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PubMed1989

[Thromboembolic risk factors in kidney transplantation: hemorheologic examination in secondary polycythemia].

Cardiovascular risk factors will increase the lethality of kidney patients being under dialysis treatment and after transplantation. This risk is additionally increased after transplantation by secondary polycythemia. The paper investigates the rheological properties of the blood of 20 patients affected by secondary polycythemia after kidney transplantation, 10 patients without polycythemia after kidney transplantation and 19 test persons. Plasma viscosity, erythrocyte aggregation and whole blood viscosity were determined. As a result, an increase of erythrocyte aggregation without their deformability being changed could be found in patients affected by polycythemia after kidney transplantation. The reduced thrombocyte aggregation identified in these patients can be explained by the influence of therapy.

Adult↗
PubMed1989

[The chemical element content of the erythrocytes in polycythemia vera].

A study is presented of the content of physiologically active erythrocytic microelements (iron, copper, manganese, cobalt and zinc) in erythrocytes of the peripheral venous blood in patients with polycythemia vera. It was found that in polycythemia vera the manganese and zinc in erythrocytes showed disturbances. These changes indicate the neoplastic character of proliferation of bone marrow in polycythemia vera. The changes are of compensatory-adaptative character and reflect the state of homeostasis in polycythemia vera.

Adult↗
PubMed1987

Polycythemia in pediatric renal transplantation.

Post-transplant polycythemia is not uncommon in adult patients and is usually transient, responding to phlebotomy. Five pediatric patients developed erythrocytosis post-transplantation. Three patients had end-stage renal disease due to cystinosis, one had reflux glomerulopathy and one had focal glomerular sclerosis. The probable causes of the polycythemia were graft arterial stenosis in three patients. In one, polycythemia occurred with nephrosis. Polycythemia with hypertension may indicate the presence of arterial stenosis in children post-transplantation.

Adolescent↗
PubMed1984

Neonatal polycythemia: I. Early diagnosis and incidence relating to time of sampling.

The dynamic changes occurring in hematocrit and blood viscosity within the first 18 hours of life were studied in 50 full-term infants who were vaginally delivered and had weight appropriate for gestational age. In all cases, the cord was clamped within 30 seconds and cord blood was collected from the vein and artery. Subsequently, samples were taken from a peripheral vein at ages 15 minutes, and 2, 4, 6, and between 12 to 18 hours. Both the Hct and blood viscosity reach their peak at age 2 hours. The incidence of neonatal polycythemia varied greatly with age. Thus at the age of 2 hours, ten infants (20%) were polycythemic, whereas by age 6 hours only six (12%) of these infants were still polycythemic and by age 12 to 18 hours only one infant (2%) was polycythemic. A linear correlation was found between cord Hct levels and peripheral venous Hct levels by age 2 hours. None of the infants with cord blood Hct levels less than or equal to 56% had developed polycythemia, whereas ten of the 12 infants with cord Hct levels greater than 56% developed polycythemia. In this particular group of infants, cord blood Hct levels may be used for the screening of neonatal polycythemia.

Blood Viscosity↗
PubMed1981

Phlebotomy with iron therapy to correct the microcytic polycythemia of chronic hypoxia.

Patients with chronic hypoxia develop a physiologically appropriate "secondary" polycythemia that improves oxygen carrying capacity. Supplemental iron is often required to maintain this. In severe cases when hematocrit levels approach 70%, iron is withheld in order to avoid dangerously high hematocrit levels and the risks of vascular sludging due to "hyperviscosity." Some patients even require reduction of viscosity by exchange of their polycythemic blood for plasma when symptoms develop. Iron deficiency with microcytic polycythemia can then develop. Management of such patients is unclear. Continued blood withdrawal will worsen the iron deficiency; iron supplementation will increase the hematocrit level and the risks of hyperviscosity. The combination of frequent phlebotomy with oral iron therapy should improve iron stores while safely maintaining a stable hematocrit level in patients with microcytic polycythemia. This combination should also have multiple beneficial effects on tissue oxygen delivery and utilization. This approach has been discussed and used for a patient with microcytic polycythemia due to Eisenmenger syndrome. While on therapy the patient's clinical symptoms decreased, and his serum iron level, hematologic indices, and treadmill tolerance tests all improved.

Administration, Oral↗
PubMed1994

Determination of serum erythropoietin. Its value in the differential diagnosis of polycythemias.

