Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We hypothesized that chart reminders would decrease the number of cases in which a low admission hemoglobin level was missed or ignored. Additionally, we compared the cost of generating the chart reminders by hand with the estimated cost of modifying the university hospital information system for this function. For three months, two medical students reviewed all abnormal hemoglobin results and assigned those more than 1 g below normal limits to a control or study group. A questionnaire, placed in all study group charts, requested an explanation for the low hemoglobin level. Eleven of 141 study cases and 16 of 150 control cases failed the audit criteria (differences not significant). The cost was $308 compared with $3,000 for altering the hospital information system. We conclude that chart reminders did not improve the detection of anemia and that it cost less to test this intervention by manually simulating the computer function.
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PMID:Chart reminders in the diagnosis of anemia. 678 72

Electrophoretic analysis of a hemolysate from a young man undergoing a routine physical examination revealed an abnormal hemoglobin with a mobility similar to Hb S on cellulose acetate (pH, 8.4). This new variant, designated Hb Connecticut, was found in three generations of a family of Polish descent. Several individuals possessing the variant exhibited mild anemia. Structural analysis of the abnormal beta-chain indicated that the amino acid substitution was at position 21 (B3), and involved the replacement of aspartic acid with glycine. Oxygen dissociation studies revealed low oxygen affinity. The alkaline Bohr effect and the degree of cooperativity were unchanged. Analysis of the crystal structure of the variant suggested that the low oxygen affinity was due to the possible disruption of salt bridges between aspartic acid 21(B3) and lysines 61(ES) and 65(E9), changes that could lead to steric interference in oxygen binding.
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PMID:Hemoglobin connecticut (beta 21 (B3) Asp leads to Gly): a hemoglobin variant with low oxygen affinity. 730 5

Coefficient of variation (C.V.) of red cell volume is inversely proportional to red cell mass in hemoglobinopathies and thalassemias. Even a subject with markedly reduced red cell survival and abnormal hemoglobin had a normal C.V. associated with normal hemoglobin level. In contrast are patients with nutritional deficiency, who have increased C.V. whether or not there is anemia, and patients with hypoplastic anemia, who have normal to near-normal C.V. independent of anemia.
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PMID:Nondiscrete heterogeneity of human blood cells. 1. Volume heterogeneity as a reflection of the quality of erythropoiesis. 732 77

Visceral leishmaniasis has been found to be associated with severe anemia and premature lysis of erythrocytes. Peroxidative damage of red cells has been noted in several hemolytic anemias. Present study shows enhanced formation of methemoglobin in hamsters infected with Leishmania donovani. Increased formation of malonyldialdehyde and diene conjugate has been noted in the erythrocytes of the infected animals with the progress of anemia. Results showed decreased activities of protective enzymes like superoxide dismutase, catalase and glutathione reductase against peroxidative attack. An increase in the membrane cholesterol/phospholipid ratio and a decrease in membrane fluidity of erythrocytes were observed under the diseased condition. Densitometric scan after SDS-PAGE of red cell membrane of the infected animals revealed significant degradation of band 3 and band 4.1 proteins. The results suggest that alteration in the membrane may lead to reduced life span of the red cells in experimental visceral leishmaniasis.
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PMID:Lipid peroxidation of erythrocytes during anemia of the hamsters infected with Leishmania donovani. 756 50

We studied the hematological effects of single and repeated exposure to 1,3,5-trinitrobenzene (TNB) in rats. Male F-344 rats were gavaged with TNB at 35.5 and 71 mg/kg in corn oil. Blood was collected 5 h and 24 h after a single oral dose or 24 h after daily oral doses for 4 or 10 d in four different set of experiments. A dose-dependent methemoglobinemia was present only in blood collected 5 h after a single dose. A highly significant dose-dependent anemia with reduced red cells, hemoglobin, and hemotocrit was present in rats receiving TNB for 4 or 10 d. A dose-dependent decrease in serum triglycerides was present in rats receiving TNB for 10 d. There was no hemolysis when rat erythrocytes were incubated with TNB (in vitro) for 9 h. Spectral changes of hemoglobin recorded during the incubation with TNB confirm methemoglobin formation and progressive denaturation of hemoglobin-forming hemichromes. The significance of methemoglobin and hemichrome formation is discussed, and a probable hypothesis for the hemolytic anemia is suggested.
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PMID:Hematological effects of 1,3,5-trinitrobenzene (TNB) in rats in vivo and in vitro. 766 94

