia, which is maintained for a long period before a rapid worsening supervenes; the reason for the latter acceleration of anemia is unknown. Most serious was the evidence that mild anemias are often ignored. Stricter attention to the established limits of normal hemoglobin values is required. These aspects of physician performance have implication for the recognition of all anemias.

Aged↗
PubMed1977

[Iron therapy and hemoglobin regeneration in pregnancy anemias and postpartum anemias (author's transl)].

The influence of oral doses of iron on the hemoglobin regeneration of pregnancy anemias and postpartum anemias was examined. The examinations were carried out in 45 pregnant women and in 70 puerperae. Other hematologic parameters besides hemoglobin were determined before, and 4 and 6 weeks during treatment with 110 mg iron sulfate daily. In pregnancy anemias, hemoglobin regeneration took place at a much slower rate under the iron therapy than was the case in postpartum anemias. Postpartum anemias of medium severity require for elevating the hemoglobin values to 12.0 g% at iron absorption rate of 22%, a treatment period of 35 days with a total amount of 3.8 g ferrous sulfate. In milder forms of anemia iron absorption diminished to 15% as hemoglobin conditions improved. An iron treatment course of 6 weeks will not be sufficient to cover the maternal iron deficiency during pregnancy and lyingin. To achieve optimum iron compensation, the daily supply of 100 mg iron will be necessary during pregnancy from the 16th week until delivery. In mild to medium anemias, postpartum iron treatment of 10 to 18 weeks' duration will be necessary until the exhausted iron deposits have been replenished.

Anemia, Hypochromic↗
PubMed1986

Failure to diagnose anemia in medical inpatients. Is the traditional diagnosis of anemia a dying art?

The diagnosis and treatment of anemia in medical inpatients were studied. Anemia was detected from the admitting complete blood cell count, the medical charts were perused for management of anemia by the physicians, and the cases of anemia were classified by the investigators, using the complete blood cell count and peripheral blood smear. Anemia was seldom diagnosed in the traditional manner. In about 25 percent of cases, it was not even recognized. In about 20 percent, it was recognized but not evaluated or treated. In the 55 percent of cases adequately diagnosed and/or treated, the diagnosis was often more "situational" than analytic, the treatment more empiric than specific. Physicians ignored or misused information from the complete blood cell count and smear description and examined the smear themselves in fewer than one in 10 anemic patients. Not all of the missed cases of anemia were mild, expected from the patient's illness, or unimportant to the patient's care.

Anemia↗
PubMed1987

Comparison of effects of vegetable protein diet and animal protein diet on the initiation of anemia during vigorous physical training (sports anemia) in dogs and rats.

The effect of the quality of dietary protein on the initiation of temporary anemia during vigorous physical training (sports anemia) was studied in dogs and rats. In the dog experiment, one group of dogs was fed a crude animal protein (AP) diet and the other a crude vegetable protein (VP) diet. After 6 weeks on the diets in a sedentary state (rest period), all the dogs were forced to run every day for two weeks (exercise period). The rat experiment was carried out using purified nutrient mixtures. Casein (C) was used as AP and gluten (G) as VP. Feeding was done for two weeks in two series with two diet groups of rats. One series was 15% protein feeding (15% C and 15% G) groups and the other 24% protein feeding (24% C and 24% G) groups. In each group, one group remained in a sedentary state (rest group), and the other ran vigorously on a treadmill every day for one week (exercise group). In a sedentary state, there was a slight tendency for the hemoglobin content or erythrocyte count to be reduced, even when the values remained within the normal range, in dogs and rats fed VP. On the other hand, after vigorous running, significant anemia (reduction of hemoglobin) appeared in the VP diet dogs and in all exercise rat groups except the 24% C group. It was confirmed that the anemia was caused by a reduction of erythrocyte resistance to hemolysis, which was closely related to changes in the lipid composition of blood (serum and especially erythrocytes). The change in lipid profile revealed by the experiments was a reduction of free cholesterol in blood associated with an increase of lysolecithin in dogs during the exercise period and in the rat exercise groups. It was suggested that repeated physical exercise increased the activity of LCAT (lecithin-cholesterol-acyltransferase) in the liver, spleen, etc., resulting in the above changes in lipid patterns in the blood. In dogs of AP and rats of 24% C, however, those changes in lipid pattern caused by exercise and sports anemia did not appear significantly. The different effects of the AP diet seemed to be due to the antagonistic effects of lysine, which was present in sufficient amounts in the diet. Thus the theoretical basis for our recommendation of a high amount of AP in the diet to prevent sports anemia was clarified by the present experiments.(ABSTRACT TRUNCATED AT 400 WORDS)

Anemia↗
PubMed1976

[The effect of mesterolone in panmyelopathic anemia and anemia of renal failure].

A controlled randomized multicenter trial was carried out to examine the therapeutic value of the androgen mesterolone in aplastic anemia and anemia of renal failure. the drug was given in a dose of 2 mg/kg orally for 6 months. Control patients received no androgens but were otherwise similarily treated. 31 patients with aplastic anemia could be evaluated. No significant difference was found between androgen treated control cases in respect to bone marrow cellularity, improvement of peripheral blood cell counts or survival. In a group of 14 patients not being hemodialyzed with anemia from renal failure, 3 of the androgen treated and none of the control patients showed progressive and significant improvement of erythropoiesis; however, this was not a statistically significant difference when the both groups of patients were compared. The results do not suggest that the androgen mesterolone is of therapeutic value in the majority of adult patients with aplastic anemia. Possible reasons of the discrepancy to positive results reported in the literature are discussed.

Adolescent↗
PubMed1992

Serum transferrin receptor distinguishes the anemia of chronic disease from iron deficiency anemia.

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.

Anemia↗
PubMed1990

Improvement of anemia by recombinant erythropoietin in patients with myelodysplastic syndromes and aplastic anemia.

Eight patients with myelodysplastic syndromes (MDS) and four patients with aplastic anemia (AA) were treated with recombinant erythropoietin (rEpo) to investigate its effect on the anemia of these patients. rEpo was administered by i.v. injection three times a week for at least four weeks. The doses were 3,000, 6,000, or 12,000 U/day. Despite an elevated "endogenous" Epo level, a greater than 1.5 g/dl increase in hemoglobin (Hb) concentration was observed in one patient with refractory anemia (RA), one patient with refractory anemia with excess of blasts (RAEB), and one patient with AA. A greater than 50% decrease in red cell transfusion requirement was observed in one patient with RA and one patient with AA. One RA patient and one AA patient have received rEpo as maintenance therapy for more than 64 and 100 weeks, respectively. They no longer need red cell transfusions and have had a normal Hb concentration and normal ferrokinetics. No side effect was seen. These results indicate that rEpo may benefit some patients with MDS and AA who are dependent on red cell transfusions while further studies will be necessary to elucidate the mechanism by which rEpo stimulates erythropoiesis and improves anemia in patients with these diseases.

Adult↗
PubMed1992

Microcytic anemia. Differential diagnosis and management of iron deficiency anemia.

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.

Anemia, Hypochromic↗