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

The erythrocyte is a highly specialized cell whose main functions are oxygen transport and the mediation of carbon dioxide transport. Energy production in the mature erythrocyte depends on glycolysis, with glucose as the principal substrate. Glycolysis and the oxidative pentose phosphate pathway generate NADH and NADPH to reduce methemoglobin, which is being continuously produced, and the antioxidant glutathione, which is present in high concentrations. Red blood cells are equipped with a highly effective antioxidant defense even without the glutathione system. Compared with other cell types, they possess high activities of the most important antioxidant enzymes. Most of the nonenzymatic antioxidant capacity of whole blood is likewise localized in the erythrocytes. Circulating red cells are mobile free radical scavengers and provide antioxidant protection to other tissues and organs. An imbalance between pro-oxidant reactions and antioxidant defense is described in patients with chronic renal failure. Oxidative stress increases as antioxidant defenses are weakened by pro-oxidant hemodialysis factors; it increases further still in renal anemia with a very low red cell count. Thus in terms of free radical metabolism, the only arguments remaining over the complete correction of renal anemia are those in favor, with none against.
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PMID:Erythrocyte free radical and energy metabolism. 1074

Sickle cell anemia, a congenital hemolytic type of anemia due to a genetic defect in the beta chain of the globin molecule can cause severe disease. During pregnancy, the risk for preeclampsia and deep venous thrombosis is increased in patients with sickle cell anemia. Occlusion of placenta blood vessels with rigid deformed erythrocytes can cause repeated miscarriages and intra-uterine fetal death. Repeated blood transfusions can prevent these complications by reducing the concentration of abnormal hemoglobin S. We report on the evolution of five pregnancies in three patients with sickle cell anemia who received multiple blood transfusions during gestation, and discuss advantages and risks involved in the care of such cases.
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PMID:[Sickle cell anemia and pregnancy: considerations on systematic prophylactic transfusion]. 1131 68

Sickle cell anemia (SCA) is a disease caused by production of abnormal hemoglobin, which binds with other abnormal hemoglobin molecules within the red blood cell to cause rigid deformation of the cell. This deformation impairs the ability of the cell to pass through small vascular channels; sludging and congestion of vascular beds may result, followed by tissue ischemia and infarction. Infarction is common throughout the body in the patient with SCA, and it is responsible for the earliest clinical manifestation, the acute pain crisis, which is thought to result from marrow infarction. Over time, such insults result in medullary bone infarcts and epiphyseal osteonecrosis. In the brain, white matter and gray matter infarcts are seen, causing cognitive impairment and functional neurologic deficits. The lungs are also commonly affected, with infarcts, emboli (from marrow infarcts and fat necrosis), and a markedly increased propensity for pneumonia. The liver, spleen, and kidney may experience infarction as well. An unusual but life-threatening complication of SCA is sequestration syndrome, wherein a considerable amount of the intravascular volume is sequestered in an organ (usually the spleen), causing vascular collapse; its pathogenesis is unknown. Finally, because the red blood cells are abnormal, they are removed from the circulation, resulting in a hemolytic anemia. For the patient with SCA, however, the ischemic complications of the disease far outweigh the anemia in clinical importance.
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PMID:Sickle cell anemia. 1145 73

Changes were studied in processes of peroxide oxidation of lipid (LPO), such as neutral lipids and phospholipids, as related to the levels of hemoglobin (Hb) and its derivatives, methemoglobin (Met-Hb) and carboxyhemoglobin (CO-Hb) in erythrocytes and blood plasma of 33 patients with iron-deficiency anemia (IDA). It has been found out that in IDA, decline in the concentration of Hb correlates with augmentation of the content of Met-Hb (r = -0.670, P = 0.038). Increase in the level of Met-Hb is accompanied by an accumulation in erythrocytes of Schiff bases as the final products of phospholipids peroxidation (r = 0.586, P = 0.004), CO-Hb-substrates of LPO (r = 0.425, P = 0.049), primary (r = 0.453, P = 0.04) and secondary (r = 0.438, P = 0.048) molecular products of peroxide oxidation of neutral lipids. A mechanism is discussed of the Hb derivatives Met-Hb and CO-Hb concurrence in the activation of LPO in IDA.
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PMID:[Hemoglobin-induced lipid peroxidation in anemia]. 1169 26

To investigate the mechanism of anemia accompanying Japanese bovine theileriosis, we examined whether production of methemoglobin (MetHB), an indicator of erythrocyte oxidation, was associated with anemia in cattle experimentally infected with Theileria sergenti. The percentage of MetHB, which is an oxidized form of hemoglobin, increased according to the onset of anemia. During severe anemia, high levels of acquired methemoglobinemia were observed in all infected cattle. A significant correlation (r=-0.649; P<0.01) between an increase in MetHB concentration and a decrease in packed cell volume (PCV) was observed. It was considered that hemoglobin oxidation may be one of the aggravating factors of anemia in T. sergenti infection.
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PMID:Acquired methemoglobinemia in anemic cattle infected with Theileria sergenti. 1170 51

