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PubMed2002

Overproduction of platelet microparticles in cyanotic congenital heart disease with polycythemia.

OBJECTIVES: We sought to clarify the role of platelets in the pathogenesis of abnormal coagulation in patients with cyanotic congenital heart disease (CCHD) with polycythemia; we evaluated the production of platelet microparticles (MPs), platelet degranulation and aggregation response, as well as the correlations of these variables with polycythemia. BACKGROUND: A shortened life span and suppressed aggregability of platelets are well known in patients with CCHD. Although platelet MPs are overproduced and play an important role in the coagulation process in various hematologic and cardiovascular disorders, the production of MPs remains to be elucidated in CCHD. We studied 19 patients who had CCHD with polycythemia and 21 age-matched subjects with acyanotic congenital heart disease (ACHD). Flow cytometry, using monoclonal antibodies, showed the presence of MPs as particles positive for the surface antigen (glycoprotein IIb/IIIa) specific to platelets, and platelet alpha-degranulation was recognized as platelets positive for the surface antigen of P-selectin. Platelet aggregation was assessed as the response to adenosine diphosphate (ADP). Relationships between these indexes and hematocrit (Hct) values were also evaluated. RESULTS: Production of MPs correlated positively with Hct and markedly increased at Hct values above 60% in patients with CCHD. Surface P-selectin and the mean platelet volume in patients with CCHD were comparable with those in patients with ACHD. The platelet aggregation response to ADP significantly and negatively correlated with Hct. In two subjects who showed hemoptysis and underwent phlebotomy, MPs were reduced 6 h after the procedure. CONCLUSIONS: Platelet MPs are overproduced in patients who have CCHD with polycythemia, probably due to a high shear stress derived from blood hyperviscosity. Circulating incompetent platelets, which have already been activated, as well as MPs, might play an important role in the coagulation abnormalities identified in such patients.

Adolescent↗
PubMed1998

Renovascular adaptive changes in chronic hypoxic polycythemia.

BACKGROUND: Chronic hypoxia in rats produces polycythemia, and the plasma fraction falls, reducing renal plasma flow (RPF) relative to renal blood flow (RBF). Polycythemia also causes increased blood viscosity, which tends to reduce RBF and renal oxygen delivery. We studied how renal regulation of electrolyte balance and renal tissue oxygenation (which is crucial for erythropoietin regulation) are maintained in rats during hypoxic exposure. METHODS: Rats of two strains with differing polycythemic responses, with surgically implanted catheters in the urinary bladder, femoral artery, and left renal and right external jugular veins, were exposed to a simulated high altitude (0.5 atm) for 0, 1, 3, 14, and 30 days, after which RPF (para-aminohippurate clearance), glomerular filtration rate (GFR, polyfructosan clearance), hematocrit and blood gases were measured, and RBF, renal vascular resistance and hindrance (resistance/viscosity), renal oxygen delivery, and renal oxygen consumption were calculated. RESULTS: During chronic hypoxia RBF increased, but RPF decreased because of the polycythemia. GFR remained normal because the filtration fraction (FF) increased. Renal vascular resistance decreased, and renal vascular hindrance decreased more markedly. Renal oxygen delivery and consumption both increased. CONCLUSIONS: During chronic hypoxia GFR homeostasis apparently took precedence over RBF autoregulation. The large decrease in renal vascular hindrance suggested that renal vascular remodeling contributes to GFR regulation. The reduced hindrance also prevented a vicious cycle of increasing polycythemia and blood viscosity, decreasing RBF, and increasing renal hypoxia and erythropoietin release.

Animals↗
PubMed2002

Concomitant primary polycythemia vera and follicle center cell non-Hodgkin lymphoma: a case report and review of the literature.