In vivo and in vitro bioassays, radio immunoassays (RIA), enzyme linked immunoassays (ELISA) and immunoradiometric assays (IRMA) have been applied to measure serum erythropoietin (Epo) levels. Results are expressed in international units (IU). In vivo bioassays are time consuming, expensive and not sensitive enough to measure the amount of Epo in normal sera. Nevertheless, this test remains the standard of comparison for the other new assays. Immunologic technics are specific, sensitive, reproducible, easy to perform, rapid and are now preferred for the measurement of Epo. Published values for non anemic human range from 6 to 32 IU/l. In the search of etiology of a polycythemia, the results of usual investigations to class the polycythemia either as primitive (P. vera) or secondary are often inconclusive. In these situations, measurement of serum Epo could be of value for accurate a differential diagnosis. However the results of the literature and our personal experience, show that the serum Epo level does not discriminate with an absolute fiability between Polycythemia Vera and secondary polycythemia because of a great overlap between the two groups.

Biological Assay↗
PubMed1994

Polycythemia in a llama.

The PCV of a llama increased from 50.8 to 74.0% during a 19-month period. The llama remained clinically normal unless stressed, when it would become dyspneic and tachypneic. Thoracic auscultation revealed sounds consistent with pneumonia, but were probably attributable to pulmonary congestion resulting from polycythemia. A diagnosis of secondary absolute polycythemia was made on the basis of high serum erythropoietin concentrations and no evidence of hypoxia. Necropsy revealed congestion of the lungs and liver. Cause of the polycythemia was not determined. Polycythemia should be considered as a differential diagnosis in a llama with exercise intolerance and harsh bronchovesicular sounds.

Animals↗
PubMedDate not supplied

Quantitative and functional studies of impaired natural killer (NK) cells in patients with myelofibrosis, essential thrombocythemia, and polycythemia vera. I. A potential role for platelet-derived growth factor in defective NK cytotoxicity.

In view of the possibility that immunological dysfunctions may be involved in initiating or contributing to the pathogenesis of myeloproliferative disease, we investigated quantitative and functional activity of natural killer (NK) cells in patients with polycythemia vera, essential thrombocythemia and myelofibrosis, and have demonstrated, especially in myelofibrosis, a measurable cytotoxic defect in the ability of their peripheral blood mononuclear cells to efficiently kill the standard NK target, K-562. Furthermore, highly purified, FACS-sorted CD16+ lymphoid cells from patients with myelofibrosis were consistently defective in their ability to lyse K-562 targets, and could not be augmented substantially with recombinant interleukin (IL)-2. Only patients with myelofibrosis had significantly lower percentages and absolute numbers of CD16+ cells as compared to patients with essential thrombocythemia and polycythemia vera. Further experiments demonstrated that patients with myelofibrosis, although having fewer CD16+ NK cells, had a significantly increased proportion of CD16+ cells with detectable platelet-derived growth factor (PDGF) on their surface. In contrast, surface PDGF was barely detectable on CD16+ cells from patients with polycythemia vera and essential thrombocythemia, as well as from normal controls. Having previously reported that physiologic quantities of PDGF significantly inhibit human NK cell cytotoxicity, and that patients with myelofibrosis and essential thrombocythemia have significantly elevated circulating levels of plasma PDGF, we now have demonstrated that pretreatment of normal NK cells with concentrated, PDGF-containing, platelet-poor plasma from patients with these diseases significantly inhibits NK cytotoxicity. This inhibitory effect was reversed by neutralization of plasma PDGF with anti-PDGF (coupled to Sepharose resin). Both the NK defects demonstrated in this study, and the abnormal plasma PDGF results reported earlier, are most striking in myelofibrosis and least abnormal in polycythemia vera, with an intermediate degree of abnormality in essential thrombocythemia. Our new findings suggest a causal correlation between abnormal platelet release, plasma accumulation of PDGF, and the observed NK immunodeficiency in these myeloproliferative patients.

Adult↗
PubMed1997

Retinopathy secondary to anemia from myeloid metaplasia in polycythemia vera.

BACKGROUND: Polycythemia vera is a chronic clonal disorder associated with excessive proliferation of erythrocytes, leukocytes, and thrombocytes, as well as an accompanying splenomegaly. Ocular manifestations of polycythemia vera include occipital cortex transient ischemic attacks, transient monocular blindness, vaso-occlusive disease, and retinal hemorrhages. CASE REPORT: A 56-year old man with longstanding polycythemia vera sought treatment for a chief symptom of blurred vision in the left eye and a red tinge to things first noticed on awakening that morning. He had preretinal and intraretinal hemorrhages and was subsequently found to be severely anemic as a result of postpolycythemic myeloid metaplasia after years of phlebotomy. Splenectomy controlled his anemia and thrombocytopenia, allowing transient improvement of the retinal hemorrhages. Acute leukemia subsequently developed and the patient died 7 weeks after initial examination. CONCLUSION: In this case, preretinal and intraretinal hemorrhages were found in a patient with longstanding polycythemia vera. The exact origin of these hemorrhages is uncertain. They are probably secondary to anemia, but the possibility that they are sites of extramedullary hematopoiesis must be considered. The appearance of retinal hemorrhages warrants careful investigation to rule out diabetes, hypertension, and anemia, as well as the various other blood dyscrasias.

