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At least 37 records · Page 2Linked to original sources
PubMed2001

Acute erythremic myelosis (true erythroleukaemia): a variant of AML FAB-M6.

AIMS: Classic erythroleukaemia (acute myeloid leukaemia M6, or M6 AML) is defined as an excess of myeloblasts in an erythroid predominant background. Leukaemia variants in which the primitive blast cells are demonstrably erythroid are extremely rare and poorly characterised. Variably referred to as "true erythroleukaemia" or "acute erythremic myelosis", they are often included within the M6 AML category even though they do not meet strict criteria for this type of AML. METHODS: Two cases of acute erythroid neoplasia are presented with clinical, morphological, immunophenotypic, and cytogenetic analysis. RESULTS: Both patients presented with profound anaemia, one in a setting of long standing myelodysplasia. Bone marrow examination revealed a predominant population of highly dysplastic erythroid cells in both cases. In one case, the liver was infiltrated by neoplastic erythroid cells. Both patients died within four months of diagnosis. CONCLUSIONS: This report illustrates that cases of acute leukaemia occur in which the dominant neoplastic cell is a primitive erythroid cell without an accompanying increase in myeloblasts. This does not preclude the neoplastic clone originating in a multipotent haemopoietic stem cell, as suggested by cases arising in patients with myelodysplasia. Acute erythremic myelosis should be recognised as a distinct variant of M6 AML.

Adult↗
PubMed1975

Cytochemical abnormalities of atypical erythroblasts in acute erythremic myelosis.

Cytochemical properties of atypical erythroblasts and 'histioid' cells from the bone marrows of two patients with acute erythremic myelosis (Di Guglielmo's disease) were studied. In addition to strong PAS and strong nonspecific esterase positivity, intense specific esterase positivity was also detected in the majority of the erythroid precursors. Since specific esterase activity is considered to be a feature of granulocytic cells, its presence in erythroid precursors raises the possibility that the atypical erythroblasts of acute erythremic myelosis may share close metabolic relationships with granulocytic cells.

Acute Disease↗
PubMed1979

[Splenectomy and polychemotherapy in chronic myelosis].

It is referred to the possibility of the splenectomy in the early phase of the chronic myelosis in the time of the first remission. The intervention cannot be recommended generally and should be used only now and then in centres which have rooms at their disposal which are poor in germs. Own experiences speak for the fact to extend the polychemotherapy of the blast crisis of the chronic myelosis to its prephase, when an increasing therapy resistance occurs, the spleen becomes clearly larger, the number of blasts in the bone-marrow increases and single blasts may be proved in the peripheral blood. Combinations of two or three medicaments, such as Busulfan, Myelobromol, Merkaleukin, Methotrexat, Hydroxyurea, Alexan, Vinkristin or Rubomycin seem to be favourable.

Busulfan↗
PubMed1977

[Pathologc findings in megakaryocytic myelosis (author's transl)].

From 1969--1975 patients with predominantly megakaryocytic myelosis were observed. Diagnosis was made up after histologic examination of iliac crest bone biopsy specimens embedded in methacrylate. From 6 patients rebiopsies and from further eleven ones the removed spleens were available. Autopsy was performed in 12 cases. In our material predominantly megakaryocytic myelosis was especially observed in male patients of advanced ages. The course of the disease was rarely acute, most often chronic and associated with the development of an extreme splenomegaly. Transition into osteomyelofibrosis or osteomyelosclerosis was frequent, the latter condition tended to develop a so-called myelosarcoma. The cause of death often was a generalized hemorrhagic diathesis with gastrointestinal hemorrhage or an fatal infection.

Adult↗
PubMed1980

Chronic megakaryocytic granulocytic myelosis-CMGM. A subtype of chronic myeloid leukemia.

In 1,083 core biopsies of the bone marrow with myeloproliferative diseases 454 cases or 42% were found to have neoplastic megakaryopoiesis. Neoplasia of megakaryocytes was assumed from the conspicuous cytological atypicality revealed by light microscopy, extending and confirming earlier ultrastructural findings. Histopathology of the bone marrow in these patients was described as chronic megakaryocytic-granulocytic myelosis - CMGM - since neutrophilic granulopoiesis is also apparently neoplastic and both cell lineages showed a complete differentiation to mature forms. CMGM should be separated from the chronic granulocytic leukemia - CGL - which consists of only a single line proliferation. The incidence of CGL in our total of 1,083 patients was 25%. Both entities are included in chronic myeloid leukemia - CML - because of the demonstration of the Philadelphia chromosome in the hematopoietic cells of these two groups of patients. Primary or idiopathic thrombocythemia has to be differentiated from CMGM since there is no evidence for malignancy of the granulocytic series.

Bone Marrow↗
PubMed1977

Chronic megakaryocytic-granulocytic myelosis--an electron microscopic study. I. Megakaryocytes and thrombocytes.