The association of myeloproliferative and lymphoproliferative disorders is well known after cytotoxic drug or radiation exposure, while it is remarkably rare prior to therapy. We report on a patient simultaneously diagnosed as having polycythemia vera and II3A follicle center cell non-Hodgkin lymphoma (grade 1). At this timepoint, he is on 12-year follow-up, characterized by post-polycythemia myeloid metaplasia with myelofibrosis and persistent complete remission of lymphoma. The conventional marrow cytogenetic analysis performed during the course of the disease demonstrated an abnormal karyotype with deletion of the long arm of chromosome 20 and trisomy 8, while molecular analysis failed to detect BCR-ABL rearrangement in peripheral blood cells. To the best of our knowledge based on a computer-aided review of the literature (MED-LINE 1966-2002), this is the sixth case of concomitant primary polycythemia vera and lymphoma of non-Hodgkin type. Besides, there is a single literature report on polycythemia vera coexisting with the Hodgkin's lymphoma. In our case as well as in the recorded ones, two independent malignant clones of myeloid and lymphoid origin, respectively, seem to have arisen. Further reports, supported by chromosomal and molecular studies, could improve our knowledge on this extremely infrequent disease association.

Aged↗
PubMed2002

Failure of polycythemia-induced increase in arterial oxygen content to suppress the anorexic effect of simulated high altitude in the adult rat.

The anorexic effect of exposure to high altitude may be related to the reduction in the arterial oxygen content (Ca(O2)) induced by hypoxemia and possibly the associated decreased convective oxygen transport (COT). This study was then performed to evaluate the effects of either transfusion-induced polycythemia or previous acclimation to hypobaria with endogenously induced polycythemia on the anorexic effect of simulated high altitude (SHA) in adult female rats. Food consumption, expressed in g/d/100 g body weight, was reduced by 40% in rats exposed to 506 mbar for 4 d, as compared to control rats maintained in room air. Transfusion polycythemia, which significantly increased hematocrit, hemoglobin concentration, Ca(O2), and COT, did not change the anorexic response to the exposure to hypobaric air. Depression of food intake during exposure to SHA also occurred in rats fasted during 31 h before exposure and allowed to eat ad libitum for 2 h during exposure. Body mass loss was similar in 48-h fasted rats that were either hypoxic or normoxic. Body mass loss was similar in normoxic and hypoxic rats, the former eating the amount of food freely eaten by the latter. Hypoxia-acclimated rats with endogenously induced polycythemia taken to SHA again had diminished food intake and lost body mass at rates that were very close to those found in nonacclimated ones. Exposure to SHA also led to a decrease in food consumption, body weight, and plasma leptin in adult female mice. Analysis of data suggest that body mass loss that accompanies SHA-induced hypoxia is due to hypophagia and that experimental manipulation of the blood oxygen transport capacity cannot ameliorate it. Leptin does not appear to be an inducer of the anorexic response to hypoxia, at least in mice and rats.

Acclimatization↗
PubMed1983

Diagnostic use of CFU-E formation from peripheral blood in polycythemia vera.

Peripheral blood mononuclear cells from five patients with polycythemia vera (P. vera) and three with other polycythemias were cultured in a methylcellulose system. Colony-forming unit-erythroid (CFU-E) colonies appeared after seven days in the absence of added erythropoietin (Ep) in all P. vera cultures. A pattern of growth similar to the one seen for P. vera patients occurred in the culture from a patient in whom that disease was suspected. In the cultures from two of the patients with other polycythemias, erythroid colonies did not appear even in the presence of Ep. These findings emphasize the potential value of culturing peripheral blood for CFU-E colonies in diagnosing polycythemia vera.

Adult↗
PubMedDate not supplied

Polycythemia and hyperviscosity of the newborn.

Polycythemia and hyperviscosity of the newborn are well-known conditions that are surrounded by controversy. The patient population most affected by polycythemia is the term or near-term infant. The true incidence of this condition is not known since the majority of infants are likely to be asymptomatic, normal newborns. Diagnosis is largely based on hematocrit values and symptoms, which can range from subtle to severe, and not on measures of viscosity. Hematocrits are not routinely drawn in this population, most likely related to the controversy surrounding the treatment of the asymptomatic infant. Presenting symptoms may be subtle and are not always attributed to polycythemia. Knowledge of the etiology, pathophysiology, and clinical signs and symptoms may contribute to the early identification and treatment of infants with polycythemia and hyperviscosity syndrome.

