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At least 19 recordsLinked to original sources
PubMed1989

[Megakaryocytic myelosis--clinical aspects, morphology and platelet function].

The study reviews 22 patients, aged between 19 to 73 years, with megakaryocytic myelosis. In the course of the disease 11 patients presented haemorrhagic manifestations, 12 patients thrombotic complications, and 6 patients the association of haemorrhage and thrombosis. The maximum platelet counts ranged from 524 to 2700 x 10(9)/l. The bone marrow showed a conspicuous megakaryocytic proliferation with polyploidy of the nuclei, giant forms and clusters. Marked alterations of erythro- and granulopoiesis were excluded. There was no evidence for a reactive thrombocytosis in any case. Patients with thrombocythaemia due to megakaryocytic myelosis (n = 14), with secondary thrombocytosis of various origin (n = 16), and a control group of healthy donors (n = 20) were investigated with respect to the aggregation behaviour and the total calcium content of blood platelets. In 9 of 14 patients with megakaryocytic myelosis platelet rich plasma did not respond to epinephrine (15 mumol/l), a concentration which induced at least weak aggregation in 14 of 16 patients with secondary thrombocytosis and also in healthy subjects. In patients with megakaryocytic myelosis the mean extent of aggregation induced by epinephrine, collagen or adenosine diphosphate was significant lower as compared to controls whereas in patients with secondary thrombocytosis in most cases this parameter did not differ significantly from that of controls. The total calcium content of platelets was significantly lower in both groups of patients as compared to controls. In 14 patients with megakaryocytic myelosis the concentration of the glycoprotein (GP) IIb-IIIa complex was estimated by crossed- and rocket-immunoelectrophoresis and found to be decreased in 8 of them.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1975

[Metabolic myelosis (author's transl)].

102 patients suffering from metabolic myelosis were studied clinically. Among the early signs and symptoms, pins and needles, freezing or burning feet, and impaired kinaesthesia were the most frequent ones. With the syndrome progressing, motor disturbances of supramotoneuronal character developed. Every third patient had neurogenic ischuria. Examinations of the cerebrospinal fluid did not reveal any deviation characteristic or "typical" of myelosis. Different pathogenic factors were detected by analysis according to the rules of internal medicine. However, no single factor defining myelosis aetiologically could be discovered. The majority of cases suggested that the metabolic steady state decompensated by the coincidence of more than one factor, thus initiating myelosis. The following pathogenic factors were observed frequently: Malabsorption, abuse or intoxication, liver cell damage, neoplasm. The great variety of pathogenic factors emphasizes that metabolic myelosis must be counted among the polygenetic identical reactions of the central nervous system. These are the organism alarming signals and they require comprehensive general examinations.

Adult↗
PubMed1975

Ultrastructural localization of histones in chronic erythremic myelosis.

The localization of histones was studied ultrastructurally with the use of the ammoniacal silver stain in erythroid precursors from 6 patients with chronic erythremic myelosis (Di Guglielmo syndrome), 3 patients with severe untreated pernicious anemia, 2 patients with untreated autoimmune hemolytic anemia, and 4 presumedly normal individuals. Silver deposits, indicative of sites of arginine-rich histone within nuclei, were not observed in proerythroblasts from any of the individuals. Small deposits of silver were seen in the heterochromatin in very early intermediate normoblasts. Differences in the amount and distribution of the silver deposits in the various types of erythroid precursors first became recognizable in the intermediate normoblast stage. In all of the individuals, the silver deposits were localized predominantly in the heterochromatic regions of the nucleus. In 6 patients with chronic erythremic myelosis, unusually, dense deposits of silver were observed in erythroid precursors having amounts of heterochromatin comparable to that found in intermediate normoblasts of intermediate megaloblasts in other conditions. In these chronic erythremic myelosis erythroid precursors, the silver deposits were larger and, in many instances, appeared to be more aggregated than in erythroid precursors obtained from 3 patients with untreated pernicious anemia, 2 patients with autoimmune hemolytic anemia, and 4 presumedly normal persons. It is possible that the findings described in this study are involved in the pathogenesis of megaloblastoid erythropoiesis as found in chronic erythremic myelosis.

Anemia, Hemolytic, Autoimmune↗
PubMed1977

[Megakaryocytic myelosis--cause of "idiopathic" thrombocythemia].

Primary thrombocythaemia is to be distinguished from the secondary type by higher counts of megakaryocytes especially of atypic and gigantic forms of these cells, showing up in adequate histological preparations of bone marrow biopsies. From the analysis of those preparations the autonomous proliferation of the megakaryocytopoiesis clearly is to be understood as the reason of the socalled primary thrombocythaemia, occurring in the forms of isolated or mixtcellular megakaryocytic myelosis of the well differentiated type. Both of these forms can convert into thrombocytopenia when atypical and immature megakaryocytes start to overcrowd the picture or when myelofibrosis develops. The latter is to be considered in causal connections with the ineffective dislocated thrombopoiesis, a common finding among megakary-ocytic myelosis complicated with myelofibrosis. Megakaryocytic myelosis therefore is the clue of three different clinical syndromes, which are alternatively marked by the haemostaseologic or the histologic consequences of the overproduction of platelets, or by the proliferation of the megakaryocytes themselves.

Bone Marrow Examination↗
PubMed1977

Chronic megakaryocytic-granulocytic myelosis--an electron microscopic study including freeze-fracture. II. Granulocytes, erythrocytes, plasma cells and myeloid stroma.