Anemia↗
PubMed1998

[A case of dilated cardiomyopathy caused by myocardial microinfarcts in the course of polycythemia vera].

This article presents a case of 45-year-old man with polycythemia vera non diagnosed before. The first symptom of polycythemia vera was acute congestive heart failure which suggested diagnosis of myocarditis. Polycythemia vera was confirmed by raised hematocrit, significantly increased platelet count, normal oxygen saturation, score for leukocyte alkaline phosphatase (LAP)-130 and splemomegaly. Echocardiography revealed left ventricular histological. Coronary arteriography showed normal coronary arteries. Finding of histological examination of the endomyocardial biopsy were described as necrosis of myocytes and abnormal blood flow in very small coronary vessels. It was the main reason of dilated cardiomyopathy caused by microinfarcts in polycythemia vera. Hematological parameters were reduced to normal levels after hydroxyurea treatment. Digitalis and ACE-inhibitor therapy quickly improved cardiovascular status from III to II NYHA class.

Biopsy↗
PubMed2004

Efficacy and safety of low-dose aspirin in polycythemia vera.

BACKGROUND: The use of aspirin for the prevention of thrombotic complications in polycythemia vera is controversial. METHODS: We enrolled 518 patients with polycythemia vera, no clear indication for aspirin treatment, and no contraindication to such treatment in a double-blind, placebo-controlled, randomized trial to assess the safety and efficacy of prophylaxis with low-dose aspirin (100 mg daily). The two primary end points were the cumulative rate of nonfatal myocardial infarction, nonfatal stroke, or death from cardiovascular causes and the cumulative rate of nonfatal myocardial infarction, nonfatal stroke, pulmonary embolism, major venous thrombosis, or death from cardiovascular causes. The mean duration of follow-up was about three years. RESULTS: Treatment with aspirin, as compared with placebo, reduced the risk of the combined end point of nonfatal myocardial infarction, nonfatal stroke, or death from cardiovascular causes (relative risk, 0.41; 95 percent confidence interval, 0.15 to 1.15; P=0.09) and the risk of the combined end point of nonfatal myocardial infarction, nonfatal stroke, pulmonary embolism, major venous thrombosis, or death from cardiovascular causes (relative risk, 0.40; 95 percent confidence interval, 0.18 to 0.91; P=0.03). Overall mortality and cardiovascular mortality were not reduced significantly. The incidence of major bleeding episodes was not significantly increased in the aspirin group (relative risk, 1.62; 95 percent confidence interval, 0.27 to 9.71). CONCLUSIONS: Low-dose aspirin can safely prevent thrombotic complications in patients with polycythemia vera who have no contraindications to such treatment.

Aspirin↗
PubMed2003

Neutrophil PRV-1 expression across the chronic myeloproliferative disorders and in secondary or spurious polycythemia.

Recent studies have demonstrated neutrophil overexpression of the polycythemia rubra vera-1 (PRV-1) gene in polycythemia vera (PV) but not in secondary or spurious polycythemia (SP). To validate as well as expand upon this novel observation, we conducted a prospective study of 88 subjects: 30 with PV, 22 with SP, 14 with essential thrombocythemia (ET), 12 with myelofibrosis with myeloid metaplasia (MMM), and 10 controls. To minimize interstudy methodologic differences, we used a published real-time polymerase chain reaction (PCR)-based assay. The proportion of patients with increased neutrophil PRV-1 expression was 83% in PV, 21% in ET, 42% in MMM, 18% in SP, and 0% in controls. All 5 MMM patients with PRV-1 up-regulation had an antecedent history of PV. We conclude that neutrophil PRV-1 up-regulation is a characteristic feature of PV that may not be affected by fibrotic transformation. However, quantifying neutrophil PRV-1 mRNA, while complementary to other tests, is not in itself sufficient for the diagnosis of PV.

Case-Control Studies↗
PubMed1984

An evaluation of serum erythropoietin estimation by a hemagglutination inhibition assay in the differential diagnosis of polycythemia.

A commercially available hemagglutination inhibition assay kit for the measurement of erythropoietin (EPO) was evaluated for its usefulness in the differential diagnosis of the polycythemic states. Serum samples were obtained from patients with polycythemia rubra vera (active and controlled), secondary and relative polycythemia and from normal controls. Firstly, we found that the mean EPO level (+/- SD) of our normal controls (81 +/- 69 miu/ml) was higher than the manufacturer's quoted normal range (15-59 miu/ml) and that there was a significant spread of values (7-233 miu/ml). Secondly, within each patient subgroup studied, the spread of data points was so wide that interpretation of individual data points would be impossible. We conclude that this assay kit is of little value for serum EPO estimation and in the differential diagnosis of polycythemia.

