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Results for “Erythrocyte Inclusions”

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At least 19 recordsLinked to original sources
PubMed1989

Investigations on beta-glucuronidase-positive erythrocytic inclusions.

Novel erythrocytic inclusion bodies, characterized by strong beta-glucuronidase activity, are described. Their physicochemical properties differ substantially from those of known inclusion bodies and they are mainly observed in patients with liver damage. Since these inclusions occur almost exclusively in erythrocytes, the intraerythrocytic beta-glucuronidase must originate from an extraerythrocytic source, perhaps entering erythrocytes via a receptor-mediated endocytotic pathway.

Adult↗
PubMed1990

The occurrence of beta-glucuronidase in erythrocyte inclusions.

This study presents erythrocytic inclusion bodies exhibiting histochemically a strong beta-glucuronidase activity. The unique occurrence of this enzyme in cells of the erythropoietic series has never been described before and characterizes a novel type of erythrocyte inclusions mainly observed in patients suffering from liver damage but also from myelodysplasia and congenital dyserythropoietic anemia type I. Since it is known that hepatocytes contain high activities of beta-glucuronidase, we supposed a relationship between an increased breakdown of liver cells and the appearance of beta-glucuronidase positive inclusions in the red cells. To prove this hypothesis, we determined the beta-glucuronidase plasma levels of 99 unselected patients suffering from various liver disorders in comparison with 19 healthy controls by use of the umbelliferone technique. Our results indicate that in cases with liver diseases beta-glucuronidase plasma levels are significantly increased as compared with normal persons. The availability of a sufficient amount of beta-glucuronidase, thus, seems to be one prerequisite for the appearance of these inclusions in erythrocytes. As demonstrated by our investigations on congenital dyserythropoietic anemia, in which the red cells also show beta-glucuronidase positive inclusions, another premise seems to be an elevated autophagolysosomal activity in the erythrocytes.

Adult↗
PubMed1985

Beta-glucuronidase-positive erythrocytic inclusion bodies--a hitherto unknown phenomenon.

A combined cytochemical and electron microscopical study has delineated a new type of an erythrocytic inclusion body. Enzyme cytochemically these inclusions are characterized by beta-glucuronidase as a marker enzyme. In part, the inclusions may contain acid phosphatase and ferritin. The inclusions develop in mature erythrocytes since beta-glucuronidase normally does not occur in erythroblasts and, in general, this type of inclusion body is not found in erythroblasts. Based upon our preliminary findings, the hypothesis is extended that beta-glucuronidase is taken up via receptor-mediated endocytosis into erythrocytes and is finally put into clustered cytolysosomal vaculoes, that account for the inclusion bodies as seen at light microscopy. Exogenous beta-glucuronidase might be contributed for by breakdown of cells (e.g. hepatocytes) producing this enzyme in considerable amounts numbers. This view is corroborated by the observation that most patients with beta-glucuronidase-positive inclusions suffered from various chronic disorders of the liver.

Acid Phosphatase↗
PubMed1990

Intrahepatocellular erythrocyte inclusions with hepatic sinusoidal infiltrates and splenomegaly.

We describe two patients suffering from a prolonged fever, pancytopenia, and splenomegaly. The spleen of both patients was grossly enlarged and the liver was moderately enlarged. The blood pictures were characterized by anemia and leukopenia to a severe degree, with moderate thrombocytopenia and moderate reticulocytosis. The serum transaminases were in the normal range, but the alkaline phosphatase was greatly increased. Splenectomy and wedge liver biopsies were performed on both patients. Histological findings of the spleen were variable. The histopathologic findings of the liver showed infiltration of lymphocytes, plasma cells, monocytes, and neutrophils into the dilated hepatic sinusoids. The sinusoidal infiltrate was more prominent in zones 1 and 2 and less prominent in zone 3 of the acinus. Erythrocyte inclusions that were confirmed by immunohistochemical methods were seen in the cytoplasm of hepatocytes. Electron microscopy revealed a penetration of erythrocytes into the cytoplasm of hepatocytes and caused leakage of cytoplasmic contents into Disse's spaces and sinusoids.

