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PubMed1992

Nucleolar organizer regions of megakaryocytes in chronic myeloproliferative disorders.

To study megakaryocyte activation, the argyrophilic staining method of nucleolar organizer regions (AgNOR) has been applied to decalcified bone marrow biopsies of 16 individuals with no haematopoietic disorders and 59 patients with chronic myeloproliferative disease. Of the 59 patients, 18 had chronic myeloid leukaemia (CML), 21 chronic megakaryocytic granulocytic myelosis (CMGM), 13 polycythaemia vera (PV) and 7 essential thrombocythaemia (ET). The AgNOR number of megakaryocytes in CML was significantly lower, and in CMGM, PV and ET significantly higher than in healthy individuals. The high number and the clusters of fine-grained AgNORs of megakaryocytes in CMGM, PV and ET are suggestive of active, proliferating cells. The AgNOR number of megakaryocytes and the platelet counts of the patients did not show a convincing correlation. In CMGM, PV and ET the pyknotic, heterochromatinized megakaryocytes with narrow rims of cytoplasm called bare (nude) nuclei, possessed few, large AgNOR granules. The AgNOR staining of bare nuclei and the roughly identical number of granules found in CMGM, PV and ET indicate a common, active mechanism of apoptosis.

Biopsy↗
PubMed1991

Megakaryocytes in chronic myeloproliferative disorders: numerical density correlated between different entities.

A morphometric evaluation of number and grouping of megakaryocytes (MK) in five different groups of chronic myeloproliferative disorders (CMPD) was performed by counting 60 high power fields equaling approximately 14.28 mm2 of haematopoiesis in each case. Twenty-one up to 29 cases were evaluated for each of five categories of CMPD and one control group; a total of 132 cases of CMPD and 33 control cases were used. The mean number of MK per square millimetre was 15.54 +/- 1.53 in chronic myeloid leukaemia of common or granulocytic type (CML.CT), 69.91 +/- 5.85 in CML with megakaryocytic increase (CML.MI), 59.59 +/- 3.27 in polycythaemia vera (P. vera), 59.85 +/- 4.59 in primary thrombocythaemia (PTH), 67.58 +/- 4.11 in chronic megakaryocytic granulocytic myelosis (CMGM), and 19.7 +/- 3.07 in controls. The distinction between free or isolated MK, and between clustered or grouped MK corresponds to the total cell counts of MK in the various groups of CMPD. Clustering of MK was significantly higher in CMGM and PTH compared to other groups, but the difference between them was not statistically significant. Significant differences in the mean number of MK were obtained between controls and CML.CT on the one hand and all other groups of CMPD on the other. The results further support the histological sub-classification of CMPD according to the primary disorders of the Hannover classification (not advanced by sclerosis, fibrosis or excess of blasts, respectively).

Blood Cell Count↗
PubMed1975

[Fine structure of megakaryocytes in aleukemic megakaryocytic meyelosis].

Megakaryocytes from a case of aleukemic megakaryocytic myelosis were examined by electron microscope. They were considerably increased in number and their ultrastructure was different from normal megakaryocytes in certain aspects. Myelinfigures became demonstrable in the cytoplasm in increased number. An effective development of the demarcation membran system could not be observed.

Aged↗
PubMed1992

Histologic findings in bone marrow biopsies of patients with thrombocythemic cell counts.

Histologic diagnoses from bone marrow biopsies were analyzed in a total of 1165 patients presenting with thrombocythemic platelet counts at initial examination. Two cut-off points suggested by the Polycythemia Vera Study Group to define thrombocythemia by platelet counts were compared: the former limiting value of 1000 x 10(9)/l platelets versus the recently proposed value of 600 x 10(9)/l. The percentage of all nonproliferative disorders was 41% under the lower, dropping to 11% under the high cut-off point. The respective figures for myeloproliferative disorders increased from 49% under the lower to 74% under the high limiting value. Primary thrombocythemia was included in 72% by the lower, and in only 40% by the high limiting value when classified by its histologic pattern in bone marrow biopsy. A striking decrease of platelet counts occurs, related to fiber increase, among each of three main groups of myeloproliferative disorders: in CML with megakaryocytic predominance from 40% down to 25%, in megakaryocytic-granulocytic myelosis (primary, i.e., agnogenic myelofibrosis) from 36.6% to 10%, and in primary thrombocythemia from 72.6% to 28.6% in cases with reticulin sclerosis.

