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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Crab-eating monkeys, Macaca fasicularis, fed a vitamin E-depleted diet for over 15 months, showed signs of anemia manifested by a lowering in hematocrit, hemoglobin concentration and red blood cell number, and by an increased susceptibility of erythrocytes to hydrogen peroxide lysis. Bone marrow pictures indicated the presence of multinucleated erythroid precursor cells and an accumulation of orthochromatophilic normoblasts. Supplementation with vitamin E resulted in reticulocytosis and a return of the normal bone marrow picture.
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PMID:Accumulation of orthochromatophilic normoblasts in bone marrow of vitamin E-deficient monkey, Macaca fasicularis. 40 14

Protein-energy malnutrition in Kivu is associated with a discrete normocytic, normochromic anemia. An attempt to define the physiopathology of this anemia disclosed the following results. As compared with local controls, both iron and total iron binding capacity were low, but with siderophilin saturation and sideroblast counts either normal or elevated; serum and erythrocyte folate was normal, plasma vitamin B12 was normal or elevated, and serum ascorbic acid was normal or elevated. The riboflavin nutritional status was normal. During refeeding, iron and riboflavin deficiencies became apparent. Characteristic findings on admission were the presence of giant erythroblasts and a diminished erythrocyte survival time implicated to an intracorpuscular hemolysis. Two results from the present study could contribute to explanation for the aforementioned abnormalities: low plasma vitamin E levels and, perhaps more importantly, low plasma selenium levels. In conclusion, the anemia of protein-energy malnutrition, as observed in Kivu, is a classifiable nonadaptive anemia that cannot be explained by isolated iron or vitamin deficiencies and whose physiopathology is distinct from that of the anemia of chronic disorders. It is suggested that a selenium deficiency may play an important role in the pathogenesis of this anemia.
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PMID:Protein-energy malnutrition and anemia in Kivu. 41 29

17 babies suffering from haemolytic disease or "hyperbilirubinaemia of prematurity" underwent exchange transfusion in the first 4 days of life. In 14 babies, including all those who had abnormally low pre-exchange serum vitamin E levels (<0.5 mg/100 ml), the vitamin E concentration rose as a result of exchange transfusion. In 3 babies the serum vitamin E concentration fell as result of exchange transfusion, but in no case was the post-exchange level below 0.5 mg/100 ml. The normal range of plasma vitamin E in stored ACD blood was 0.44--1.24 mg/100 ml. It was concluded that although vitamin E deficiency might be a factor in the aetiology of the anaemia of prematurity, prior subjection to exchange transfusion is unlikely to make a significant contribution to the vitamin E deficiency.
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PMID:Exchange transfusion and serum vitamin E (tocopherol) concentration in the newborn. 57 29

Hens were fed a diet low in selenium made up mostly of corn and torula yeast. Egg production and hatchability increased significantly when selenium was supplemented, while the percentage of infertile eggs and early dead embryos decreased. Anemia also resulted from the deficiency. A total of .05 mg. selenium per kg. (.04 from the basal diet plus .01 supplemental) was adequate to prevent signs of deficiency in a diet which contained no supplemental vitamin E or antioxidant. In a second experiment the anemia was classified as macrocytic.
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PMID:The selenium requirements of the hen and effects of a deficiency. 61 92

Rabbits fed a vitamin E-deficient diet developed severe muscular dystrophy in 3-4 wk, but they did not become anemic. Nevertheless, reticulocyte counts increased in deficient rabbits (3.2%) compared to control rabbits (0.9%), and erythroid hyperplasia was evident in the bone marrow. Comparing deficient rabbits to controls, the plasma iron concentration was lower (134.4 versus 206.6 microgram/dl); the TIBC was higher (335.9 versus 228.3 microgram/dl); the whole blood protoporphyrin concentration was higher (131.6 versus 81.7 microgram/dl); and the total iron content was lower in spleen (71 versus 153 microgram), higher in skeletal muscle (4956 versus 3054 microgram), and unchanged in bone marrow, liver, and heart. Studies of iron absorption and excretion using 59Fe showed no abnormalities in deficient rabbits. There were abnormalities of ferrokinetics, however. The half-time of disappearance of 59Fe was shorter (100.6 versus 169.4 min), the plasma iron turnover was greater (1.25 versus 0.95 mg/dl blood/day), and the reappearance of 59Fe in circulating erythrocytes at day 9 was greater (77.2% versus 57.2%) in deficient rabbits. Anemia induced by phlebotomy accentuated the abnormal iron metabolism of deficient rabbits, and the animals were unable to correct the anemia. These findings show that vitamin E deficiency in rabbits causes abnormal erythropoiesis associated with abnormal iron metabolism and sequestration of iron in skeletal muscle.
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PMID:Abnormalities of iron metabolism and erythropoiesis in vitamin E-deficient rabbits. 65 27

Vitamin E deficiency in premature infants has been described as being associated with low hemoglobin levels in the 2nd month of life. Recently, low vitamin E concentrations were suspected as being associated with sudden death in infancy. As vitamin E is absorbed incompletely from the premature's intestine, vitamin E levels in the serum were determined in 80 prematures on the 10th day of life. The result was correlated to the clinical course of the infants and to the hemoglobin levels up to the 30th day. Low concentrations of vitamin E and lower hemoglobin levels were found more frequently in new borns, whose clinical course was characterized by additional complications and who received parenteral nutrition. A group of uncomplicated newborns showed no correlation of vitamin E to hemoglobin values. Thus early diagnosis of vitamin E-dependent anemia is not possible and the usefulness of vitamin E should be investigated only in newborns with an uneventful clinical course.
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PMID:Vitamin E concentrations in term and preterm newborns and their clinical course. 82 May 58

