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

Rates of glucose, glycine, and folic (pteroylglutamic) acid absorption were determined for a 30 cm jejunal segment in vivo, with a double-lumen tube perfusion system, in 10 Zambian African women with a mean haemoglobin concentration of 5-1 (3-5-9-2) g/dl. In four the anaemia was megaloblastic (due to folate deficiency) and in six hypochromic. Perfusion solutions contained (1) glucose 200 mmol/1, (2) glycine 100 mmol/1, and (3) folic acid 250 mug/1. D-xylose absorption after a 25 g oral load was determined in them, and also in 18 additional patients (11 had megaloblastic and seven either hypochromic or haemolytic anaemia). Xylose absorption tests were significantly impaired in the patients with megaloblastic compared with hypochromic or haemolytic anaemia (P less than 0-001); those with untreated megaloblastic anaemia had a greater abnormality than those who had started treatment. Mean glucose, glycine, and folic acid absorption rates were similar to those in controls, and the rates in patients with megaloblastic and hypochromic anaemia were not significantly different. Correlation between glucose absorption rate and xylose excretion was, however, significantly (P less than 0-02). If more patients had been studied it seems likely therefore that a significant impairment of glucose absorption rate in the presence of megaloblastic anaemia would also have been demonstrated. In this investigation anaemia per se did not affect glucose, glycine, or folic acid absorption rates or xylose absorption, but xylose absorption was reduced in patients with megaloblastic anaemia. That abnormality was probably related to folate deficiency, and the underlying mechanism seems to be different from that causing impairment of monosaccharide absorption in patients with systemic bacterial infections. Mean glycine and folic acid absorption rates were not altered by megaloblastic anaemia, indicating that folate deficiency does not cause a general depression of absorption.
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PMID:Absorption of xylose, glucose, glycine, and folic (pteroylglutamic) acid in Zambian Africans with anaemia. 97 99

Thymidine kinase has been measured in phytohaemagglutinin (PHA)-stimulated lymphocytes from 13 normal subjects and eight patients with megaloblastic anaemia. The levels in normal subjects ranged from 0.20 to 2.10 units/mg protein (mean 0.903 units/mg protein) and in megaloblastic anaemia from 2.99 to 9.97 units/mg protein). All the patients showed raised levels of the enzyme which were partly but not completely reduced to normal by addition of folic acid in vitro. Vitamin B12 in vitro had a lowering effect in the five vitamin-B12-deficient patients and two patients with combined deficiencies but not in one 'pure' folate-deficient patient. Thymidine kinase activity was highest in the cells of the least anaemic patients, suggesting that the degree of anaemia in megaloblastic anaemia may be determined in part by the ability of the cells to utilize thymidine by the 'salvage' pathway when the de novo pathway of thymidylate synthesis is failing. The rise in thymidine kinase activity in megaloblastic anaemia is presumably due to induction of the enzyme. Addition of methotrexate or 5-fluorouracil, drugs known to inhibit de novo thymidylate synthesis, caused an increase in thymidine kinase activity in normal PHA-stimulated lymphocytes after 24 h (but not after 1 h) which could be completely blocked by addition of puromycin. Thymidine mono- and di-phosphate kinases were also measured in normal PHA-stimulated lymphocytes. The activities were substantially higher than that of thymidine kinase and their activities were unaffected by methotrexate addition.
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PMID:Thymidine kinase in megaloblastic anaemia. 100 25

Azaribine is an effective agent in the treatment of psoriasis. In this investigation the extent of clinical dermatologic remission appeared to correlate with the degree of metabolic block induced by 6-azauridylic acid, as quantitated by the urinary excretion of orotic acid and orotidine, and the development of anemia. Following azaribine therapy there was a coordinate rise of the specific activities of erythrocyte orotate phosphoribosyltransferase and orotidine-5'-monophosphate decarboxylase. There was no correlation between the pretreatment activity of these enzymes and the clinical response to azaribine. The anemia of azaribine therapy was mile and of a megaloblastic type. Uridine effectively corrected the azaribine-induced anemia, but led to exacerbation of the patients' psoriasis. Following uridine therapy there was a reduction in the urinary excretion of orotic acid and orotidine, presumable reflecting end-product inhibition or repression of the first steps of a repeated pyrimidine biosynthesis.
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PMID:Anemia of azaribine in the treatment of psoriasis. 103 74

