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Query: UMLS:C0002874 (aplastic anemia)
 5,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a method involving elution of hemoglobin bands from cellulose acetate strips following electrophoresis of hemolysates, hemoglobin A2 (Ab A2) was quantitated in bloods from 300 healthy individuals and 904 patients. The percentage of Hb A2 was elevated in beta-thalassemia heterozygotes and some patients who had megaloblastic anemia. In the latter, the highest Hb A2 levels were observed in patients with the most severe anemia. Low Hb A2 percentages were found in iron-deficiency anemia, hereditary persistance of fetal hemoglobin, and Hb H disease. In iron-deficiency anemia, the lowest levels of Hb A2 were observed in association with the most severe anemia. Iron and folate deficiency each suppressed Hb A2 levels in beta-thalassemia heterozygotes; however, vitamin B12 deficiency did not alter the percentage of Hb A2 in thalassemia. Malignant tumors, renal and hepatic insufficiency, chronic infections and inflammation, hemolytic disease, lead poisoning, aplastic anemia, leukemia, myelofibrosis, and hypothyroidism did not change Hb A2 levels. The pathogenesis of altered Hb A2 levels and their clinical significance in various diseases are discussed.
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PMID:Hemoglobin A2 levels in health and various hematologic disorders. 26 35

One hundred consecutive patients with hemoglobin concentration less than 3.5 g/dL (hematocrit reading, less than 10%) were admitted to the University of Baghdad Teaching Hospital, Iraq, during a 30-month period. Twenty-eight patients had aplastic anemia, 27 had leukemia or other hemopoietic malignancies, 16 had chronic renal failure, eight had iron-deficiency anemia, eight had hemolytic anemia, seven had thalassemia major, and six had other conditions. Twenty-three patients died within seven days of admission, mostly due to the underlying disease or complications thereof. Heart failure developed in ten patients, and five had retinal exudates and hemorrhages attributed to severe anemia. Arrhythmias and ECG abnormalities were noted in 20 of 68 patients. Blood transfusion was instituted in all but three patients, whose anemia was corrected with specific therapy without blood transfusion. The tolerance of the 100 patients to such severe anemia was remarkable.
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PMID:Severe anemia. Clinical observations in 100 patients with very low hemoglobin levels. 47 23

Results of the investigation of 3 children aged from 2 to 7,5 with diagnosed aplastic anemia of Fanconi type are presented. Two children were females and one child was a male. Their illness symptoms appeared at the age of one, three and four respectively. All three patients had similar symptomes: palenes, tiredness, epistaxis, appearance of hemorrhagic syndrome and delayed growth. The following anomalies were also present: small size, microcephaly, mandibular hypoplasia, high palate and malformation of the urinary tract. In one child ductus Botalli persistens was also revealed. The laboratory findings showed presence of pancytopenia of the blood and increased level of both iron and erythropoietin in the serum. The karytype of two children revealed several cells with broken chromatin and with polyploid and tetraploid cells. The meiogram showed presence of all cells in bone marrow but in lowered number. Celularity I.
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PMID:[Congenital aplastic anemia-Fanconi]. 61

Several forms of drug-induced anemia are discussed. Anemia resulting from toxic effects on the marrow may occur after large doses or long treatment courses of alkylating agents, the plant alkaloids vinblastine and vincristine, and antibiotics used in cancer chemotherapy. A lesion of the stem cells in bone marrow is thought to be caused. Aplastic anemia has been produced by chloramphenicol in a small percentage of cases. This has led to its disuse except when no suitable alternative is available or where the mortality of the disease being treated is high. Some nonnarcotic analgesics, e.g., amidopyrine, have caused agranulocytosis. Gold injections have also been implicated. Insecticides or an inhaled agent such as benzine or a glue solvent may cause hypoplastic anemia. A list is given of drugs that have been reported as having caused aplastic anemia. Chromosomal changes have rarely been reported. An alleric mechanism is sometimes responsible for drug-induced aplastic anemia. There may be individual variations in ability to metabolize a drug. Treatment of drug-induced aplastic anemia requires transfusions. Bone marrow transplants have also been used. Antibiotic therapy is needed. Oral contraceptives may be of value if there is menorrhagia. Megaoloblastic anemia may be due to defective metabolism of folate. Anticonvulsant drugs may also cause megaloblastic anemia, especially primidone. Giving folic acid with these drugs may prevent this development. Oral contraceptives have been reported to cause folate depletion but megaloblastic anemia has not been shown to follow. Alimentary bleeding with peptic ulcer or following drug use may cause anemia. Sideroblastic anemia may be a congenital abnormality of iron metabolism or an acquired form induced by drugs or lead poisoning. Pyridoxine therapy is used. Drug-induced leukemia may follow use of radioactive compounds or may develop in patients with a drug-induced aplastic anemia.
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PMID:Drug-induced anaemias. 78 36