Weanling male rats were fed a Torula yeast diet supplemented with selenium, vitamin E, or both for 3 months. Of rats fed each diet, one group received 250 ppm lead in the drinking water and another group did not. In rats not poisoned with lead, neither vitamin E nor selenium deficiency affected spleen weight, hematocrit value, or erythrocyte mechanical fragility. Vitamin E deficiency increased the splenomegaly, anemia, and mechanical fragility of red cells of lead-poisoned rats, whereas selenium deficiency did not. Addition of 0.5 ppm selenium to the vitamin E-supplemented diet increased slightly the splenomegaly and anemia in lead-poisoned rats. Excess levels of selenium (2.5 and 5 ppm) in the vitamin E-deficient diet had little or no effect on spleen size or hematocrit of rats not receiving lead, but partially prevented the splenomegaly and anemia of red cells from either non-poisoned or lead-oisoned vitamin E-deficient rats, but not as effectively as vitamin E. These results show that vitamin E status of rats is more important that selenium status in determining response to toxic levels of lead. Excess dietary selenium did protect partially against lead poisoning in vitamin E-deficient rats, but the levels of selenium used were toxic in themselves.
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PMID:Comparative effects of selenium and vitamin E in lead-poisoned rats. 84 75

The role of vitamin E in human nutrition was studied by investigation of patients with cystic fibrosis (CF) and associated pancreatic insufficiency. Vitamin E status was assessed by measurement of the plasma concentration of the principal circulating isomer, alpha-tocopherol. Results of such determinations in 52 CF patients with pancreatogenic steatorrhea revealed that all were deficient in the vitamin. The extent of decreased plasma tocopherol varied markedly but correlated with indices of intestinal malabsorption, such as the serum carotene concentration and percentage of dietary fat absorbed. Supplementation with 5-10 times the recommended daily allowance of vitamin E in a water-miscible form increased the plasma alpha-tocopherol concentrations to normal in all 19 CF patients so evaluated. Studies on the effects of vitamin E deficiency focused on possible hematologic alterations. An improved technique was developed to measure erythrocyte hemolysis in vitro in the presence of hydrogen peroxide. While erythrocyte suspensions from control subjects demonstrated resistance to hemolysis during a 3-h incubation, all samples from tocopherol-deficient CF patients showed abnormal oxidant susceptibility, evidenced by greater than 5% hemoglobin release. The degree of peroxide-induced hemolysis was related to the plasma alpha-tocopherol concentration in an inverse, sigmoidal manner. The possibility of in vivo hemolysis was assessed by measuring the survival of (51)Cr-labeled erythrocytes in 19 vitamin-E deficient patients. A moderate but statistically significant decrease in the mean (51)Cr erythrocyte half-life value was found in this group. Measurement of erythrocyte survival before and after supplementation of 6 patients with vitamin E demonstrated that the shortened erythrocyte lifespan could be corrected to normal with this treatment. Other hematologic indices in deficient subjects, however, were normal and did not change upon supplementation with vitamin E. It is concluded that CF is invariably associated with vitamin E deficiency, provided that the patient in question has pancreatic achylia and is not taking supplementary doses of tocopherol. Concomitant hematologic effects consistent with mild hemolysis, but not anemia, occur and may be reversed with vitamin E therapy. Patients with CF should be given daily doses of a water-miscible form of vitamin E to correct the deficiency.
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PMID:The occurrence and effects of human vitamin E deficiency. A study in patients with cystic fibrosis. 87 86

Either simultaneous or separate dietary deficiencies of vitamin E and selenium in Atlantic salmon during first 4 weeks of feeding caused twice the mortality shown in fish fed both supplemental vitamin E (0.5 IU/g dry diet) and selenium (0.1 mug/g). Subsequent dietary repletion with both vitamin E and selenium significantly reduced mortality during the following 2 weeks. Larger salmon (0.9 g initial mean weight), with vitamin E deficiency with or without selenium resulted in the following deficiency signs: extreme anemia, pale gills, anisocytosis, poikilocytosis, elevated plasma protein, exudative diathesis, dermal depigmentation, in vitro ascorbic acid-stimulated peroxidation in hepatic microsomes, yellow-orange liver color, yellow-brown intestinal contents, enlarged gall bladder distended with dark green bile, low vitamin E in carcass and hepatic tissue, muscular dystrophy, increased carcass fat and water, and a response to handling characterized by a transitory fainting with interruption in swimming. A deficiency of dietary selenium suppressed plasma glutathione peroxidase activity. Supplemental selenium with vitamin E significantly increased tocopherol activity in hepatic, but not carcass tissues. Supplements of both vitamin E and selenium were necessary to prevent muscular dystrophy.
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PMID:Vitamin E and selenium interrelations in the diet of Atlantic salmon (Salmo salar): gross, histological and biochemical deficiency signs. 93 27

alpha-tocopherol and placebo were compared by a double-blind trial to study their preventive effect on secondary anemia in a sample of low birth weight (less than or equal 2,500 g) infants. In the 7th week of life, hematological data from each of the two groups of infants (receiving vitamin E or placebo) were compared either by covariance analysis or by the t test of comparison of means. The infants who were given vitamin E have a higher serum level of vitamin E, a lower hemolysis, a higher erythrocyte count and a higher hemoglobin level than infants given the placebo. No significant difference was observed with respect to hematocrit or reticulocyte count. Thus, it appears that vitamin E has an effect on some of the factors in the anemia of infants of low birth weight.
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PMID:[Double blind study of vitamin E compared to placebo in the prevention of anemia in the low birth weight infant during the 7th week of life: therapeutic study]. 98 78


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