The fine structure of the bone marrow in chronic megakaryocytic-granulocytic myelosis (CMGM) was studied in 5 nontreated patients to investigate possible malignant proliferation of megakaryocytes and the role of megakaryopoiesis in fibrillogenesis, terminating in osteomyelofibrosis. In comparison with normal megakaryopoiesis there is an enormous increase of the megakaryocytic cell line and many immature and atypical forms are seen. Most conspicuous are microforms, nuclear-cytoplasmic disorganization and nuclear inclusions. Asynchrony of maturation causes abnormal thrombocytogenesis with premature detachment of platelets resulting in immature and peculiar giant forms of thrombocytes. Besides megakaryocytes appearing superficially normal the maturation anarchy of many cells is so severe that by analogy with observations in other leukaemic cells these abnormalities are thought to be representative of a malignant growth. Moreover, there is a striking accumulation of microfibrils and single collagen fibres around megakaryoblasts. Since these cells contain all those organelles commonly associated with fibre production the initial step for fibrillogenesis may therefore arise from the megakaryoblasts prior to platelet release, or any fibroblast proliferation.

Blood Platelets↗
PubMed1976

Ultrastructure of chronic megakaryocytic-granulocytic myelosis.

To study chronic megakaryocytic-granulocytic myelosis, bone marrow biopsies from 5 patients were obtained. Ultrastructural quantitative and qualitative assessments demonstrate proliferation of both the megakaryocytic and granulocytic cell lines. Factors indicative of malignant growth in megakaryocytes included atypical maturation, nuclear-cytoplasmic asynchrony, nuclear inclusions and production of micromegakaryocytes. Abnormal thrombocyte delineation provoked giant platelet production. The neutrophil series also presented atypia as generally observed in chronic myelogenous leukemia. Even in cases without evidence of myelofibrosis under the light microscope, megakaryoblasts were associated with fibrillar structures. These cells may be responsible for the initial step in fibrillogenesis by providing a medium conductive to the collagen formation found in later stages of this disease.

Blood Platelets↗
PubMed1977

Freeze-fracture of the normal and pathological megakaryocyte lineage in chronic megakaryocytic-granulocytic myelosis.

Freeze-fracture and thin sections were performed on human bone marrow of chronic megakaryocytic-granulocytic myelosis (CMGM) to study the three-dimensional fine structure and maturation of normal and atypical megakaryocytes and thrombocytes. In the many normally maturing megakaryocytes the development of the demarcation membrane system (DMS) was best investigated by comparison of thin sections with freeze-fracture replicas. The DMS shows no connections with the Golgi apparatus or rough-surfaced endoplasmic reticulum, but originates from tubular infoldings of the plasma membrane. These infoldings are always in continuity with the extracellular space and form an intracellular membranous pool by branching and coalescing of flattened tubules from which finally the perforated cisternae of the DMS arise. Freeze-fracture of the normal thrombocytes confirms earlier findings. The abnormal giant platelets seen in CMGM display extensive areas of smooth membranes of a spongy structure consisting of dense tubules surrounded by the labyrinth of the surface-connected system. Their physiological significance in these atypical platelets remains unsolved.

Blood Platelets↗
PubMed2000

Erythremic myelosis (AML6er) in a cat.

A 4-year-old male European domestic cat was presented with dysorexia, weakness and depression. Normocytic normochromic non-regenerative anaemia, leucopaenia and thrombocytopenia were detected. Rubriblasts were detected both in the blood and in the bone marrow. Tests of blood chemistry revealed no alterations of renal and hepatic function and a positive reaction to FeLV antigen was detected in the cat's serum. Neoplastic cells did not show positive to cytochemical reactions against granulocytes, monocytes and lymphocytes. According to haematological and bone marrow cytological findings, a diagnosis of erythremic myelosis (AML6er) was made. Histopathology showed extramedullary haematopoiesis in the liver, spleen, kidney and lymph nodes and chronic nephropathy and degenerative signs in the liver.

Animals↗
PubMed1975

Chronic erythremic myelosis profiling a refractory anemia.

Chronic erythremic myelosis is a myeloproliferative disorder of unknown etiology that is characterized by refractory macrocytic anemia and marked megaloblastoid erythroid hyperplasia of the bone marrow. Ferrokinetic and cytologic evidence indicates that the disorder demonstrates ineffective erythropoiesis. Certain cytochemical tests may help both to substantiate the diagnosis and to provide insight into some of the biochemical abnormalities in the erythroid precursors. Therapeutic trials of androgen or pyridoxine (vitamin B6) or both may be of value in some cases but ineffective in others, and some patients may require administration of blood transfusions. Why an erythroid disorder characterized by a uniquetype of megaloblastoid erythropoiesis should be the forerunner of acute leukemia is one of the many unanswered questions in this often therapeutically frustrating disorder.

Adult↗
PubMed1975

Phosphorylase activity in chronic erythremic myelosis.