Biopsy↗
PubMed1982

Abnormalities of megakaryocytes in myelitis and chronic myeloproliferative diseases.

A planimetric study of megakaryopoiesis in various chronic myeloproliferative diseases (CMPD) was performed and the results compared with those from controls and myelitis of rheumatic origin. Morphometric measurements included at least 200 megakaryocytes in each case observed in Giemsa-stained semithin sections of resin-embedded core biopsies. Twenty specimens were evaluated from the controls and inflammatory disorders and from each of the following CMPD: 1, chronic granulocytic leukaemia (CGL); 2, polycythaemia vera (P. vera); 3, chronic megakaryocytic-granulocytic myelosis without or with minimal increase in reticulin fibre content (CMGM); 4, myelofibrosis or osteomyelosclerosis (MF/OMS). Megakaryocytes were classified as follows: 1, normal megakaryocytes at all stages of maturation; 2, giant forms; 3, microforms; 4, intussusceptions; 5, a-nuclear cytoplasmic fragments; 6, naked nuclei or necrotic forms. The results of this study demonstrate obvious abnormalities of megakaryopoiesis in addition to the increase in absolute numbers of megakaryocytes per marrow area and their different sizes as reported earlier (Thiele et al. 1982). Aberrations are particularly conspicuous when pure granulocytic proliferation or neoplasia of CGL is compared with the so-called mixed cellularity of megakaryocytes and granulocytes in CMGM including MF/OMS. Abnormalities of the giant forms of megakaryocytes are especially evident and comprise irregular cellular and nuclear perimeters (as calculated by a modified shape factor) in the two latter entities (CMGM-MF/OMS). This remarkable feature is associated with a disorganization of nuclear development and/or a disproportionate nuclear-cytoplasmic ratio which has never been observed in CGL previously. In combination with this striking cellular anomaly, which is compatible with an extreme amoeboid shape of giant forms in CMGM and MF, intussuceptions and a-nuclear cytoplasmic fragments are frequently encountered. The final stage of megakaryopoiesis, i.e. naked nuclei, are increased in number in all CMPD, probably because of enhanced proliferation and platelet shedding. Naked nuclei are often small in CGL (as remnants of the frequent micromegakaryocytes) and large in P. vera and CMGM/MF (depending on the high incidence of giant megakaryocytes in these latter disorders).

Bone Marrow↗
PubMed1991

Planimetric analysis of megakaryocytes in the four main groups of chronic myeloproliferative disorders.

Planimetry of megakaryocytes (MK) was performed in bone marrow biopsies (BMBs) from patients with chronic myeloproliferative disorders (CMPD) to substantiate cytomorphologic differences in this cell lineage between the four main groups of CMPD. The biopsy specimens were classified histologically prior to morphometry, according to the Hannover Classification of CMPD. Five histological groups were investigated, evaluating between 21 and 30 biopsies in each group. The five groups were as follows: (1) Chronic myelocytic leukemia (CML) of common type (CML.CT), (2) CML with megakaryocytic increase (CML.MI), (3) polycythemia vera (P. vera), (4) primary thrombocythemia (PTH), and (5) chronic megakaryocytic-granulocytic myelosis (CMGM). The results of five variables, i.e. the cellular and nuclear size, the cellular and nuclear form factor, and nuclear segmentation, were determined in at least 50 MK per BMB. The results reveal significant differences in MK nuclear and cellular size, as well as in nuclear segmentation between CML and the three other groups in that the nuclear and cellular size of the MK in CML are smaller than in P. vera, PTH, and CMGM. Moreover, the degree of nuclear segmentation or lobulation differs significantly between the three disorders characterized by large MK. Discriminant analysis permits 78-100% reliability of reclassification by morphometry compared with the histologic classification. A reduced reliability of the morphometric classification to around 80% was found between P. vera and PTH, as well as between P. vera and CMGM. In the design of this study, morphometry of MK lends added weight to the subjective classification of these disorders.

Biopsy↗
PubMed1993

Evidence from molecular genetic and cytogenetic analyses that bone marrow histopathology is reliable in the diagnosis of chronic myeloproliferative disorders.