Ten healthy volunteers and 38 patients with iron deficiency anemia, aplastic anemia, chronic lymphadenosis, myelofibrosis were examined. On the base of the results from the kinetics of iron-59 and the marked with chromium-51 erythrocytes and from the corrected per cent reticulocytes, the authors set up the task to evaluate the etythropoetic potentialities of bone marrow and the severity of erythrocyte balance disorder, studying the quantity of produced and destroyed erythrocytes daily and comparing the data obtained with those from aspiration biopsy and treparobiopsy. The results, obtained by the authors, reveal the high potentialities indicated by the isotope investigation with iron-59 and chromium-51 as well as the corrected per cent of reticulocytes, for the evaluation of the erythropoetic potentialities of bone marrow and the high correlation between the results obtained and the clinical picture.
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PMID:[Quantitative changes in produced and destroyed erythrocytes in hemopathy]. 87 47

In 11 patients with megaloblastic anemia, transfusion of packed erythrocytes or washed erythrocytes invariably resulted in a decline in plasma iron concentration to a range of 20-90 microgram/dl (3.6-16 mumol/l) after 36 to 48 hours. The same phenomenon was observed in two of six cases of ineffective erythropoiesis without megaloblastosis and in none of five cases of aplastic anemia. The observed changes did not result from a specific hematinic response or from iron uptake by a non-erythroid compartment. In megaloblastic anemia, alteration in marrow function in response to transfusion was reflected by plasma iron kinetics and serum lactate dehydrogenase values, which indicated marked reductions in both marrow hyperplasia and ineffective erythropoiesis. Transfusion in megalobastic anemia was also responsible for a 50% reduction in platelet count after 2 to 6 days. The significance of these changes is discussed.
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PMID:Effects of transfusion on serum iron, serum lactate dehydrogenase and platelets in megaloblastic anemia. 90 75

The incorporation of [15N]delta-aminolaevulinic acid and [15N glycine into haemoglobin haem and early labelled bilirubin was measured in subjects with various haematological disorders. The clearance of [14C bilirubin was used to measure bilirubin production rate, and the magnitude of the various sources of bilirubin production and the percentage ineffective erythropoiesis were calculated. Ineffective erythropoiesis was found to be a major factor in the production of the anaemia in patients with the following disorders: megaloblastic anaemia associated with the Lesch-Nyhan syndrome, thalassaemia intermedia, sideroblastic anaemia, and the anaemia of chronic disorders. In three patients with iron-deficiency anaemia ineffective erythropoiesis was increased, but was of minor importance in the production of the anaemia, while in two patients with aplastic anaemia and one with macrocytosis of alcoholism there was no increase in ineffective erythropoiesis.
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PMID:Quantitation of ineffective erythropoiesis from the incorporation of [15N] delta-aminolaevulinic acid and [15N] glycin into early labelled bilirubin. II. Anaemic patients. 95 67

The lack of a simple, rapid, and quantitative test of the functional activity of the monocyte has hampered studies of the contribution of this cell type to host defense and human disease. This report describes an assay of antibody-dependent cellular cytotoxicity, which depends exclusively upon the monocyte as the effector cell and therefore provides a convenient test of monocyte function. In this system, mononuclear leukocytes (MNL) obtained by Ficoll-Hypaque separation of whole blood are cytotoxic for 51Cr-labeled human erythrocyte targets coated with anti-blood group antibody. Removal of phagocytic monocytes from the MNL by iron ingestion, followed by exposure to a magnetic field, completely abolishes all cytotoxic activity from the remaining MNL population. Similarly, in severely mono-cytopenic patients with aplastic anemia, cytotoxic effector activity is absent. In normals and less severely monocytopenic aplastic anemia patients, cytotoxicity correlates significantly (p less than 0.001) with monocyte number. Application of this monocyte-mediated antibody-dependent cellular cytotoxicity assay to the study of patients with the Wiskott-Aldrich syndrome has revealed defective monocyte cytotoxic activity in spite of normal monocyte numbers, suggesting that this test may be useful for the assessment of monocyte function in a variety of clinical situations.
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PMID:Monocyte-mediated antibody-dependent cellular cytotoxicity: a clinical test of monocyte function. 100 82

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

Dose-related blood dyscrasias during treatment with either chloramphenicol or thiamphenicol chiefly include erythroid suppression and may be recognized at an early stage by observation of reticulocytopenia and an increased serum iron concentration. Ferrokinetic studies show the typical features of sideroblastic anemia. Whilst chloramphenicol is conjugated with glucuronic acid in the liver, thiamphenicol is predominantly eliminated by the kidney in its unmodified form. Sensitization against both drugs has been described and may, following reexposure, lead to dangerous granulocytopenia. Potentially the most dangerous late complication after chloramphenicol treatment, i.e. aplastic anemia, has not thus far been observed in patients treated with thiamphenicol.
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PMID:[Blood damage due to chloramphenicol and thiamphenicol]. 116 96


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