Cytoplasmic and intranuclear annulate lamellae in the erythroblasts from patients with dyserythropoietic anaemia (megaloblastic anaemia, dysplastic anaemia and erythroleukaemia) are described. Annulate lamellae have mainly been observed in oocytes, in embryonic tissues and in malignant cells. Their occurrence in dyserythropoietic anaemia may be related to the reappearance of fetal characteristics in the erythroblasts and erythrocytes.
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PMID:Dyserythropoiesis and annulate lamellae. 105 75

Cell-mediated immunity has been studied in patients with 1) megaloblastic anemia of folic acid deficiency, 2)megaloblastic anemia of pregnancy, or 3) iron-deficiency anemia. Using dinitrochlorobenzene skin tests, phytohemagglutinin-stimulated lymphocyte transformation, and rosette inhibition by antilymphocyte globulin, we have shown that cell-mediated immunity is depressed in megaloblastic anemia due to folate deficiency; this depression was reversed by folate treatment. Cell-mediated immunity was not impaired by iron-deficiency anemia. Suggested interactions between iron deficiency and folate metabolism were not clarified by these studies.
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PMID:Depressed cell-mediated immunity in megaloblastic anemia due to folic acid deficiency. 111 20

We have described a case of chronic arsenic intoxication associated with pancytopenia and megaloblastic erythropoiesis. The patient had the typical laboratory manifestations of effective erythorpoiesis due to a megaloblastic process, including macroovalocytes, mild pancytopenia, low reticulocyte index, increased marrow cellularity with erythroid hyperplasia, and morphologic evidence of megaloblastic maturation in the marrow. The patient's serum folate and vitamin B12 were normal, and the anemia regressed without therapy. Our case suggests that the combination of megaloblastosis with normoblastic or megaloblastic karyorrhexis,should raise the suspicion of arsenic intoxication in the mind of the observer. In addition, arsenic should be added to the list of agents causing a reversible megaloblastic anemia.
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PMID:Arsenic intoxication as a cause of megaloblastic anemia. 112 Jan 85

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..
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PMID: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. 113 Jan 21

With the purpose of analyzing the evolution in weight before and after treatment of megaloblastic anemia with folic acid, we studied the clinical changes and the evolution in weight in 8 malnourished children who developed this type of anemia during their recovery. Seven out of the 8 cases were less than 20 months of age; 5 of them came from mothers who had had five or more pregnancies; in 7 a history of diarrhea of prolonged course was presented and 2 cases had been given sodium diphenylhydantoin. Increase in weight before treatment of anemia with folic acid was lesser than the one for the days following treatment in seven of the patients. Simultaneously, an important change in behavior was appreciated, without being possible to atribute this change or the increase in weight to a quantitative change favorable to the ingestion of proteins and calories.
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PMID:[Megaloblastic anemia in the recovery of the malnourished child]. 127 58

The clinical picture and the course of the disease of seven patients with the 5q-syndrome are described. Examination of peripheral blood revealed refractory anaemia with macrocytosis, anisocytosis, poikilocytosis of erythrocytes, and platelet anisocytosis with some giant platelets. Characteristic bone marrow findings are megaloblastic dyserythropoiesis and micromegakaryocytes with hypolobulated nuclei. Cytogenetically, an interstitial deletion of the long arm of chromosome 5 is always found, associated with a haploid loss of the genes for the growth factors GM-CSF, M-CSF and IL-3. The disease is usually chronic, and only in the case of clonal evolution is there a considerable risk of leukemic transformation occurring. In the chronic phase, infusion of packed red cells as required individually has proved a reliable form of treatment. The results of chemotherapy have disappointed both in the chronic and acute phases of the disease.
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PMID:[Refractory anemia with 5q--anomaly. Clinical picture and follow-up of seven patients]. 140 72

We describe the first reported case of resistance to human recombinant erythropoietin (rhEPO) treatment caused by vitamin B12 deficiency in a chronic hemodialysis patient. Despite a normal B12 level before rhEPO treatment, resistant anemia together with a low B12 level and a megaloblastic bone marrow developed after only 8 months of rhEPO. There was a rapid reticulocyte response to B12 supplements, and transfusion requirements dropped from 2 units monthly to nothing. Atrophic gastritis was diagnosed through endoscopy and biopsy. Because of the fall in B12 level after 8 months of rhEPO treatment, we analyzed the results of routinely measured B12 levels in 30 hemodialysis patients treated with rhEPO, and found the mean B12 levels to be unchanged before and after rhEPO treatment. Although we found screening for B12 deficiency of little benefit, any patient with rhEPO resistance should have B12 levels tested, given the potentially serious extra-hematological effects of B12 deficiency.
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PMID:Erythropoietin resistance due to vitamin B12 deficiency. Case report and retrospective analysis of B12 levels after erythropoietin treatment. 141 79


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