[Paraproteinemia and its possible prognostic significance in chronic myelosis].
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To assess the role of the ultrasonic imaging evaluation of articular lesions suspected to be the initial presentation of heterotopic ossifications (HO) 59 consecutive spinal cord injured patients were studied. 32 out of 59 patients showed clinical signs of local inflammation in one of the articular sites of the upper or lower limbs, sonographic scans proved to be diagnostic of HO in 7 out of those 32 patients before a their radiographic findings. Serial sonographic examinations were performed utilising a 7.5 MegaHertz transducer probe for 2 months. The imaging abnormalities were correlated with biochemical levels of serum alkaline phosphatase, modifications of radiographic features and bone 99mTC scintigraphy. Scintigraphy revealed to have a high sensitivity but a low specificity for the diagnosis of HO. Also the serum levels of alkaline phosphatase was not a sensitive indicator of early HO in our group of patients. Moreover serial sonographic scans confidently excluded the HO in the 25 patients with no initial signs of the disease without any false negative results. Thus, early sonographic assessment of patients with spinal cord injury in which local signs of inflammation suggest initial HO formation revealed to be superior to the other utilized technique for the diagnosis of HO and may be considered a valuable alternative in particular to evaluate the evolutive pattern of this disease.
A myeloproliferative disorder in a cat was characterized by abnormal proliferation of megakaryocytes in the bone marrow and by severe, nonregenerative anemia. The number of circulating thrombocytes was increased markedly, with many giant and morphologically bizarre forms. Terminally, the circulating blood contained large numbers of undifferentiated blast cells. The spleen and liver were infiltrated by megakaryocytes and mononuclear mesenchymal cells of uncertain identity.
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76 cases of CML were divided according to clinical parameters (duration of illness prior to diagnosis, size of spleen, leucocyte and platelet counts, ALP index, bone marrow cytology and others) into groups showing a classical or an atypical course of the disease. All patients were submitted to bone marrow biopsy, using the method of Jamshidi and Swaim. The histological subtypes of CML, i.e. chronic granulocytic leukaemia and chronic megakaryocytic granulocytic myelosis were correlated with the two clinical types of disease. The classical form of CML was histologically inhomogeneous and was subdivided into 40% cases of chronic granulocytic leukaemia and 60% cases of chronic megakaryocytic granulocytic myelosis. At the time of bone marrow biopsy 20% of patients with classical leukaemia were already found to have myelofibrosis. The atypical myeloses consisted of chronic megakaryocytic granulocytic myelosis only and myelofibrosis was present initially in 50% of patients. In view of these findings agnogenic myeloid metaplasia is considered to be merely a variant of chronic myeloid leukaemia and the term "atypical myelosis" is preferred.
The wide clinical range of CMPD can be understood as leukaemia of pluripotent stem cells according to the pathogenic concepts reviewed above. Blastic metamorphoses of CMPD are regressions to a more primitive level of cellular differentiation. The predominant proliferative cell line characterizes the classical entities of PV, PT and CML, and their different prognoses. Pure erythrocytic and megakaryocytic proliferations are more compatible with sustained physiologic bone marrow functions than granulocytic proliferations. The combinations of granulocytic and megakaryocytic growth are especially prone to develop MF/OMS, in which participation of immune reactions, of granulocytic and of platelet factors is probable. An etiologic role for ineffective thrombocytopoiesis is supported by experimental as well as by histologic evidence. Myelofibrosis and osteomyelosclerosis may have similar causes, but develop independently. The prevalence of the female sex among thrombocythaemic patients was proven statistically also for the increase of giant type megakaryocytes in the form of clusters in the bone marrow, and for longer median survival of females in CMPD, especially when there is megakaryocytosis in the bone marrow. It is assumed that females may be better protected against the detrimentous effects of abnormal platelet production. An arbitrary classification according to haematologic and histologic criteria was applied to PV, PT and CML, and groups with typical and atypical haematologic and histologic signs were distinguished. The latter cannot be separated from each other by their various haematologic manifestations, but by histology and their different propensity to progress into more immature and/or fibrotic stages. Three major groups are characterized by histology: mixed granulocytic-megakaryocytic myelosis with giant megakaryocytic clusters, a similar variant with diffuse distribution of giant megakaryocytes, and immature and/or pleomorphic megakaryocytic myelosis. Transitions from each of these groups have been observed as well as transitions from each of the typical CMPD-entities into these less typical forms. CML, frequently accompanied by dwarf-megakaryocytes, often develops into pleomorphic megakaryocytic or blastic myelosis. Blastic dedifferentiation and myelofibrosis manifest themselves as closely related end stages, to which principally all groups proceed after a longer or shorter period of time, modified by the proliferating cell lines in each group. Clinical, experimental and histologic evidence of this natural history has been reviewed, with special emphasis on the re-evaluation of technically optimal bone marrow biopsies of untreated patients.(ABSTRACT TRUNCATED AT 400 WORDS)
Sixty-one patients with essential thrombocythemia (ET) were followed from 1974 through 1987 at the Medizinische Poliklinik. Fifty-one patients (84%) presented with thromboembolic complications, and eight patients (13%) with hemorrhages. In seven patients (12%), a thrombocytosis was detected accidentally. Disturbances of the microcirculation (67%), mainly of the fingers and toes (53%), were the most frequent thromboembolic symptoms. The mean age of all patients was 58 years (male patients, 61 years; female patients, 56 years). The average platelet count at diagnosis was 897,000/microliter. The average maximal platelet count was 1.231 X 10(6)/microliter (range, 500,000/microliter to 4 X 10(6)/microliter). Seventy-two percent had a moderate leukocytosis (average, 12,400/microliter), 34% a splenomegaly, 29% a hepatomegaly. Signs of hypermetabolism were infrequent, lactate dehydrogenase (LDH) and uric acid elevations, if present, were moderate. Bleeding time and viscosity were normal in most patients. Spontaneous platelet aggregation was increased in 81% of patients (n = 40). Platelet aggregation studies with the aggregation inducing substances adenosine diphosphonate (ADP), platelet activating factor (PAF), thrombin, collagen, and adrenalin showed hypoaggregation in most patients. Adrenalin-induced aggregation distinguished best between ET-patients and reactive thrombocytosis showing hypoaggregation in all ET-patients tested (n = 16) and in none of 22 controls. Bone marrow studies were performed in 57 patients. The histologic studies (done in 49 patients) were consistent with a chronic myeloproliferative disorder in all cases. In 41 cases (84%) the picture of a megakaryocytic myelosis was found, in 12 of these a granulocyte-rich form of megakaryocytic myelosis. Cytologic studies only (eight patients) did not differentiate ET well from reactive thrombocytosis. Platelet aggregation studies and bone marrow histology may be of help in the diagnosis of difficult cases of thrombocytosis. The Philadelphia status was negative in all cases studied (14 patients). Fourteen patients died. The causes of death were thromboembolic complications in probably 11 and acute leukemia in two patients. The probability of 10-year survival is 64% after a mean follow-up time of approximately 5 years. It appears that considering the average age of ET patients at diagnosis, life expectancy is close to normal.