Diagnosis, Differential↗
PubMed2005

Diagnosis of polycythemia vera based on bone marrow pathology.

The diagnostic criteria of the Polycythemia Vera Study Group (PVSG) do not include bone marrow (BM) examinations. The aim of this review is to elucidate whether distinctive patterns of histopathology exist which discriminate reactive (secondary polycythemia) from autonomous (polycythemia vera) erythrocytosis. When accompanied by an elevated platelet count, the initial stages of PV may clinically mimic essential thrombocythemia because they are not recognized by the conventional diagnostic criteria. Our data are derived from previous studies and evaluations of 362 patients with a borderline to marked increase in hemoglobin. PV revealed a trilineage myeloproliferation (panmyelosis) with a pleomorphous appearance (ie, differences in size) of loosely clustered megakaryocytes that failed to show gross cytological anomalies. Distinction from SP was accomplished by regarding megakaryopoiesis and the stromal changes (perivascular plasmacytosis, eosinophils, cell debris, and iron deposits). Discriminant analysis of standardized BM features, based on semiquantitative evaluation, yielded a sensitivity of 96% concerning the clear-cut separation of PV from SP.

Biopsy↗
PubMedDate not supplied

Plasma homocysteine levels in 10 patients with polycythemia.

Polycythemia and hyperhomocysteinemia are risk factors for thrombosis. Since red blood cells actively metabolize methionine to homocysteine, we investigated whether or not patients with polycythemia have increased plasma levels of homocysteine, which might contribute to their increased thrombotic risk. In ten patients with polycythemia, the plasma homocysteine levels were measured before phlebotomy, three days after the procedure and 1-2 months later. The baseline mean plasma homocysteine levels in patients (9.7 +/- 1.6 mumol/L [+/-SD]) did not differ significantly from that found in 30 sex- and age-matched healthy controls (12.2 +/- 6.9). Despite a fall in the patients' mean [+/-SD] hematocrit from 0.50 +/- 0.02 at baseline to 0.47 +/- 0.03 three days after phlebotomy (significant at 95%) and to 0.48 +/- 0.02 after 1 to 2 months (not significant), the mean plasma homocysteine levels did not change significantly (9.9 +/- 2.3 mumol/L at 3 days and 9.7 +/- 2.1 mumol/L at 1-2 months). It is unlikely that high plasma homocysteine levels contribute to the increased thrombotic risk of polycythemic patients.

Adult↗
PubMed1977

Prolonged remission of leukemia associated with polycythemia vera.

A patient with polycythemia vera (PV) received successive treatment by phlebotomies, radioactive phosphorus, myleran and cyclophosphamide. Sixteen years after the diagnosis, he developed acute myeloblastic leukemia. A complete remission was achieved following two courses of COAP (cyclophosphamide, vincristine, Cytosine Arabinoside, and prednisone) therapy. Four months later, while still in leukemic remission, he became mildly polycythemic again and the treatment with phlebotomies and cyclophosphamide was resume. The patient has subsequently been in complete remission of leukemia for over three years and his polycythemia is controlled by small doses of cyclophosphamide. This appears to be a unique case of such a prolonged remission of leukemia in the course of PV, with a return to a mild polycythemia state.

Aged↗
PubMed1984

Development of polycythemia vera and chronic lymphocytic leukemia during the course of refractory idiopathic thrombocytopenic purpura.

A case in which polycythemia vera and chronic lymphocytic leukemia (CLL) developed during the course of idiopathic thrombocytopenic purpura (ITP) is described. Observations in this case suggest that ITP was a pre-monitor of the clinical development of CLL and preceded the manifestation of polycythemia vera. The polycythemia was mild, requiring infrequent phlebotomies, and, as the CLL progressed, the requirement for phlebotomy diminished. Evidence of both CLL and myeloid proliferation, as well as severe immune thrombocytopenia, persisted throughout her course. Studies on lymphocytes revealed characteristics of those of CLL. Excellent therapeutic response of the CLL was observed with the use of vinblastine and steroids.

Female↗
PubMed1987

Malignant histiocytosis occurring with acute myelogenous leukemia in a patient with longstanding polycythemia vera.

A 52-year-old man with polycythemia vera of 20 years duration with progression to myelofibrosis developed a mass arising from the sternum. The mass consisted of large poorly differentiated cells infiltrating skeletal muscle, with cytochemical and ultrastructural features of malignant histiocytosis. At autopsy 6 weeks later, his bone marrow and spleen were involved by acute myelogenous leukemia. This is the first reported case of malignant histiocytosis occurring in a patient with polycythemia vera, and the second report of its association with acute myelogenous leukemia. There is suggestive evidence in this case that the malignant histiocytosis may possibly have arisen from the polycythemia vera clone.

Antibodies, Monoclonal↗