Blood Viscosity↗
PubMed1998

Embryonal adenoma of the kidney associated with polycythemia and von Willebrand disease.

PURPOSE: We studied the significance, identification and management of acquired von Willebrand disease and polycythemia associated with benign renal tumors in children. MATERIALS AND METHODS: Two patients who presented with polycythemia and a renal mass were also found to have acquired von Willebrand disease. One patient was treated with radical nephrectomy and 1 was treated with partial nephrectomy. The patients have been followed for 19 and 10 months, respectively. RESULTS: Excision of the renal mass resulted in prompt resolution of polycythemia and von Willebrand disease in each patient. Perioperatively 1-deamino-(8-D-arginine)-vasopressin was given to control bleeding. Each patient had benign embryonal adenoma of the kidney. CONCLUSIONS: Polycythemia and von Willebrand disease may be associated with benign kidney neoplasms. Children and adolescents with a renal mass may benefit from preoperative screening for coagulopathy.

Adenoma↗
PubMed1991

Immunohistochemical study of erythropoietin in cerebellar hemangioblastomas associated with secondary polycythemia.

Although cerebellar hemangioblastomas are known to be associated with secondary polycythemia, the cellular derivation of erythropoietin (EPO) in hemangioblastomas still remains obscure. Specimens from 18 patients with cerebellar hemangioblastomas were immunohistochemically studied using anti-EPO monoclonal antibody. Eight cases of brain tumors, including 2 meningiomas, 2 medulloblastomas, 2 glioblastomas, and 2 metastatic brain tumors were studied as controls. In 9 of 18 cases, EPO-positive cells were scattered around the capillaries and were ultrastructurally shown to be mast cells. These cases were not, however, associated with secondary polycythemia. In contrast, the stromal cells were positive for EPO in 3 cases. Among them, one was associated with secondary polycythemia. Furthermore, one-half of the control cases of brain tumor contained EPO-positive mast cells. Accordingly, it was suggested that mast cells (or small granulocytes) have little relationship to the release of EPO; however, some stromal cells might release EPO with a resultant polycythemia.

Adolescent↗
PubMed2004

Familial and congenital polycythemias: a diagnostic approach.

The rare absolute polycythemias with an innate and hereditary character can be grouped together under the heading "familial and congenital polycythemias" (FCPs). Primary forms, due to an intrinsic defect in the erythroid progenitor cells, and secondary forms, resulting from extrinsic factors such as an elevated erythropoietin level, have both been reported. Despite the widely divergent characteristics of the different FCPs, the range of possible diagnoses is much more restricted and the distribution of disorders markedly different compared with polycythemias in general. Therefore, in FCP, one can argue against following the algorithm of the Polycythemia Vera Study Group for the evaluation of an elevated hematocrit level, following instead a more specific algorithm. In this article the authors describe a child with primary FCP, review the different FCPs, and propose an adapted work-up scheme.

Adolescent↗
PubMed2004

Cutaneous sarcoidosis and polycythemia vera.

Polycythemia vera is classified with myelogenous leukaemia, agnogenic myeloid metaplasia and primary thrombocythemia as a myeloproliferative syndrome. Cutaneous symptoms have been reported with polycythemia vera, including facial plethora, aquagenic pruritus, urticaria, purpura, Sweet's syndrome and pyoderma gangrenosum. However, polycythemia vera associated with systemic sarcoidosis has been rarely reported. An unusual case of polycythemia vera associated with cutaneous sarcoidosis is described.

Aged↗
PubMed1980

The effect of polycythemia on blood flow in working and non-working skeletal muscle.