Methylene blue trihydrate is used widely as a dye and therapeutic agent. Methylene blue was administered by gavage to 30 animals/sex/dose group in a 0.5% aqueous methylcellulose suspension at doses of 0, 25, 50, 100, and 200 mg/kg. Blood samples from 10 animals/sex/dose group were collected at the end of study weeks 1, 6, and 13. Methylene blue treatment resulted in methemoglobin formation and oxidative damage to red blood cells, leading to a regenerative anemia and a variety of tissue and biochemical changes secondary to erythrocyte injury. An early change was a dose-related increase in methemoglobin, where the response of rats and mice was similar in magnitude. Mice appeared to be more sensitive than rats to the formation of Heinz bodies and the development of anemia that was characterized by a decrease in hemoglobin, hematocrit, and erythrocyte count. Splenomegaly was apparent in all treated mice and in the 100 mg/kg (males only) and 200 mg/kg rats at necropsy. There was a dose-related increase in absolute and relative spleen weight for both species. Microscopic examination revealed increased splenic hematopoiesis in all mice treatment groups and in rats at the 50 mg/kg dose level and above. Splenic congestion and bone marrow hyperplasia were also observed in these rat-dose groups. Mice at the higher doses showed hematopoiesis in the liver and accumulation of hemosiderin in Kupffer cells. These gross and microscopic findings are consistent with the development of hemolytic anemia. A dose-related increase in the reticulocyte count during study weeks 6 and 13 suggested a compensatory response to anemia.
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PMID:Hematological effects in F344 rats and B6C3F1 mice during the 13-week gavage toxicity study of methylene blue trihydrate. 1175 92

A new compact-type latex photometric immunoassay system, SPOTCHEM IM SI-3510 (ARKRAY, Inc., Kyoto, Japan), which assays three kinds of inflammatory markers-neutrophil count (NPC), C-reactive protein (CRP), and anti-streptolysin O (ASO)-was evaluated. Hemoglobin (Hb), which is a good marker for anemia, can also be measured with it. NPC and CRP are measured using antibodies against neutrophilic elastase and CRP, purified streptolysin O was used for ASO determination, and Hb was measured by an azide-methemoglobin method. Whole blood, serum, and plasma specimens can be used as samples with this system. In this study, whole blood treated with dipotassium ethylenediamine tetraacetic acid was used for evaluation. Linearity and reproducibility were good for all of the items studied. Good correlations were observed between the results obtained by this system and those obtained by routine methods. Since NPC exhibited a high correlation with the routine white blood cell (WBC) counts, it was judged to be useful as a substitute for WBC counting. Since this system is small and easy to operate, and evaluation revealed reliable results, it was judged to be practical for small laboratories, and satellite testing in hospitals and physicians' office laboratories for patients suspected to have acute inflammation.
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PMID:New compact-type latex photometric immunoassay system for hemoglobin and three acute inflammation markers: neutrophil count, C-reactive protein, and anti-streptolysin O. 1194 99