The reliability of histopathological diagnosis in bone marrow specimens from patients with chronic myeloproliferative disorders (CMPD) was evaluated by correlating the histological findings with molecular genetic and cytogenetic analyses of the Ph1-translocation. A rearrangement of m-bcr was detected only in patients (28/30) diagnosed histologically as chronic myeloid leukemia (CML). This finding was supported by the presence of a Ph1-chromosome in 24/26 patients with CML examined. All the patients with other types of CMPD, including polycythemia vera (PV), primary thrombocythemia (PTH) and chronic megakaryocytic-granulocytic myelosis (CMGM), as well as those with unclassifiable CMPD (CMPD.UC) were Ph1-negative (n = 38). The histopathological discrimination of CML from Ph1-negative varieties of CMPD was also reliable for patients with myelofibrosis complicating CML, CMGM and CMPD.UC. The results demonstrate that bone marrow histopathology allows a reliable diagnosis of CML. This is in contrast with hematological data such as high platelet counts which show considerable overlapping in the various forms of CMPD.

Adult↗
PubMed2000

[Masked autoimmune polyendocrine syndrome caused by sequelae of diabetes mellitus].

BACKGROUND: In most cases Type I diabetes is immunologically mediated. Complications after long duration of the disease are commonly observed. Further autoimmune mediated diseases are rare, but more often diagnosed in diabetics than in the general population. The combination of 2 autoimmune endocrinopathies is subsumed under the term autoimmune polyendocrine syndrome (APS). Depending on the endocrine gland involved disorders are classified as APS Type I, II or III. CASE REPORT: We report on a 64-year-old diabetic patient presenting with repeated nightly hypoglycemia. Diabetes was first diagnosed 12 years before. Clinical examination revealed a café-au-lait like color of the skin and severe peripheral polyneuropathy. Surprisingly, laboratory testing revealed a hemoglobin concentration of 6.8 g/dl. Further examinations led to the diagnosis of pernicious anemia and funicular myelosis. Screening for potentially associated autoimmune diseases showed also features of autoimmune thyroid disease. CONCLUSION: Despite of late manifestation of disease Type I diabetes should be considered if the clinical features correspond to an autoimmune induced disorder. Associated autoimmunopathies have always to be considered. Early diagnosis of commonly with diabetes associated autoimmunopathies can prevent as severe manifestations of disease as reported in this case.

Diabetes Mellitus, Type 1↗
PubMed1995

[Morphometry of megakaryocytes for supporting the histologic diagnosis of chronic myeloproliferative diseases].

Morphometric analysis of sections of biopsy specimens from patients with chronic myeloproliferative disorders (CMPD) can complement the individual histological diagnosis and help to distinguish the four groups of CMPD. A total of 130 diagnostic biopsies from 29 cases of chronic myelocytic leukemia (CML.CT), 26 cases of (CML.MI), 28 of essential thrombocythemia (PTH), 26 cases of chronic megakaryocytic granulocytic myelosis (CMGM), and 21 of polycythemia vera (P. vera), and 30 from healthy control persons were evaluated morphometrically in sections of undecalcified plastic-embedded core biopsies. Clear distinctions were revealed in size of megakaryocytes, nuclear lobulation, clustering, and the nuclear size and shape of megakaryocytes. Nuclear size and cellular size were significantly less in CML (range of means of cellular size: 220-360 microns2) than in the other three Ph1-negative groups (range of means: 480-750 microns2). Nuclear lobulation was more distinct in PTH than in P. vera, and especially in CMGM. Clustering of megakaryocytes was more than twice as frequent in CMGM (8.0-10.5%) as in any of the other three groups (0.1-7.0%). Naked nuclei were more numerous in all groups of CMPD. The main topic of the study is the different size of megakaryocytes in the four main groups of CMPE, allowing a distinction between small-megakaryocytic Ph1-positive CML and large-megakaryocytic Ph1-negative forms of CMPD.

Biopsy↗
PubMed1995

[Histopathology of Ph1-negative chronic myeloproliferative diseases].