Phosphorylase activity was detected in the cytoplasm of erythroid precursors of 6 of 7 patients with chronic erythremic myelosis (Di Guglielmo syndrome), in proerythroblasts and megaloblasts from 3 patients with pernicious anemia and in 2 patients with severe folate deficiency in neoplastic lymphocytes from 2 patients with acute lymphoblastic leukemia, and in 1 patient with leukemic lymphosarcoma. In all of these patients, most of the erythroid precursors and/or neoplastic lymphocytes contained increased amounts of glycogen when stained with the PAS reagent. Phosphorylase activity was not detected in erythroid precursors obtained from 6 presumed normal individuals or from 3 of 7 patients with a variety of other types of anemia in which the erythroid precursors were PAS-negative. Similarly, phosphorylase activity was absent in lymphocytes obtained from presumed normal individuals. Although the mechanisms responsible for the pathogenesis of PAS positivity are unclear, it is possible that the increased phosphorylase activity found in cells that are PAS-positive may reflect a disorder in the biosynthetic pathway of glycogen.

Anemia, Hemolytic↗
PubMed1977

Nonspecific esterase activity in pernicious anemia and chronic erythremic myelosis: a cytochemical and electrophoretic study.

Cytochemically, nonspecific esterase activity was detected in megaloblasts from three patients with severe untreated pernicious anemia, in megaloblastoid erythroblasts from five patients with chronic erythremic myelosis (DiGuglielmo syndrome), and in normoblasts from a patient with severe untreated iron-deficiency anemia. Nonspecific esterase activity in all of these erythroblasts was inhibited by sodium fluoride. Enzymatic activity could not be detected in normoblasts from normal marrows. Electrophoretically, three bands of nonspecific esterase activity could be visualized in marrow sonicates from the anemic patients and normal persons. All of these bands were inhibited by sodium fluoride. The results demonstrate that electrophoretically and in terms of fluoride inhibition, nonspecific esterases obtained primarily from erythroid precursors in various types of anemias are similar to nonspecific esterases found in normal marrows presumably containing a more heterogeneous population of cells.

Anemia, Pernicious↗
PubMed1975

[Association of chronic myelosis and cancer].

During the period between 1948-1963 a total of 3,200 tumor patients were treated in the First and Second Medical Clinics of Tg.-Mures. In these tumor patients as well as the skin cancer patients who were treated with radiotherapy the authors found in 1.5% of the patients a leukocytosis of more than 20,000. In the last ten years (1964-1974), however, in the Second Medical Clinic only, 5% of 516 tumor patients showed a leukocytosis exceeding 20,000. In the first group of patients (3,200 cases) 0.03% showed more than 50,000 leukocytes, in the other group of 516 patients 0.2% showed more than 50,000 leukocytes. These values point towards a leukemoid reaction. A shift to the left to the myelocytes or beyond in the blood picture was found in the Second Medical Clinic in 10% of patients with carcinoma during the year of 1974. In 6% of the cases erythroblasts in the peripheral blood were seen, too. This deviation occurred often independent of the total number of leukocytes and was of a temporary nature. During the same time (1949-1974) 128 patients with chronic myeloid leukemia were treated in both departments as in-patients. 6 cases (i.e., 4.6%) had a chronic myelosis simultaneous with carcinoma, in one case together with an osteosarcoma. The diagnosis was confirmed in all cases by autopsy.

Autopsy↗
PubMed1975

[Acute erythremic myelosis as a terminal phase of polycythemia rubra vera].

A male, 66, developed Acute Erythremic Myelosis in the course of Polycythemia Vera. The time of onset of Polycythemia Vera could not be determined, his first symptoms being vascular complications. He received treatment with Phlebotomies and Myleran. Five years later he became ill with malaise, fever, splenomegaly; in the peripheral blood profound pancytopoenia with immature, bizzare erythro-and megaloblasts have been found. Bone marrow was full of atypical megaloblasts, some of them having two or more nuclei. The number of mitoses was increased. Chromosomal abnormalities consisted of ane-uploid cells, chromatid breakes and translocations (G to A-1). The therapy with B12, Cytosin-Arabinoside, Oncovin and Blood transfusions was unsuccessful. He died 21 days after being admitted to the Hospital.

Acute Disease↗
PubMed1976

[Chronic myelosis].

After introducing remarks concerning the character of chronic myelosis and epidemiological data the clinical symptomatology and diagnostic criteria including differential diagnosis are discussed. The possibilities of the cytostatic or radiological therapy in the different stages of disease are explained.

Adult↗
PubMedDate not supplied

[Analysis of cases of funicular myelosis].

In a material of 14 cases of funicular myelosis the authors demonstrated frequent presence of peripheral signs, psychic changes and rare occurrence of such infrequent syndromes as transverse myelitis, cerebellar syndrome, optic nerve atrophy. Diagnostic difficulties are discussed in cases of pernicious anaemia without blood changes, without gastric achylia, or in patients with vitamin B12 deficiency, malabsorption syndromes and other more infrequent pathological conditions. The importance of such investigations as Schilling's test in atypical cases and the necessity of regular, long-term substitutive treatment with B12 are stressed.

Adult↗