The effect of acutely induced polycythemia on blood flow and viscosity in the vasodilated vascular bed of working and non-working skeletal muscle was studied. In 12 mongrel dogs anesthetized with thiopental sodium the calf muscle of one hind limb was isolated. Vasodilation was induced either by sciatic stimulation setting the muscle at maximal work or by i.a. infusion of papaverine. Blood flow was measured at different perfusion pressure before and after infusion of 300 ml packed homologous red cells. Blood viscosity in vitro was determined in a coneplate viscometer. Apparent viscosity in vivo was analyzed by comparing pressure-flow relationships for blood and a reference solution. Polycythemia decreased blood flow by 35% in the non-working muscle but less than 10% in the working muscle at comparable perfusion pressures. Blood viscosity in vitro increased by 35% at low shear rates. Apparent viscosity in vivo increased by 35% in the non-working muscle but less than 10% in the working muscle. The flow impairment induced by polycythemia was far more pronounced in the non-working skeletal muscle indicating a flow facilitation by the rhythmic muscle contractions. Erythrocyte flow in fact increased in the working muscle after induced polycythemia while decreased in the non-working muscle.

Animals↗
PubMed2005

Regulation of oxygen delivery during induced polycythemia in exercising dogs.

Previous studies have concluded that polycythemia decreases oxygen delivery primarily because of a large fall in cardiac output associated with a rise in systemic vascular resistance that has been attributed to increased blood viscosity. However, because other studies have shown that polycythemia may not reduce oxygen delivery, an alternative hypothesis is that cardiac output falls in response to a rising oxygen content, thereby maintaining oxygen delivery constant. To determine whether oxygen content participates in the regulation of cardiac output during polycythemia, we studied eight chronically instrumented dogs trained to exercise on a treadmill. The dogs underwent exchange transfusion with packed red blood cells containing methemoglobin, which caused an increase in hematocrit from 35 +/- 1 to 50 +/- 1% and in viscosity, with little change in oxygen content. The expected fall in exercise cardiac output failed to occur after exchange transfusion with red blood cells containing methemoglobin (7.5 +/- 4 vs. 6.8 +/- 0.5 l/min; P = not significant), and there was no rise in systemic vascular resistance. Methylene blue was then administered intravenously to facilitate conversion of methemoglobin to oxyhemoglobin, which increased oxygen content (12.8 +/- 0.9 vs. 18.4 +/- 0.9 vol%; P < 0.01) with no change in hematocrit or viscosity. Resting cardiac output did not change significantly, but there was a significant decrease in exercise output (6.8 +/- 0.5 vs. 5.8 +/- 0.4 l/min; P < 0.05). Thus we conclude that the fall in cardiac output seen in acute polycythemia results in part from the regulation of oxygen delivery and is not due solely to increased blood viscosity.

Animals↗
PubMed1988

Ventilation-perfusion relationships during induced normovolemic polycythemia in dogs.

Previous studies on normal subjects and patients with polycythemia have given conflicting results of the effect of polycythemia on pulmonary gas exchange. We studied acutely induced normovolemic polycythemia in the dog and measured arterial blood gases and ventilation-perfusion (VA/Q) relationships using the multiple inert gas elimination technique. The mean base-line hematocrit of 43 +/- 5% was increased to 57 +/- 4 and 68 +/- 8%, respectively, after two exchange transfusions of packed erythrocytes. Subsequent plasma exchange transfusions returned the mean hematocrit to 44 +/- 4%. Polycythemia caused no significant arterial hypoxemia; indeed there was a slight improvement in the alveolar-arterial PO2 difference. The multiple inert gas elimination measurements showed no increase in VA/Q inhomogeneity with no increase in log SD ventilation (V) or log SD blood flow (Q). There was a shift of mean V and mean Q to high VA/Q areas because of a decrease in cardiac output, presumably caused by increased blood viscosity. This study showed no deleterious effects on pulmonary gas exchange within the hematocrit range of 36-76%.

Animals↗
PubMed2003

Early cord clamping protects at-risk neonates from polycythemia.

