Electron Microscopic Observations on Bone Marrow and Liver Tissue in Non-Hereditary Refractory Sideroblastic Anaemia

A Comparative Electron Microscopic Study of Refractory and Alcoholic Sideroblastic Anaemia

“…The results of this study are in agreement with those obtained in previous examinations of various sideroblastic anaemias, i.e., that erythroblasts contain a visible excess of iron expressed particularly as abnormal mitochondrial accumulations (Bessis and Breton-Gorius, 1962;Sorenson, 1962;Larizza and Orlandi, 1964;Bessis and Jensen, 1965;Petz et al, 1966;Tanaka et al, 1966;Goodman and Hall, 1967). In the present RSA cases most of the cellular iron occurred as iron micelles within the mitochondria but also was present as fcrritin in 'micropinocytotic' vesicles or in aggregates.…”

“…Coated vesicles and smooth thick vesicles, with or without ferritin, were seen in all cases, as were ferritin aggregates.Ring-sideroblasts have been observed in an increasing number of haematological disorders (Dacie and Mollin, 1966;Hines, 1969). The ultrastructural characteristics of pathological sideroblasts (RSA) have been reported previously (Bessis and Breton-Gorius, 1962;Larizza and Orlandi, 1964;Goodman and Hall, 1967; Petz, Goodman, Hall and Fink, 1966;Tanaka, Brecher and Bull, 1966). The purpose of this communication is to describe and compare the electron microscopic features of erythroid cells$ in patients with 'primary' and 'secondary' types of RSA (Mollin, 1965) and in patients with reversible sideroblastic anaemia associated with severe alcoholism (Hines, 1969).…”

Porphyrin biosynthesis in the erythrocytes of patients with sideropenic anaemias

“…Formerly accepted views that the number of sideroblasts is decreased and that there exists a shift of iron from the intraerythroblastic pool into the extraerythroblastic one, namely, into reticuloendothelial cells of the bone marrow (Kaplan, Zuelzer, and Mouriquand, 1954;Mouriquand, 1958;Mouriquand, Lejeune, Germain, and Maitrepierre, 1962;Larizza and Orlandi, 1964), is no longer generally accepted. Breton-Gorius (1961 and have observed large amounts of ferritin dispersed in the cytoplasm of erythroblasts from patients with inflammatory diseases.…”

Microspectrophotometric and Electron Microscopic Studies of Bone Marrow in Hereditary Sideroblastic Anaemia

“…However, as the proportion of cells in G-z was highest in those early polychromatic erythroblasts with the largest accumulations of stainable iron and because only a small proportion of early polychromatic ring sideroblasts were found to be in DNA synthesis, the abnormalities were attributed to an arrest of proliferation caused by the pathological accumu lation of iron within these cells. In support of this hypothesis was the electron microscopic demonstration of iron-laden mitochondria in the early and late erythroblasts in this disease [6,11], and the fact that mitochondrial damage is known to produce a G2 arrest [4]. In the 3 cases of hereditary sideroblastic anaemia, there was no 'pile up' of basophilic or early polychromatic erythroblasts in G> and only a small number of 'U' cells were present.…”