Red‐Cell Acetylcholinesterase Activity in Physiological and Pathological Reticulocytosis

Sabine, Jean C.

doi:10.1111/j.1365-2141.1965.tb06573.x

Cited by 7 publications

(3 citation statements)

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“…The present investigation shows that red cell AChE activity in AIHA is below normal, as previously reported by Tanaka et al(1964) and Brabec et a1 (1965). Others (De Sandre et al, 1963;Kaplan et al, 1963;Sabine, 1965;Hansen, 1968;Sabine & Kwok, 1968; Rueda et a!, 1969), however, have found normal AChE values in this disorder. The reasons for this discrepancy are presumably multiple and related to both the biological and technical variability occurring in enzyme activity determination.…”

Section: Discussionmentioning

confidence: 99%

“…The determination of red cell acetylcholinesterase (AChE) in AIHA is of particular interest since this enzyme is located in the cell membrane, where the primary action of the antibody takes place. As far as we know, AChE has been determined in approximately 50 cases of AIHA (De Sandre et a1, 1963;Kaplan et al, 1963;Tanaka et al, 1964;Brabec et al, 1965;Choremis et al, 1965;Sabine, 1965;Hansen, 1968;Kovalev & Zefirov, 1968;Sabine & Kwok, 1968;Rueda et al, 1969) and found subnormal in somewhat more than half. It is interesting that AChE activity is also subnormal in ABO haemolytic disease of the newborn but not in Rh disease (Kaplan et al, 1964;Sirchia et al, 1965), both of which are immunohaemolytic disorders.…”

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Red Cell Acetylcholinesterase Activity in Autoimmune Haemolytic Anaemias

et al. 1970

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Summary. Red cell acetylcholinesterase activity was determined in 59 patients suffering from autoimmune haemolytic anaemia, classified according to the types of erythrocyte‐coating globulins. The enzyme activity was found significantly subnormal in the γG and the γG+C' types of AIHA, while it was not significantly lower than normal in the group of patients where complement (C') alone coated the red cells. These results suggest that different types of autoantibodies are able to cause different biochemical alterations of the red cells.

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Section: Discussionmentioning

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Red Cell Acetylcholinesterase Activity in Autoimmune Haemolytic Anaemias

et al. 1970

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“…Deficiency of AChE, the most likely explanation, is characteristic of paroxysmal nocturnal haemoglobinuria (PNH) (Auditore and Hartmann, 1959;Metz, Bradlow, Lewis and Dacie, 1960). It is a common finding in Coombs positive haemolytic disease (Tanaka, Valentine and Schneider, 1964) and in myelophthisic anaemia or leucoerythroblastosis frequently associated with malignant disease (Sabine, 1965).In several cases, however, it appeared more likely that an over-abundance of G6PD not reflecting red cell youth was present. A clear example occurred in an elderly man with 507…”

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Observation of Four Age‐Related Parameters in the Red Cells of Various Disease States

Sabine

Kwok

1968

Br J Haematol

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Simultaneous determinations of anaerobic glycolysis, hexokinase activity (HxK), glucose‐6‐phosphate dehydrogenase activity (G6PD) and acetyl‐cholinesterase activity (AChE) were made in the whole red cell populations of patients and of healthy subjects, and in the layers of the centrifuged cell packs of selected patients to give regression lines for each parameter plotted against each of the others. Apparently normal interrelationships were found in blood loss and in haemolytic disease of various origins. Abnormalities were revealed which would escape notice if a single parameter were assayed. These were relative, not absolute, deficiency of anaerobic glycolysis in a case of congenital nonspherocytic haemolytic disease with no deficiency of G6PD, HxK or pyruvate kinase; of HxK in a case of unexplained anaemia; and of AChE in a case of Coombs positive haemolytic disease. In a case of paroxysmal nocturnal haemoglobinuria AChE was severely deficient while glycolysis, HxK and G6PD were extraordinarily high and appeared normally interrelated. The patient had been transfused just before these studies, and calculations based on the enzyme data led to the hypothesis that in this case the donor cells were rapidly destroyed. Observations in normal blood showed that values for G6PD and AChE occur as two independent normal distributions. The same was true for glycolysis and AChE. Glycolysis and G6PD were correlated but did not approach a perfect functional relationship. There is evidence that high G6PD unrelated to red cell age occurs in malignant disease, but it is not conclusive.

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