Chlorinated anilines are used as intermediates in the manufacture of dyes, drugs, and agricultural agents. In comparative 13-week studies conducted to determine the structure-toxicity relationships of o-, m-, and p-chloroaniline, groups of 10 male and 10 female F344/N rats and B6C3F1 mice were administered 0, 10, 20, 40, 80, or 160 mg o- or m-chloroaniline per kilogram body weight in dilute hydrochloric acid by gavage. Animals were evaluated for hematology, clinical chemistry, histopathology, and reproductive system effects. Genetic toxicity studies of o- and m-chloroaniline in vivo and in vitro were also conducted. The results of the o- and m-chloroaniline studies were compared to results from the p-chloroaniline studies performed previously under similar experimental conditions by the same laboratory; doses in the p-chloroaniline studies were 0, 5, 10, 20, 40, and 80 mg/kg for rats and 0, 7.5, 15, 30, 60, and 120 mg/kg for mice. The hematopoietic system was the target of o-, m-, and p-chloroaniline in rats and mice. Neither the o- nor the p- isomer had an adverse effect on survival; the death of one female rat in the 160 mg/kg m-chloroaniline group during week 12 was possibly secondary to methemoglobinemia. The final mean body weights and weight gains of male rats in the highest dose group in each study and female mice in the 160 mg/kg group in the o-chloroaniline study were significantly less than those of the respective controls. Clinical findings of toxicity included a transient bluish discoloration of the genital and footpad regions in rats administered o- or m-chloroaniline and tremors in rats and mice administered o-chloroaniline and in mice administered m-chloroaniline; these effects occurred primarily in the 80 and 160 mg/kg groups. Methemoglobin concentrations were increased in dosed rats and mice in all studies and resulted in a secondary anemia; the severity of the anemia increased with increasing dose. Microscopic lesions considered related to chemical administration in rats and mice included hemosiderin pigmentation in the bone marrow, kidney, liver, and spleen; hematopoiesis in the liver and spleen; and erythroid cell hyperplasia in the bone marrow. These lesions reflected the response to hemolytic anemia and methemoglobinemia induced by the chloroanilines. A comparative analysis of the results suggests that p-chloroaniline is the most potent of the chloroaniline isomers in the induction of methemoglobin formation in rats and mice, followed by m-chloroaniline and then by o-chloroaniline. This order of potency was also observed for changes in other hematology parameters and in spleen weights, gross and microscopic lesions, and the severity of hemosiderin deposition. Although the o-, m-, and p- isomers of chloroaniline all exhibit genetic toxicity, the profiles of activity among the three isomers are not identical. p-Chloroaniline was mutagenic in all assays in which it was tested, including the Salmonella assay, the mouse lymphoma assay, in vitro Chinese hamster ovary cell cytogenetics assays, and the in vivo mouse bone marrow micronucleus assay; in contrast, o- and m-chloroaniline gave mixed results among the various assays in which each was tested. In conclusion, chloroaniline isomers are hematotoxic and have the same pattern of toxicity in rats and mice. Hematotoxicity occurred at all doses in these studies. p-Chloroaniline induces the most severe hematotoxic effect, followed by m-chloroaniline, then o-chloroaniline. Each of the three isomers is more toxic to rats than to mice. p-Chloroaniline is clearly genotoxic in various test systems, while the results for the o- and m- isomers are inconsistent and indicate weak or no genotoxic effects.
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PMID:NTP Comparative Toxicity Studies of o-, m-, and p-Chloroanilines (CAS Nos. 95-51-2; 108-42-9; and 106-47-8) Administered by Gavage to F344/N Rats and B6C3F1 Mice. 1196 42

A functional requirement for all hemoglobin-based oxygen carriers (HBOCs) is the maintenance of the heme-iron in the reduced state. This is necessary for the reversible binding/release of molecular oxygen and minimization of methemoglobin (Fe+3) formation. Acellular hemoglobins are especially susceptible to oxidation and denaturation. In the absence of the intrinsic reducing systems of the red blood cell, the reduced heme-Fe+2 can be oxidized to form increasing levels of methemoglobin that can give rise to free radicals and oxidative cellular damage. If acellular HBOCs are to be utilized as red cell substitutes for oxygen delivery, these carriers must be stabilized in the plasma, the carrier medium. Normal plasma contains reducing components, such as ascorbic acid and glutathione, that can afford protection to these acellular HBOCs through electron-transfer mediated processes. For these components to provide effective reduction to an HBOC, a favorable reduction potential difference must exist between the reducing agent and the HBOC. Using a modified thin-layer spectroelectrochemical method, a determination of the formal reduction potential (vs. Ag/AgCl) of several oxygen carriers, including monomeric myoglobin, tetrameric HbA and HbS, chemically cross-linked HbXL99alpha, polymerized oxyglobin (FDA approved for canine anemia), and the natural cross-linked polymeric Lumbricus hemoglobin, have been determined. In contrast to the negative formal reduction potentials (-155 to -50 mV) obtained for Mb, HbA, HbS, HbXL99alpha, and oxyglobin, Lumbricus hemoglobin exhibited a positive formal reduction potential (approximately 100 mV). These results may help explain the greater effectiveness of the tested reducing agents to reduce met Lumbricus hemoglobin, compared to the other HBOCs, back to the required reduced form necessary for physiological binding/release of oxygen. Each reducing agent was capable of reducing met Lumbricus hemoglobin to the fully reduced state, although the kinetics of these reactions were different. HbA, HbXL99alpha, and oxyglobin were only partially reduced (10 to 37%) by glutathione, beta-NADH, and ascorbic acid under similar conditions.
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PMID:Role of redox potential of hemoglobin-based oxygen carriers on methemoglobin reduction by plasma components. 1200 Feb 25

Sickle cell disease (SCD) is a term used to describe a group of genetic disorders of hemoglobin production characterized by a predominance of the abnormal hemoglobin known as hemoglobin S. Common acute complications of SCD in children requiring hospitalization include painful episodes, febrile illness, and splenic sequestration. The staff nurse has an important role in providing prompt treatment and instituting preventative measures to avoid the adverse clinical outcomes of SCD such as acute chest syndrome, severe anemia, cardiovascular instability, and bacterial sepsis. A basic understanding of the pathophysiology of vaso-occlusion, the immune system, hemolysis, and the spleen is essential in the care of a child during an acute complication of SCD. Additionally important are a knowledge of the genetics, pathophysiology, medical and nursing management, and a familiarity with patient and family education material relating to sickle cell disease.
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PMID:Care of the child with sickle cell disease: acute complications. 1202 71


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