Hb Washtenaw [beta 11(A8)Val-->Phe] is a new, low oxygen affinity variant with a previously undescribed substitution, identified in seven members over three generations of a Hungarian-American family. The hemoglobin is mildly unstable and the family members studied are clinically asymptomatic but mildly cyanotic, and some exhibit mild anemia. The index case had severe pulmonary hypertension and some of the family members had increased pulmonary vascular resistance on echocardiography. An association between the inheritance of this abnormal hemoglobin and the pathogenesis of primary pulmonary hypertension is suggested but the mechanism is unclear.
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PMID:Hb Washtenaw [ beta 11(A8)Val-->Phe]: an electrophorectically silent, unstable, low oxygen affinity variant associated with anemia and chronic cyanosis. 785 83

DQ-2511, a new anti-ulcer drug, was administered to beagle dogs for 4 weeks to investigate the mechanism whereby this drug induced hemolytic anemia and its reversibility in comparison with beta-acetylphenylhydrazine. Hemolytic anemia accompanied by an increase in the number of cells containing Heinz bodies that was preceded by a marked decrease in blood-reduced glutathione concentration was observed in dogs receiving 600 mg/kg of DQ-2511, but only a slight increase in the methemoglobin level was noted. beta-Acetylphenylhydrazine, however, caused hemolytic anemia accompanied by marked increases in both Heinz body-containing cells and methemoglobin concentration, but the blood-reduced glutathione concentration was not decreased consistently with the formation of Heinz bodies. Hemolytic anemia disappeared after a 4-week recovery period in the dogs that received DQ-2511. These results suggest that decreases in reduced glutathione in erythrocytes play an important role in the anemia and Heinz body formation induced by DQ-2511, but not by beta-acetylphenylhydrazine.
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PMID:Heinz body hemolytic anemia induced by DQ-2511, a new anti-ulcer drug, in dogs. 844 84

Hb Questembert [alpha 131(H14)Ser-->Pro] was found in several members of a French family suffering from congenital Heinz body anemia. The unstable hemoglobin was expressed in the peripheral red blood cells at a very low level. Globin biosynthetic studies revealed a high specific activity of the abnormal chain and an alpha-/beta-labeling ratio similar to that of beta-thalassemia trait. Hb Caen [alpha 132(H15) Val-->Gly] is another unstable variant with the same globin biosynthesis abnormality. In both cases the structural modification is localized at the end of the H helix, a region encoded by the third exon. The mechanism for the unbalanced globin synthesis is not yet clear. It may be related 1) to a defect in chain assembly, 2) to an increased rate of degradation of the variant chain followed by the release of unlabeled beta-chains from the abnormal hemoglobin, thus leading to an apparent suppression of beta-chain synthesis, or 3) to a modified stability of the abnormal alpha-globin mRNA.
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PMID:Unstable alpha-chain hemoglobin variants with factitious beta-thalassemia biosynthetic ratio: Hb Questembert (alpha 131[H14]Ser-->Pro) and Hb Caen (alpha 132[H15]Val-->Gly). 849 87

A 9-year-old girl was admitted to Mie University Hospital June 25, 1992, complaining of fever, skin rash and pallor. Physical examination revealed anemia and hepatosplenomegaly. Laboratory findings showed normocytic normochromic anemia, increased reticulocyte counts and remarkably decreased haptoglobin level. Red blood cells had no morphological abnormality. Bone marrow examination showed erythroid hyperplasia without abnormal cells. Hemoglobin electrophoresis showed an abnormal band. The amino acid structure and sequence of the abnormal hemoglobin was determined to be an unstable hemoglobin, Hb Buenos Aires [beta 85 (F1) Phe-->Ser]. Sequence of genomic DNA and cDNA was compatible to Hb Buenos Aires. Parvovirus B19 infection was thought to have caused severe anemia due to hemolytic crisis in this patient because its IgM antibody was positive on admission. She recovered soon without any treatment and has been followed in the outpatient clinic. Her parents and brother showed no hemoglobin abnormality.
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PMID:[The first case in Japan of unstable hemoglobin, Hb Buenos Aires [beta 85 (F1) Phe-->Ser], with parvovirus B19 infection (first case in Japan)]. 858 69

The ready access to blood (plasma and formed cellular elements) makes it unusually susceptible to the deleterious effects of pollutants whose origins may be in the air. The red blood cells' hemoglobin may be rendered useless for oxygen transport by combination with carbon monoxide or conversion to methemoglobin or sulfhemoglobin. Lead and arsine can damage the erythrocytes' membranes, resulting in anemia. Metabolites of benzene and other volatile polycyclic hydrocarbons are implicated in the causation of leukemias. The extensive use of pesticides and herbicides may be associated with the development of Hodgkin's disease, non-Hodgkin's lymphoma, and aplastic anemia. The carcinogenic risks from ionizing radiation, especially for leukemia, are well known. More information is needed concerning the epidemiology of environmental factors responsible for damage to blood. Enhanced knowledge about the molecular biology of toxins' effects on the hematopoietic system and improved detection and prevention technologies are needed to answer environmentally related health questions.
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PMID:Blood and air pollution: state of knowledge and research needs. 863 33


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