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Query: UMLS:C0032463 (polycythemia vera)
 3,374 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polycythemia vera, a rare and poorly documented disease in cats, was diagnosed in a 4-year-old domestic shorthair cat admitted because of seizures. The diagnosis was made on the basis of high PCV, normal serum erythropoietin concentration (as determined by bioassay, using rabbit bone marrow cells), and elimination of secondary polycythemia as a diagnosis. Cardiac hypertrophy, which might have been secondary to blood hyperviscosity, also was diagnosed. The cat has been treated by periodic phlebotomy and has been without clinical signs of disease for more than 20 months.
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PMID:Polycythemia vera in a cat with cardiac hypertrophy. 297 Apr 51

The haematological, biochemical and clinical features of six patients with polycythaemia after renal transplantation were studied. The patients had an absolute increase in red cell mass, but normal plasma and whole blood volumes. Primary proliferative polycythaemia was excluded. Polycythaemia developed within one year of transplantation and persisted for 3-7 years. Chronic rejection, renal artery stenosis, severe hypertension and corticosteroid therapy were probably not the cause of the polycythaemia. There were no occlusive vascular lesions during the observation period and venesections were generally not required. The polycythaemia is probably the result of the cumulative production of erythropoietin by the donor and recipient kidneys.
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PMID:Polycythaemia after renal transplantation. 331 62

Marrow cells from seven untreated patients with polycythemia vera (PV) were used to initiate standard single inoculum long-term marrow cultures. The numbers, erythropoietin independence, and cycling behavior of all detectable classes of erythroid, granulopoietic, and multilineage progenitors were then evaluated and the results obtained compared with preculture values. Time course studies showed that the long-term marrow culture system supports the continuous proliferation of primitive neoplastic progenitor cells from PV patients for many weeks. However, these progenitors fail to respond to signals from the adherent layer that return their counterparts in normal long-term marrow cultures to a quiescent state 5-7 d after each medium change. This abnormal cycling behavior of PV cells in the long-term culture system appears to mimic that operative in vivo, where primitive hemopoietic progenitors are also in a continuous state of turnover, in contrast to similar primitive progenitor compartments in normal individuals, which are quiescent. The long-term marrow culture system thus offers new possibilities for the further analysis of abnormal cellular and molecular mechanisms underlying clonal expansion at the stem cell level in PV.
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PMID:Unregulated proliferation of primitive neoplastic progenitor cells in long-term polycythemia vera marrow cultures. 333 45

We investigated the influence of T-cell depletion on BFU-E and CFU-GM colony growth in vitro from normal individuals and patients with chronic granulocytic leukemia (CGL), idiopathic myelofibrosis (MF), and polycythemia vera (PV). Preincubation of mononuclear cells with the complement-fixing monoclonal antibody OKT11A, which is cytotoxic to T-lymphocytes, significantly reduced the number of erythropoietin (epo)-dependent BFU-E colonies cultured from normal bone marrow and normal peripheral blood, as well as from the blood of patients with CGL, PV, and MF. In contrast, the numbers of epo-independent ("endogenous") BFU-E colonies cultured from the blood of PV and MF patients were the same before and after T-cell depletion. The blood and marrow of CGL patients and normal individuals produced no epo-independent BFU-E proliferation. The growth of day-7 and day-14 CFU-GM was not significantly influenced by T-cell depletion in the majority of experiments. We conclude that T cells promote the growth of epo-dependent BFU-E colonies in vitro, but they do not influence the growth of "endogenous" BFU-E colonies from patients with myeloproliferative disorders.
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PMID:Endogenous erythroid colony formation in myeloproliferative diseases does not depend on T cells. 348 53

An analysis of the results of determination of erythropoietin in the blood plasma of patients with polycythemia vera and data on the kinetics of erythroid cell proliferation led to a conclusion that erythrocytapheresis more than bloodletting stimulated the production of erythropoietin and the cell proliferative potential. Activation of regenerative processes probably determined by deinhibition of the normal clone of bone marrow erythroid cells, can account for the mechanism of a therapeutic effect of erythrocytapheresis in patients with polycythemia vera.
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PMID:[Erythron in patients with polycythemia vera during treatment by erythrocytapheresis and bloodletting]. 362 98

The definite differential diagnosis between spurious polycythemia (SP) and pure erythrocytosis (PE) was tested. Serum erythropoietin (EPO) levels in 6 patients with PE were 12.8 +/- 3.7 mU/ml and were significantly lower than those of both 19 normal controls (28.5 +/- 15.0 mU/ml) and 9 patients with SP (21.3 +/- 10.2 mU/ml). Three of 11 patients with SP and 1 of 3 patients with PE had significantly higher marrow erythroid progenitor cells (CFU-Es) than those of the normal controls. Spontaneous CFU-E growth (CFU-E growth in the absence of added EPO) was found in 4 of 11 patients with SP, 1 of 3 patients with PE, and all patients with polycythemia vera. However, the number of spontaneous CFU-E was low in SP and PE. The measurements of serum EPO levels and CFU-E growth did not provide differentiation between PE and SP. Even if some patients, whose total red cell volumes are either higher than 12.5% above the mean predicted values or their CFU-E growth is great, are diagnosed as SP, consideration should be made that they might, in fact, have PE.
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PMID:Differential polycythemia: a comparative study between spurious polycythemia and pure erythrocytosis. 368 23

