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Results for “Erythrocytes, Abnormal”

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At least 19 recordsLinked to original sources
PubMed1976

Biochemical studies on abnormal erythrocyte membranes. Protein abnormality of erythrocyte membrane in biliary obstruction.

Biochemical studies on erythrocyte membranes from eleven obstructive jaundice patients (due to various disorders) have been undertaken, By scanning electron microscopic observation these erythrocytes were spur and target in appearance. The lipid composition showed a marked increase in both cholesterol and phosphatidylcholine. In addition to these changes, it was unexpectedly demonstrated by polyacrylamide gel electrophoresis in sodium dodecyl sulfate that a specific membrane protein component 4.2 was reduced or absent in all cases tested. This membrane protein abnormality was identical with that of hereditary spherocytosis erythrocyte membranes. It is of particular interest to note that after surgical relief of biliary obstruction in a typical case of common duct cholelithiasis, the disc electrophoretic pattern of erythrocyte membranes became normal and both lipid composition and red cell morphology returned to normal.

Cholestasis↗
PubMed1993

Lymphocyte cytotoxicity and erythrocytic abnormalities induced in broiler chicks by fumonisins B1 and B2 and moniliformin from Fusarium proliferatum.

Peripheral blood lymphocytes were isolated from broiler chicks that had ingested feed amended with autoclaved Fusarium proliferatum culture material containing fumonisin B1 (FB1), fumonisin B2 (FB2) and moniliformin. Lymphocyte viability was determined for birds that were placed on amended rations at day 1 or day 7 of age at three different levels of mycotoxins, ranging from 61-546 ppm FB1, 14-94 ppm FB2 and 66-367 ppm moniliformin. Reduction of the tetrazolium salt, MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide], to yield MTT formazan, based on mitochondrial metabolic activity, was used to assess cell viability. Lymphocyte cytotoxic effects were observed in all treatment groups on day 21; chicks that started on amended feed at day 1 of age were affected more than those that started at day 7. Abnormal erythrocytes resembling early stages of erythroblasts were observed in peripheral blood from test chicks. Abnormally shaped red cells (poikilocytes) having a spindle-shape with one or both ends pointed were present. Some red cells appeared to be undergoing mitosis. Both reduced lymphocyte viability and abnormal erythrogenesis occurred in chicks given feed amended with F. proliferatum culture material containing FB1, FB2 and moniliformin.

Animal Feed↗
PubMed1991

The influence of fractions of abnormal erythrocytes on aggregation.

Erythrocytes with abnormal shapes and deformability reduce cell aggregation and hence sedimentation. It is not known what influence small fractions of these abnormal cells have on the sedimentation behaviour of normal cells. We have used three different methods to alter erythrocyte properties (glutaraldehyde, heat treatment, and metabolic depletion). The admixture of such cells in increasing fractions to normal cells affected the sedimentation behaviour in three different ways. Heat-treated erythrocytes decreased the sedimentation proportionally. Small fractions of glutaraldehyde-treated cells increased the sedimentation, which was explained by a pro-aggregatory change of surface properties by glutaraldehyde. With 50% or more glutaraldehyde-treated cells sedimentation was inhibited, which was due to excessive formation of aggregates occupying the entire tube. The presence of small fractions of echinocytes produced by metabolic depletion decreased cell sedimentation disproportionally, which was explained by an inability of spiculated cells to form aggregates with normal erythrocytes. These results indicate that erythrocyte sedimentation is affected by fraction of abnormal cells in a complex way. Many diseases are characterized by fractions of abnormal erythrocytes. Our results may, therefore, contribute to a better understanding of these conditions.

Adenosine Triphosphate↗
PubMed1979

Chronic myelomonocytic leukemia associated with hereditary pyruvate kinase deficiency and multiple acquired erythrocyte abnormalities.

