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At least 217 records · Page 12Linked to original sources

Polycythemia and steroid overproduction in a gonadotropin-secreting seminoma of the testis.

While investigating the cause of mild polycythemia in a young man, a testicular seminoma was discovered with unusual and tumor-dependent features: an absolute polycythemia with high plasma erythropoietin (EPO) levels, an overproduction of estradiol and testosterone, and a dramatic Leydig cell hyperplasia surrounding the tumor tissue. The authors attempted to gain insight into the relationship between this testicular tumor and the hormonal overproduction, i.e., of EPO, estradiol, and testosterone. Their results favored the conclusion that the high EPO levels and the polycythemia were an indirect effect secondary to the steroid overproduction rather than a direct EPO-producing activity. Moreover, the steroid overproduction by the testis could be caused by a paracrine mechanism through human chorionic gonadotropin activity on the Leydig cells.

Adult↗

Polycythemia vera in childhood: case report and review of the literature.

A patient presented at 5 years of age with polycythemia vera. He subsequently developed splenic infarctions and died at 20 years of age following cerebral hemorrhage and infarctions. Two months before his death, he developed hypertension and had biochemical evidence of primary hyperparathyroidism and possibly pheochromocytoma. Only nine reported childhood cases of polycythemia vera fulfill the criteria of the Polycythemia Vera Study Group. These cases are summarized and the complications discussed. Although none have progressed to myeloid metaplasia or acute leukemia, these patients are at risk of developing thrombo-hemorrhagic complications; available evidence indicates that they should be managed to keep the hematocrit between 40 and 45%.

Bloodletting↗

Acute lymphoblastic leukemia in a patient with longstanding polycythemia vera: cytogenetic analysis reveals two distinct abnormal clones.

A 68-year-old female patient is described in whom acute lymphoblastic leukemia followed a long course of polycythemia vera. Chromosomal analysis of a peripheral blood specimen at the time of blastic transformation revealed two distinct clones: one characterized by a chromosomal abnormality frequently noted in polycythemia vera and the other by a rearrangement characteristically observed in lymphoid malignancies. These findings suggest the existence of two independent hematologic diseases: this phenomenon would not support the speculation from previous reports that lymphoproliferative disorders in patients with polycythemia vera arise from clonal evolution.

Aged↗

Hemoglobin Villejuif [beta 123(H1) Thr----Ile]: a new variant found in coincidence with polycythemia vera.

A new abnormal hemoglobin, Hb Villejuif [beta 123(H1) Thr----Ile] has been discovered during the exploration of a polycythemia in a 87-year-old patient of French origin. The isoelectric focusing of the lysate revealed the presence of a variant hemoglobin with an isoelectric point very close to that of HbA. The oxygen binding properties of the patient's red blood cells being normal, it was clear that the polycythemia was not a consequence of the presence of this hemoglobin. In fact, the red blood cell morphology and the involvement of the other blood cell lines, demonstrating excessive hemopoiesis, led to the diagnosis of polycythemia vera.

Aged↗

Leukemic transformation in polycythemia vera: analysis of risk factors.

Forty-eight patients with polycythemia vera (PV) were retrospectively studied for incidence of acute leukemia over a 12 year period. Initial clinical features, hemogram, RBC mass, B12 levels, neutrophil alkaline phosphatase (NAP), and therapy given were studied for association with development of acute leukemia. There were 25 males and mean age at diagnosis was 61.4 years. Initial Hg was 18.38 +/- 1.86 g/dl, WBC 16.44 +/- 12.92 (x 1,000/mm3), platelets 632.94 +/- 303.81 (x 1,000/mm3), B12 1,030.93 +/- 445.20 pg/ml, and neutrophil alkaline phosphatase (NAP) score 136.63 +/- 55.14. Twenty-three patients were treated with phlebotomy alone and 25 received additional myelosuppressive therapy as follows--2 received p32 alone, 4 alkylating agents alone, 8 hydroxyurea (HU) alone, and 11 received 2 or more (multiple) of these agents. None of those treated with phlebotomy alone but 6 of 25 (24%) patients given myelosuppressive therapy developed acute leukemia (P = .03) after a mean period of 46.8 months from start of myelosuppressive therapy. Four of the 11 patients (36%) receiving multiple agent therapy developed acute leukemia (P = .019). Initial hemoglobin levels, but not the other clinical parameters, were significantly higher in patients who developed acute leukemia (P = .002), and this difference persisted in various subgroups receiving myelosuppressive therapy. Thus, high initial hemoglobin and use of any myelosuppressive therapy are associated with an increased risk of leukemic transformation in polycythemia vera. This risk becomes substantial with the use of two or more myelosuppressive agents. Since myelosuppressive therapy does not prolong survival, its role in the management of polycythemia vera should be reexamined.

Acute Disease↗

Pulmonary hypertension in polycythemia vera.