The Ph1-negative groups of chronic myeloproliferative diseases (CMPD) are described, and histopathological criteria that distinguish them from each other are given. These are based upon observations in primary biopsies from 2,331 patients with CMPDs among a total of 34,160 patients referred between 1 January 1989 and 30 June 1994 to the Bone Marrow Registry. These cases of CMPD break down into the main groups as follows: CML 23.2%, megakaryocytic myelosis consistent with agnogenic myeloid metaplasia 22.3%, essential thrombocythemia 22.1%, and polycythemia vera 20.4%; 12.0% of cases were unclassifiable. Histological progress in each group is characterized by (1) increasing number and pleomorphy of megakaryocytes, (2) increasing fibrosis, and (3) excess of blasts. These three features can be observed in diagnostic biopsies before any therapy. Therefore, it is recommended that such alterations be reported semiquantitatively. A staging system with four stages from 0 to 3 for each of the three features is introduced. Its application allows staging for the individual patient on the basis of diagnostic biopsies.

Bone Marrow↗
PubMed1978

A new observation in the clinical spectrums of erythroleukemia. A report of 46 cases.

Erythroleukemia is a disease manifested by an abnormal proliferation of erythroid and myeloid precursors, generally consisting of a primary erythroid phase (chronic erythemic myelosis), a transition phase involving erythroid and myeloid precursors (erythroleukemia) and, finally, the purely myeloblastic (acute myeloblastic leukemia) phase. The experience at Memorial Sloan-Kettering Cancer Center is reported. Presenting signs and symptoms are consistent with prior reports. The chemotherapy results in the past have been poor; because of the poor results, chemotherapy is started only if one of the following criteria are present: (1) frequent transfusion requirements; (2) rapidly increasing peripheral white blood cell count or percentage of leukemic blast forms; (3) frequent recurrent infectious and/or hemorrhagic complications. A hitherto unrecognized association of erythroleukemia and symptomatic rheumatic disease and numerous immunologic abberations are reported. The symptoms related to this rheumatic disorder do not seem to be relieved by therapy directed at the leukemic process, but rather by the use of simple anti-inflammatory agents.

Adolescent↗
PubMed1981

Three or four copies of a dicentric 17q isochromosome in an acute myeloproliferative disorder.

The majority of metaphases in the bone marrow of a male patient aged 72 with a rapidly evolving aleukemic erythremic myelosis had 48 chromosomes with three copies, or 49 chromosomes with four copies, of an i(17q), which was seen to be dicentric in C-banded and Giemsa-11-banded preparations. There was also loss of a chromosome No. 5 and the addition of a chromosome resembling a No. 22. The presence of multiple copies of the isochromosome is postulated to be related to the acuteness of the condition.

Acute Disease↗
PubMed1998

Myeloproliferative disease in a calf.

A myeloproliferative disease was found in a 128-day-old Holstein female calf. The tumour consisted chiefly of primitive cells, and more mature cells, many of which were positive for haemoglobin, were admixed with them. Binucleated cells at various stages of maturation were occasionally seen, and siderosomes were confirmed in both primitive cells and more mature cells by electron microscopy. The primitive cells resembled proerythroblasts, and this tumour, thought to be an acute type neoplasm of the erythroid system, was distinguishable from chronic erythremic myelosis and polycythemia vera.

Animals↗
PubMed1993

Megakaryocyte markers in myeloproliferative disorders.

Identification of megakaryocyte precursors with immunohistochemical methods in bone marrow trephine biopsy specimens (embedded in a plastic resin, Immuno-Bed) was performed from patients with blastic phase of chronic granulocytic leukaemia (five cases), from chronic megakaryocytic-granulocytic myelosis (four cases) and from acute megakaryoblastic leukaemia (11 cases). In megakaryoblasts of bone marrow biopsies immunohistochemical reactions using the ABC method and monoclonal antibodies against von Willebrand antigen and GpIIb/IIIa (CD41) were visible in various percentages depending on the maturation's degree of megakaryocyte precursors. The number of circulating blast cells determined by flow cytophotometry was nearly similar to those of observed in biopsies. The greatest bone marrow reticulin content could be detected in acute megakaryoblastic leukaemia cases. Despite the different clinicopathological entities, the presence of the same phenotype (megakaryoblasts) was associated with a short survival in these haematological malignancies (in CGL MKB phase 4.0, in CMGM MKB phase 4.2, and in AML M7 5.8 months, respectively).

Adult↗
PubMed1990

Quantitative cytomorphology of megakaryocytes in chronic myeloproliferative disorders--analysis of planimetric and numeric characteristics by means of a knowledge based system.

