Estimation of Foetal Haemoglobin in Leukaemia

Bartolozzi, G; Marianelli, L

doi:10.1159/000209126

Cited by 12 publications

(3 citation statements)

References 10 publications

(11 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results obtained in the present study confirm previous observations that in most forms of leukaemia elevated Hb F levels may be found at some stage of the illness (Beaven et al, 1960;Weatherall & Walker, 1965;Bartolozzi & Marianelli, 1966;Miller, 1969;Ozsoylu & Balci, 1970;Newman et al, 1973;Walker & Ali, 1973). This observation poses several questions.…”

Section: Discussionsupporting

confidence: 92%

The Patterns of Fetal Haemoglobin Production in Leukaemia

et al. 1976

View full text Add to dashboard Cite

Elevated levels of haemoglobin F (Hb F) have been foudn in a wide range of haematological malignancies, but very high levels were found only in juvenile chronic myeloid leukaemia (JCML), and erythroleukaemia occurring in infancy. In both these disorders a reversion to a fetal form of erythropoiesis may occur, as judged by both the structure of the Hb F and by the disappearance of Hb A2 and the carbnoic-anhydrase isozymes during the course of the illness. The clinical picture of JCML is not always associated with a reversion to fetal erythropoiesis; there appears to be a heterogeneity of conditions with this clinical label. Thus the reversion to a completely fetal pattern of erythropoiesis seems to occur in a variety of leukaemias which start in early life. This change is associated with a uniformly bad prognosis. Of a group of 17 patients with acute myeloid leukaemia 15 developed an increase in the level of Hb F about 60 days after the commencement of treatment; significantly greater increases were observed in those achieving a clinical remission. The level of Hb F usually declined during remission but high levels persisted in a few cases. Increased levels of Hb F were found also in patients with other haematological malignancies who had undergone periods of marrow aplasia during treatment. In all cases the Hb F was heterogeneously distributed throughout the red cells. Analysis of gamma15 or gammaCB3 peptides of Hb F from a variety of leukaemias gave glycine compositions ranging from 0.20 to 0.85 residues with many values in the fetal range; all cases with a reversion to fetal erythropoiesis had values in the fetal range. Attempts to confirm the 'fetal' origin of the cells containing Hb F by means of other markers was possible only in the cases of JCML and in one child with erythroleukaemia. These studies indicate that in some forms of leukaemia there may be a genuine reversion to fetal erythropoiesis while in others the emergence of cells containing Hb F appears to be part of a rapid regeneration process occurring after a period of marrow aplasia. The diagnostic and prognostic value of these observations is discussed.

show abstract

Section: Discussionsupporting

confidence: 92%

The Patterns of Fetal Haemoglobin Production in Leukaemia

et al. 1976

View full text Add to dashboard Cite

show abstract

“…The second hypothesis put forward by Rochant et a1 (1972) is that there is a partial reversion to a fetal form of erythropoiesis in some acquired blood disorders. Fetal characteristics which have been reported in the haematological disorders described here include raised fetal haemoglobin (Beaven et al, 1960;Bartolozzi & Marianelli, 1966;Shahidi et al, 1962) and loss of I-antigen (Salmon et a!, 1966). The most obvious exception in acquired disorders is that of PK activity which, as shown in this study, often has a reduced activity.…”

Section: Discussionmentioning

confidence: 76%

Acquired Erythroenzymopathies in Blood Disorders: Study of 200 Cases

et al. 1975

View full text Add to dashboard Cite

Enzyme abnormalities are frequently found in the red cells of patients with various acquired blood disorders. In leukaemias, preleukaemic states and bone marrow insufficiencies with or without sideroblastosis, changes in enzyme activity are usually characterized by the coexistence of deficiency of some enzymes and an increased activity of others. The most frequently decreased activities are those of pyruvate kinase, phosphofructokinase,2,3-diphosphoglycerate mutase and adenylate kinase; the most frequently increased activities are those of hexokinase, aldolase, enolase, 6-phosphogluconate dehydrogenase and glucose-6-phosphate dehydrogenase. In primary myelofibrosis and in polycythaemia rubra vera, enzyme deficiencies are infrequent and differ from those observed in leukaemias and related disorders. Phosphohexose isomerase and phosphoglucomutase deficiencies seem relatively specific for polycythaemia rubra vera. Explanations for the acquired enzymopathies are still at the stage of hypothesis. The theory of multiple genetic damage may explain some findings but has not yet been proved right. The possibility of post-translational molecular modification is suggested as a working hypothesis.

show abstract

“…t 12 casj still alive at time of report had a mean age of 31 years. Note-The references to the 94 cases on which this Table is based are as follows:Bartolozzi et al (1965);Brodie and Dallaire (1962);Brown, Hale, and Porter (1964); Brown, Patterson, and van Mierrop (1962);Brunelli and Rosti (1966);Burks and Sinkford (1964);Butler et al (1965);Cernea et al (1966);Edwards et al (1960);El-Alfi, Biesele, and Smith (1964);Finley, Finley, and Carte (1963);Ganassi et al (1965);German et al (1962);Gottlieb et al (1962);Grutta et al (1966);Gustavson et al (1962);Hansen et al (1963);Hecht et al (1963);…”

mentioning

confidence: 99%