We assessed the diagnostic value of determinations of serum levels of immunoreactive erythropoietin in 90 patients referred for the investigation of a raised packed red-cell volume (hematocrit) and possible erythrocytosis (a red-cell volume greater than that predicted by weight, body-surface area, or both). The mean values for erythropoietin were 16 mIU per milliliter (range, 8 to 22) in patients with polycythemia rubra vera (n = 24), 30 mIU per milliliter (range, 14 to 123) in patients with secondary erythrocytosis (n = 12), 27 mIU per milliliter (range, 13 to greater than 400) in patients with erythrocytosis of unknown origin (n = 19), and 25 mIU per milliliter (range, 18 to 35) in normal controls (n = 25). The values in the patients with polycythemia rubra vera were lower than those in the other three groups (P less than 0.01, P less than 0.05, and P less than 0.0001, respectively). In subjects with an increased packed red-cell volume but without erythrocytosis (n = 35), the levels of serum erythropoietin were the same as those in normal controls. Among patients with erythrocytosis with an unknown cause, abnormally high serum erythropoietin levels were found in 3 of 19 subjects, and in 1 of these 3 the abnormality was intermittent. Thus, measurement of serum erythropoietin in a single sample may be misleading and may not have high discriminatory value in distinguishing between polycythemia rubra vera and secondary erythrocytosis. This assay is useful in identifying patients with secondary erythrocytosis who have inappropriate erythropoietin secretion.
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PMID:Determination of serum immunoreactive erythropoietin in the investigation of erythrocytosis. 372 21

The diagnostic value in polycythemia of the presence of endogenous erythroid colonies derived from bone marrow cells (EECs) was assessed in a prospective study on 108 patients referred for polycythemia (Hb greater than g/dL in men, greater than 16 g/dL in women) with normal plasma volume by comparison with the standard criteria, the bone marrow grade, and the serum erythropoietin (Epo) level. Total red cell volume (TRCV) was high (greater than 36 mL/kg in men, 32 mL/kg in women) in 87 cases (group A) and slightly increased in 21 cases (group B). Standard criteria were applicable in 63 of 108 cases (57%); 46 were PV and 17 were secondary polycythemia (SP). Standard criteria were nonapplicable in 45 cases. EECs were present in 65 cases (60%) with a ratio of EEC/Epo-stimulated colonies of 39.5% +/- 18% (extremes 10% to 80%). EECs were noted in 43 of 46 polycythemia vera (PV) and 0 of 17 SP. Among the 45 unclassified cases, EECs were noted in 22: 18 of 29 cases from group A (10 with 2 major and 1 minor criteria; 8 with 2 major criteria) and 4 of 16 cases from group B (with variable standard criteria, 2 belonging to a PV family). In group A, there was a positive significant correlation between EECs and the presence of two major and 1 minor criteria (P less than .0001). In group B, there was a positive significant correlation between EECs and the presence of at least 1 major criterion and 2 minor criteria or a family background (P less than .0001). The unclassified polycythemias with EECs in the bone marrow are characterized by a bone marrow grade and a mean serum Epo level not different from that of patients with PV and an active course of the disease. The unclassified polycythemias without EECs in the bone marrow are a heterogeneous group corresponding in some cases to SPs of unknown origin (slightly increased bone marrow grade and/or high serum Epo level), and in others cases to spurious polycythemias (normal bone marrow grade and/or normal Epo level). In conclusion, EECs were of great value in differentiating PV from SP (P less than .001), and in allowing the diagnosis of PV in the absence of all the standard criteria even when TRCV was slightly increased. In our study, EEC improved the classification of polycythemia by 22%. The recommended diagnostic steps for the evaluation of polycythemia must be reconsidered.
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PMID:A prospective study of the value of bone marrow erythroid progenitor cultures in polycythemia. 376 35

Burst-promoting activity (BPA) in the sera of patients with various types of anemia and polycythemia was compared with that of normal subjects by an in vitro method using mouse bone marrow cells. The control culture contained normal human AB serum instead of sample materials. Results were expressed as a percentage of burst numbers in control cultures. Serum erythropoietin (Epo) levels were determined by a radioimmunoassay. Serum BPA in patients with aplastic anemia (155.4 +/- 56.7%, mean +/- SD) was significantly higher than that in normal subjects (112.1 +/- 29.1%, Wilcoxon's rank sum test, P less than 0.05). However, serum BPA in patients with uremic anemia (122.2 +/- 26.5%), polycythemia vera (101.9 +/- 19.5%) and stress polycythemia (115.5 +/- 25.6%) was not significantly different from normal subjects. There was a correlation between serum BPA and Epo titers in patients with aplastic anemia and paroxysmal nocturnal hemoglobinuria (r = 0.81, t test, P less than 0.001).
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PMID:Burst-promoting activity in anemia and polycythemia. 395 12

The mechanism of polycythemia associated with the Budd-Chiari syndrome is unknown. Erythropoiesis in 10 patients with Budd-Chiari syndrome was studied in an attempt to distinguish prior unrecognized polycythemia vera from secondary polycythemia. Serum erythropoietin was assayed using a mouse fetal liver erythroblast assay. High concentrations of serum erythropoietin were observed in 6 of 7 patients with acute primary Budd-Chiari syndrome. Levels were normal in four patients who were investigated during the chronic phase and were increased in one with persisting polycythemia. In one patient, erythropoietin concentration in the hepatic vein was twice the level measured in peripheral, caval and renal venous blood. Bone marrow erythroid progenitors developed in vitro in the absence of exogenous erythropoietin in all polycythemia vera cases studied in acute and chronic phases, whether polycythemia persisted or not. These findings indicate that hepatic erythropoietin production occurs in the acute phase of Budd-Chiari syndrome and suggest that, in some cases of Budd Chiari syndrome, polycythemia which resolves after the acute phase may be secondary to liver disease.
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PMID:Polycythemia and the Budd-Chiari syndrome: study of serum erythropoietin and bone marrow erythroid progenitors. 402 96


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