Erythrocytes↗
PubMed1997

Intrahepatocellular erythrocyte inclusions and increased calcium precipitation in canine endotoxic shock.

AIMS: To investigate the electron microscopic localization of membrane-bound and exchangeable calcium with specific calcium precipitation techniques during endotoxic shock in the dog. METHODS: Ten pentobarbital anesthetized, mechanically ventilated, and paralyzed dogs were studied. Six dogs received 2 mg/kg E. coli endotoxin i.v. followed by a continuous 0.9% saline infusion to restore and maintain baseline cardiac filling pressures. Four dogs served as time-matched controls. Each experiment lasted for 3 h. After the completion of study, the livers of four endotoxic and two control dogs were fixed by perfusion of 3% glutaraldehyde via the portal vein. Liver sections were then prepared for electron microscopy and calcium localization studies. RESULTS: Hepatocytes of endotoxic animals completely lost their plasma membrane-bound calcium. The most severely damaged cells showed extensive "blebbing" of the plasma membrane and contained numerous cytoplasmic erythrocyte inclusions. Endotoxin administration also caused excessive calcium precipitation inside hepatocytes in areas with pronounced sinusoidal damage. CONCLUSIONS: In this acute model of fluid-resuscitated endotoxic shock in dogs, the use of specific calcium localization techniques enables the demonstration of disturbances in hepatocellular calcium handling, which appear to be closely related to structural alterations of the hepatocyte cell membrane. Erythrocyte uptake by hepatocytes is a previously undescribed phenomenon in canine endotoxic shock and may serve as an additional histologic marker of ultrastructural cell (membrane) damage.

Animals↗
PubMed1990

Hb Mizuho [beta 68(E12)Leu----Pro]. Second occurrence identified in a Caucasian child with hemolytic anemia and dense erythrocyte inclusions.

Hb Mizuho [beta 68(E12)Leu----Pro] was identified in a child of Italian/Sicilian descent who exhibited severe, transfusion dependent hemolytic anemia which improved following splenectomy. The patient's peripheral blood smear, which prior to splenectomy demonstrated coarse erythrocytic basophilic stippling, showed large, dense erythrocytic hemoglobin inclusions following splenectomy. Whole blood oxygen equilibrium results were consistent with the presence of a hemoglobin component exhibiting increased oxygen affinity with decreased cooperativity. The abnormal beta chain was characterized by high performance liquid chromatography analysis of the isopropanol precipitable hemoglobin fraction.

Amino Acid Sequence↗
PubMed1991

Congenital dyserythropoietic anaemia with novel intra-erythroblastic and intra-erythrocytic inclusions.

A hitherto undescribed form of congenital dyserythropoietic anaemia is reported. The patient was severely anaemic and hydropic at birth and is now 8 years old. She has a moderate normochromic normocytic anaemia. HbF level of 50%, reticulocyte count of 5-12% and hyperbilirubinaemia. Bone marrow smears showed intense normoblastic erythroid hyperplasia with morphological evidence of dyserythropoiesis; the most common dysplastic features were basophilic stippling of polychromatic erythroblasts and erythrocytes and marked abnormalities of nuclear shape in polychromatic erythroblasts. Electron microscope studies showed that some polychromatic erythroblasts and several erythrocytes contained inclusions which were rounded, elongated or irregular in outline or were doughnut-shaped. These inclusions consisted of compact masses of tubules and saccules which may represent smooth endoplastic reticulum together with Golgi cisternae. The ultrastructural studies also revealed peculiar membrane-bound cylindrical structures in a rare late erythroblast, and phagocytosed erythroblasts within some macrophages. The technique of combined Feulgen microspectrophotometry and 3H-thymidine autoradiography demonstrated a pile-up of early polychromatic erythroblasts in the G1 and G2 phases of the cell cycle, indicating a prolongation of, or an arrest at, these phases. Furthermore, nearly a quarter of all erythroblasts failed to incorporate 3H-leucine into protein. Thus the anaemia appeared to be due to a combination of disordered erythroblast function, increased ineffectiveness of erythropoiesis and peripheral haemolysis. The primary defect may be an excessive synthesis or impaired degradation of intracytoplasmic membranes.

Anemia, Dyserythropoietic, Congenital↗