Fixation procedures (Bessis and Weed, 1972) ] for the SEM observation of erythrocytes nowadays prove reliable, so that most artifacts are prevented from occurring. Thus SEM results in a useful method for examining normal and haemolytic patterns. Normal reticulocytes are polylobulate since they undergo through the splenic slits shape remodeling and foreign body extrusion. In premature infants the latter may occur spontaneously throughout the circulation owing to spleen immaturity. Spherocytosis is due to ATP depletion in the oldest cells and thus represents the normal pre-lytic stage. Such deformation is present in most erythrocytes during the haemolytic bouts of hereditary spherocytosis and in most defects of anaerobic glycolysis. Like hereditary spherocytosis, also elliptocytosis is caused by protein n~mbrane defects. The hallmark of thalassaemias is anisopoikilocytosis, due to increased membrane-haemoglobin content ratio. To overlapping unbalance of the globin chain synthesis ratio, more marked surface deformations in alpha- than in beta-thalassaemia correspond. In Hb H disease chain excess precipitates peripherally, in Cooley's anaemia centrally as large clusters. This is due to the more hydrophylic conditions of beta chains (Zavagli et al., 1982) 2 . Thalassaemia may be associated with other abnormal haemoglobins, such as Hb S. Haemolysis may also be due to physical agents, namely shearing stress caused by (a) fibrin deposition throughout the microcirculation, such as in Moschkowitz and Gasser syndromes, (b) prosthetic heart valves, and (c) march haemoglobinuria. IgG-caused haemolytic anaemia may or mav not be associated with complement involvement: early stages may occur intravascularly, but lysis is completed in the spleen and liver through phagocytic receptors. Conversely paroxysmal noctural haemoglobinuria (PNH) is exclusively complement-mediated owing to the characteristic red cell susceptibility to such lytic system. Scanning can reliably distinguish PNH II from PNH III cells (Zavagli et al., 1978).

SCANNING ELECTRON-MICROSCOPY (SEM) IN HEMOLYSIS

RICCI, Giorgio
1984

Abstract

Fixation procedures (Bessis and Weed, 1972) ] for the SEM observation of erythrocytes nowadays prove reliable, so that most artifacts are prevented from occurring. Thus SEM results in a useful method for examining normal and haemolytic patterns. Normal reticulocytes are polylobulate since they undergo through the splenic slits shape remodeling and foreign body extrusion. In premature infants the latter may occur spontaneously throughout the circulation owing to spleen immaturity. Spherocytosis is due to ATP depletion in the oldest cells and thus represents the normal pre-lytic stage. Such deformation is present in most erythrocytes during the haemolytic bouts of hereditary spherocytosis and in most defects of anaerobic glycolysis. Like hereditary spherocytosis, also elliptocytosis is caused by protein n~mbrane defects. The hallmark of thalassaemias is anisopoikilocytosis, due to increased membrane-haemoglobin content ratio. To overlapping unbalance of the globin chain synthesis ratio, more marked surface deformations in alpha- than in beta-thalassaemia correspond. In Hb H disease chain excess precipitates peripherally, in Cooley's anaemia centrally as large clusters. This is due to the more hydrophylic conditions of beta chains (Zavagli et al., 1982) 2 . Thalassaemia may be associated with other abnormal haemoglobins, such as Hb S. Haemolysis may also be due to physical agents, namely shearing stress caused by (a) fibrin deposition throughout the microcirculation, such as in Moschkowitz and Gasser syndromes, (b) prosthetic heart valves, and (c) march haemoglobinuria. IgG-caused haemolytic anaemia may or mav not be associated with complement involvement: early stages may occur intravascularly, but lysis is completed in the spleen and liver through phagocytic receptors. Conversely paroxysmal noctural haemoglobinuria (PNH) is exclusively complement-mediated owing to the characteristic red cell susceptibility to such lytic system. Scanning can reliably distinguish PNH II from PNH III cells (Zavagli et al., 1978).
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/462920
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