A congenital erythrocyte pyruvate kinase (PK) deficiency was found in a 72-year old female patient with chronic myelomonocytic leukemia (CMML). Erythrocyte PK deficiency was associated with an increase in the activity of hexokinase, 6-phosphogluconate dehydrogenase and glutathione peroxidase in erythrocytes as well as a decrease in acetylcholinesterase, glutathione reductase and glucosephosphate isomerase activities. The enzymatic abnormalities were accompanied by alterations in hemoglobin and in i antigen content of erythrocyte membrane. In addition, bone marrow ultrastructural studies showed dyshemopoietic changes in all blood cell lines and especially in erythroblasts. The present findings confirm the close relationship between CMML and acquired dyserythropoietic syndromes and constitute a new observation of the infrequent association of hereditary erythrocyte enzymopathies and leukemia. A survey of the literature is presented.

Acetylcholinesterase↗
PubMed1983

[Cranio-facial and dental manifestations of erythrocyte abnormalities].

Various types of erythrocyte lesions are observed: hemoglobin anomalies, enzyme disorders, membrane anomalies. This leads to a reduction in the duration of life of the erythrocytes or to abnormal erythropoiesis with, in both cases, reactive development of hematopoietic tissue. This extension of the medullary field in bones results in alterations that are initially visible on radiography, and then, in the severe forms, in the development of mainly craniofacial and dental dysmorphia with, in some cases, additional secondary enamel and dentine anomalies of the hemolytic origin. These anomalies were present to varying degrees in a series of patients in whom cranial radiographies were performed. In two cases there was a fortuitous association of dental anomalies of the melanodontia and opalescent dentine types. These patients may raise particular problems during dental care and treatment: risk of infection, respect of drug contraindications, latent cardiac insufficiency.

Adult↗
PubMed1993

Abnormal erythrocyte rheology in patients with morbid obesity.

The objectives of this study were to investigate the rheological properties of the erythrocyte in patients with morbid obesity and to follow them up after a short-term weight loss. A fluorescent polarization method was used to assess erythrocyte membrane biorheology and to measure its fluidity. Eighteen subjects participated in the study: 8 healthy controls and 10 patients with morbid obesity. The erythrocyte membrane fluidity was obtained in the healthy subjects and in the patients with morbid obesity prior to and after a ten-day zero-calorie diet. Fluidity was determined by steady-state fluorescence polarization after incorporation of the lipophilic probe 1,6-diphenyl-1,3,5 hexatriene (DPH). With this method, the anisotropy parameter at 37 degrees C, which is inversely related to membrane fluidity, was obtained. The patients with morbid obesity revealed an abnormal erythrocyte rheology. The exhibited an abnormally low erythrocyte membrane fluidity as compared with normal subjects. The anisotropy parameter at 37 degrees C was 1.417 +/- 0.093 in these obese patients compared with 1.279 +/- 0.043 in normal-weight controls (p < 0.01). Upon a short-term significant weight loss from a body mass index (BMI) (weight/height2) of 39 +/- 5 to 36 +/- 5 kg/m2 (p < 0.05), the anisotropy parameter did not change (1.401 +/- 0.190). Thus, fluidity measurements permit recognition of an abnormal erythrocyte rheology in patients with morbid obesity. This abnormality may partially explain the excess cardiovascular and thromboembolic morbidity in morbid obesity.

Adult↗
PubMed1997

Abnormal erythrocyte endothelial adherence in hereditary stomatocytosis.

Hereditary stomatocytosis is a red cell membrane protein disorder, which results in hemolytic anemia. Some patients with hereditary stomatocytosis experience dyspnea, chest pain, and abdominal pain, particularly after splenectomy. These symptoms may represent vaso-occlusion secondary to adherence of an abnormal erythrocyte membrane to vascular endothelium. We studied three members of a family with varying clinical expression of hereditary stomatocytosis. Adherence of red cells to endothelium was quantified by measuring the shear force required to separate individual cells from endothelial monolayers using a micropipette technique. Two patients with symptoms of in situ thromboses had a higher percentage of adherent cells compared with their asymptomatic sibling and normal controls. Correlation between this in vitro phenomenon and the clinical course suggests that flow abnormalities in the microcirculation attributable to erythrocyte endothelial adherence may play an important pathogenetic role in the illness. When the proportion of adherent red cells was reduced by a chronic transfusion program in one patient and pentoxifyllin therapy in another, the vaso-occlusive complications were eliminated.

Adult↗