Numeric and planimetric parameters of megakaryocytes have been analyzed in 162 bone marrow biopsies of patients with chronic myeloproliferative disorders--CMPD--and controls by means of an inductive knowledge-based system in combination with a multivariate data analysis. To achieve a reliable differential diagnosis between the different entities of CMPD and controls, decision trees and the rank order of the best discriminating parameters have been calculated. The cases measured were defined by 3 histopathologists who were involved in the elaboration of the Hannover Classification of CMPD. The results demonstrate striking numeric and morphologic characteristics of the megakaryopoiesis in each separate primary category of CMPD, that is (1) chronic myeloid leukemia of the common type and (2) with megakaryocytic increase, (3) polycythemia vera, (4) primary or idiopathic thrombocythemia, and (5) chronic megakaryocytic-granulocytic myelosis. Thus, the morphometric measurements did confirm the validity of the Hannover Classification of CMPDs. In order to evaluate the information contained in large quantitative and semiquantitative data bases and diagnostic decisions, knowledge-based expert systems seem to represent a valuable addition to conventional statistics.

Cell Count↗
PubMed1993

Myelofibrosis in chronic myeloproliferative disorders. Incidence among subtypes according to the Hannover Classification.

The distribution and the development of fibrosis were evaluated from bone marrow biopsies of patients with chronic myeloproliferative disorders (CMPD), regarding two groups of patients: (1) 564 with follow-up biopsies over a period of up to twelve years observation time, and (2) 1.787 diagnostic bone marrow biopsies from CMPD patients. Fibrosis was divided into three grades of fiber increase: early myelosclerosis, myelofibrosis, and advanced myelofibrosis. The first group of sequential BMB showed a significant progress to myelofibrosis in so-called "Chronic Megakaryocytic-Granulocytic Myelosis"--CMGM-, which corresponds to Agnogenic Myeloid Metaplasia-AMM-in 72.4% (21/29 patients), as well as in CML with megakaryocytic increase-CML.MI-in 39.2% (20/51). In the second group of diagnostic biopsies, only 30% of CMGM cases showed no fibrosis. In P. vera, 16.2% (18/111) developed myelofibrosis up to twelve years later. This figure was 4.3% (2/46) in Primary Thrombocythemia. Increase of megakaryocytes in CML indicates a high risk for developing fibrosis, combined with reduced life expectancy.

Biopsy↗
PubMed1982

Natural history of smouldering leukaemia.

The natural history of 45 cases of smouldering leukaemia has been studied. Males and females were equally represented, with a median age of 60.5. The median survival of the whole group was only 20 months, but rare cases lived 10 years or longer. 38% developed acute leukaemia; the remainder usually died of the results of marrow failure. Although it was possible to divide these marrow dysplasias morphologically into 3 major subgroups (refractory anaemia with excess of myeloblasts, chronic myelomonocytic leukaemia and chronic erythraemic myelosis), several displayed transitional features. Many showed refractory macrocytosis at diagnosis. The survival of the 3 groups was similar, though patients with high monocyte counts tended to present with less anaemia and fared rather better than the others. Statistical analysis suggests that increasing age, severe anaemia, thrombocytopenia and hepatomegaly are associated with a poor prognosis. Chemotherapy, when attempted, was usually unsuccessful.

Adult↗
PubMed1976

[Differential diagnosis of atypical chronic myeloid leukaemia].

Observations in six adult patients with leukaemic differential white counts, predominantly mature-celled, and with hepatosplenomegaly show that the mature-celled but fulminant (para-)neutrophil leukaemia must be differentiated from Ph1-positive chronic myeloid leukaemia. This (para-)neutrophil leukaemia is probably identical with the previously described atypical chronic myelosis of the adult, chronic myeloid leukaemia of childhood and the Pelger-like chronic myeloid leukaemia. Cardinal signs are a mature-celled differential count, short life expectancy (1 year), initial platelet deficiency, increased activity of granulocyte alkaline phosphatase, absence of Ph1-chromosome, and poor therapeutic response to busulfan. This curious and yet apparently not uncommon disease has been observed in the adult age group predominantly in men. The frequently high HbF level observed in juvenile chronic myeloid leukaemia could not be demonstrated in adults. Some of these neutrophil leukaemias are characterized by medullary fibrosis and terminal increase of immature blast cells (blast crises?) of which the diagnostic reliability is still disputed.

Aged↗