In 5 patients with chronic megakaryocytic-granulocytic myelosis (CMGM) bone marrow specimens were studied by electron microscopy to investigate possible abnormalities of the granulocytic cell lineage. Thin sections were compared with freeze-fracture replicas to elucidate further aspects of leucocyte cytology. The atypia exhibited in these cells (eosinophils, basophils and neutrophil granulocytes) consisted mostly of a disorganization of granulopoiesis with hyper- and hypogranulation, a pathological increase in the number of nuclear blebs and a maturation asynchrony sometimes leading to Pelger-like cell forms. Moreover, a presumptive stem cell was demonstrated in the erythopoietic and granulocytic cell lines resembling CFU cells. In conclusion, granulopoiesis in CMGM exhibited abnormalities as generally observed in chronic myelogenous leukaemia. When considered with our previous finding of malignancy in megakaryopoiesis, CMGM has to be classified as a myelosis of mixed cellularity.

Bone Marrow↗
PubMed1978

Arginine methyltransferase activity in chronic erythremic myelosis (Diguglielmo syndrome).

Activity of S-adenosylmethionine-dependent arginine methyltransferase was substantially higher in sonicated bone marrow samples from 6 patients with chronic erythremic myelosis than in bone marrow from 3 patients with untreated pernicious anemia, 2 patients with autoimmune hemolytic anemia, and 4 normal persons. Increased activity of this enzyme may be one of the factors contributing to the pathogenesis fo methylated arginines in histones of erythroblasts from patients with chronic erythremic myelosis.

Arginine↗
PubMed1977

[Megakaryocytic myelosis: clinical and morphological features (author's transl)].

In general, megakaryocytic myelosis is nowadays considered to be a separate disease entity, one of the myeloproliferative syndromes. Morphologically there are localised or diffuse proliferations of usually large pleomorphic megakaryocytes and immature atypical megakaryocytes up to megakaryoblasts in the bone marrow, in the sense of a haemoblastosis. In the course of the disease megakaryocytic splenomegaly develops. A sarcomatous form (megakaryoblastoma, megakaryo-sarcoma) is rare. Megakaryocytic myelosis may arise from chronic meyloid leukaemia or polycythaemia vera, rarely as a transitional stage to an acute myeloblastic leukaemia or megakaryoblastic leukemia in the sense of a blast crisis. The mature form of the disease, which has an age peak at 59 years and is not sex-linked, often takes a course over years with increasing splenomegaly, anaemia, moderate leucocytosis and usually marked thrombocytosis (average value of 720 X 10(9)/1). Life threatening complications are haemorrhages, thromboembolism and increased frequency of infections due to antibody deficiency in the advanced stage.

Adult↗
PubMed1977

Cytochemical detection of homocysteine in pernicious anemia and in chronic erythremic myelosis.

Utilizing a unique ability of homocysteine to form a yellow-brown precipitate with nickel chloride, a cytochemical test was developed in an effort to identify this amino acid. Among a variety of types of anemias studied, bright yellow-colored erythrocytes and erythroid precursors were found only in marrows from patients who had untreated pernicious anemia and chronic erythremic myelosis. The results of the study support the "methyltetrahydrofolate-trap" hypothesis in vitamin B12 deficiency, in which decreased activity of the methylocobalamin-dependent methyltransferase enzyme is believed to lead to accumulation of methyltetrahydrofolate and homocysteine in the deficient cells. The findings also raise the possibility that similar intracellular accumulations of homocysteine may occur in chronic erythremic myelosis, perhaps as a result of a defect in the methyltransferase enzyme.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1980

Acute myelogenous leukemia with megakaryocytic myelosis.

A case of acute myelogenous leukemia terminating in megakaryocytic myelosis is reported. There was a severe, apparently neoplastic proliferation of megakaryocytes so different from that seen in acute granulocytic leukemia or myelofibrosis that a diagnosis of acute megakaryocytic myelosis was warranted. The clinical and pathologic findings of the case are presented in detail. The literature of this extremely rare hematologic disease is reviewed, and differentiation from chronic and malignant myelosclerosis is discussed.

Aged↗
PubMed1995

Anerythremic form of acute erythremic myelosis (Di Guglielmo's syndrome) causing hepatosplenomegaly due to the infiltration of hemoglobin-bearing blast cells: an autopsy case.

An autopsy case of a 42 year old man with the anerythremic form of acute erythremic myelosis (Di Guglielmo's syndrome) is reported. The patient was admitted because of a 1 month history of fatigue and fever. Physical examination showed hepatosplenomegaly. Laboratory data showed leukopenia, mild normocytic anemia, and high levels of serum lactate dehydrogenase and vitamin B12. Bone marrow aspirate revealed an elevated number of erythroblasts, with dyserythropoiesis (E/M = 3.7). After admission, thrombocytopenia progressed rapidly, but blast cells were not seen in the peripheral blood throughout the clinical course. On the 56th hospital day, the patient died of pneumonia. At autopsy, the spleen weighed 550 g and the liver 1800 g. Histologically, the white and red pulps of the spleen and the portal region and sinusoid of the liver were diffusely infiltrated by blast cells that were positive for anti-hemoglobin (Hb) antibody on immunoperoxidase staining. The bone marrow, the lymph nodes, the adrenal glands, the pancreas, and the heart were also infiltrated by the blast cells. This was thus considered to be a rare case of the anerythremic form of acute erythremic myelosis (Di Guglielmo's syndrome), the findings showing that Hb immunoperoxidase staining is useful for the diagnosis of this condition.

Adult↗