UNLABELLED: Neonatal polycythemia is a potentially lethal, multi-organ disease. We have performed a prospective, open-label study to test the hypothesis that an early cord clamping proximally to the neonate's abdomen could avert from the neonatal circulation a blood volume critical to the occurrence of polycythemia in at-risk neonates. Newborns were divided into group 1 (clamping time within 10 s) and group 2 (clamping time 11-120 s). Group 1 had statistically significant more blood volume sequestered in the cord and less manifestations of polycythemia. CONCLUSION: An early cord clamping is an effective and zero-cost way to prevent polycythemia in at-risk neonates.

Blood Volume↗
PubMedDate not supplied

A unique form of polycythemia associated with minimal change disease.

OBJECTIVE: To present a case with nephrotic syndrome due to minimal change disease and polycythemia. CLINICAL PRESENTATION AND INTERVENTION: A 20-year-old female was admitted to our clinic for edema and severe proteinuria present with minimal change disease since the age of 7 years. Polycythemia was found during the last activation of nephrotic syndrome. The patient was placed on glucocorticoid therapy that caused disappearance of edema, proteinuria and polycythemia. Ten months later both hemoglobin and hematocrit levels were within normal range. CONCLUSION: This patient with nephrotic syndrome due to minimal change disease and polycythemia was successfully treated with glucocorticoid.

Adult↗
PubMed1992

Isolated cerebellar infarction as a presenting symptom of polycythemia vera.

Although polycythemia vera is one of the reported causes for cerebral infarction, isolated cerebellar infarction, a rare disorder, was never reported in combination with polycythemia vera. This is a report of a 72-year-old woman in whom isolated cerebellar infarction was the presenting manifestation of polycythemia vera. The patient was treated with recurrent phlebotomies until the hematocrit decreased to < 45%. This treatment was followed by marked neurological improvement. A better awareness of the possibility of cerebellar infarction in polycythemia vera may disclose additional cases.

Aged↗
PubMed1985

Hemodynamic response to normovolemic polycythemia at rest and during exercise in dogs.

Very little is known about the influence of polycythemia on oxygen transport during exercise. We studied chronically instrumented dogs trained to run on a treadmill before and after their hematocrit had been increased by isovolemic exchange transfusion with packed red blood cells. With normovolemic polycythemia, cardiac output fell in a linear fashion as hematocrit was increased to 65%, but these changes were balanced by an increasing oxygen content resulting in constant systemic oxygen transport. Oxygen consumption was unchanged both at rest and during exercise after induction of polycythemia. To investigate the effect of polycythemia on oxygen transport further, we measured both mixed venous Po2 and lactate. Mixed venous Po2 increased and lactate remained unchanged both at rest and in exercising polycythemic dogs. Thus, we conclude that, in conscious animals, systemic oxygen transport is well preserved with increasing hematocrit to at least 65%.

Animals↗
PubMed1978

Polycythemia vera. The in vitro response of normal and abnormal stem cell lines to erythropoietin.

Bone marrow cells from two glucose-6-phosphate dehydrogenase (G-6-PD) heterozygotes with polycythemia vera were cultured to determine whether progenitors which wre not of the polycythemia vera clone were present, and, if present, which cell lines contributed to the increase in erythroid colonies observed in response to added erythropoietin (ESF). To accomplish this, the G-6-PD isoenzyme activity of individual erythroid colonies was determined. All of the erythroid colonies analyzed in cultures without added ESF, contained the G-6-PD isoenzyme type characteristic of the abnormal clone. With higher ESF concentrations in the culture, however, there was an increase in the colonies that were not of the polycythemia vera clone. Analysis of the ratio of the various types of colonies indicated that normal and polycythemia vera cells are capable of responding to ESF in vitro. In selected patients, this technique permits analysis of the ratios of normal to abnormal cells during the course of the disease, in response to therapy and during late complications, such as myelofibrosis or leukemic transformation.

Clone Cells↗