Thromboembolic events occur in about 27% of the patients with polycythemia vera and account for 31% of the deaths. These include cerebrovascular accidents, myocardial infarction, peripheral vascular occlusions, pulmonary infarctions, and venous thrombosis. We report two cases with polycythemia vera who presented with pulmonary hypertension in the absence of previous thromboembolic complications of any kind. One patient died suddenly, with evidence of extensive bilateral thrombosis of prelobular pulmonary arteries at autopsy. In the second patient, local thrombosis in the pulmonary vasculature or recurrent silent pulmonary emboli appear to be responsible for the development of pulmonary hypertension. After institution of anticoagulant therapy, he is able to maintain his functional status. The purpose of this report is to alert clinicians to the development of this insidious, but potentially fatal complication in patients with polycythemia vera.

Humans↗

Hepatic vascular disease and portal hypertension in polycythemia vera and agnogenic myeloid metaplasia: a clinicopathological study of 145 patients examined at autopsy.

The pathogenesis of portal hypertension arising in patients with myeloproliferative disorders has been difficult to understand because liver biopsy findings often show minimal changes. It has been suggested that increased splenic blood flow, hepatic infiltration with hematopoietic cells or sinusoidal fibrosis may be important. We have reviewed the autopsy findings and clinical histories of 97 patients with polycythemia vera and 48 patients with agnogenic myeloid metaplasia collected from three institutions and from the Polycythemia Vera Study Group. Cirrhosis was present in seven patients, one of whom had bleeding varices. Esophageal varices were present clinically in 10 patients without cirrhosis (seven polycythemia and three agnogenic myeloid metaplasia). All of these patients had lesions in small or medium-sized portal veins and four had stenosis of the extrahepatic portal vein with histology compatible with organized thrombi. Nodular regenerative hyperplasia occurred in 14.6% and correlated closely with the presence of portal vein lesions. Thirty patients had greater than 500 ml of ascites, seven of these patients also had varices and six of them had hepatic vein thrombosis. Ascites also correlated with hepatic vein disease confined to small intrahepatic branches. No correlation was seen between hepatic hematopoietic infiltration and signs of portal hypertension. We conclude that esophageal varices are common and are almost always associated with portal vein lesions visible by light microscopy. These portal vein lesions, and the secondary effects of nodular regenerative hyperplasia and portal hypertension, are most likely a result of portal vein thrombosis in patients with myeloproliferative disorders.

Adult↗

Multiple functioning paraganglioma associated with polycythemia.

Multiple retroperitoneal functioning paraganglioma complicated by polycythemia is reported in the case of a girl who, at the age of 13 years complained of headache, palpitation, and faintness preoperatively. In the retroperitoneal cavity, there were 21 paragangliomas larger than 1 cm in diameter. All were removed surgically in two sections, the first in 1979 and the second in 1983. Bilateral adrenals were macroscopically normal, and her symptoms disappeared. Now the recurrence of retroperitoneal paraganglioma is likely, although there have been no symptoms for 8 years, since the first operation. It is difficult to conclude that the tumors were benign or malignant in this case. Though complication of polycythemia had been diagnosed before the operation, the symptom continued even with the serum erythropoietin level kept in the normal range. Association of polycythemia with paraganglioma is extremely rare, and it is also rare to find more than 10 paragangliomas. Only a limited number of reports have been made on each case in the literature.

Adolescent↗

Burst-promoting activity in anemia and polycythemia.

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).

Anemia↗

32P-therapy in polycythemia vera.

A group of 52 consecutive patients with polycythemia vera was submitted to long-term therapy with radioactive phosphorus (32P). Initial phase of therapy induced complete remissions (normalization of hematogram; spleen not palpable) in 45% of the patients, and partial remissions in the remaining 55%. During maintenance therapy of the complete remission group, mean remission time was about 3.5 years. Individual remission times ranged between 1 and 6 years. In the group of patients with incomplete remission, mean remission time increased with the progression of the disease due to gradual development of "spent" -polycythemia. In patients with splenomegaly, remission time was negatively correlated to spleen size. In both groups the increment of annual accumulated dose averaged 2.4 mCi 32P. When considering polycythemia related causes of death only, mean survival time attained 12 years after initial treatment with 32P. Acute leukemia occurred in 2 patients (4%).

Adult↗

Polycythemia in the newborn.

Polycythemia is defined as a venous hematocrit above 65%. The relationship between viscosity and hematocrit is almost linear till 65% and exponential thereafter. Increased viscosity of blood is associated with symptoms of hypo-perfusion. The hematocrit in a newborn peaks at 2 hours of age and decreases gradually after that. The etiology of polycythemia is related either to intra-uterine hypoxia or secondary to fetal transfusion. Clinical features related to hyperviscosity may affect all organ systems and this entity should be screened for in high-risk infants. Polycythemia maybe symptomatic or asymptomatic and guidelines for management of both types are provided in the protocol.

Blood Viscosity↗

Transient polycythemia and multi-organ failure due to acute alcohol ingestion.

Relative polycythemia is characterized by elevated hematocrit with normal red cell mass and results from decreased plasma volume. We present a case of a 39-year-old man who had at least two episodes of severe relative polycythemia and multi-organ failure following acute alcohol ingestion. Although the acute dehydrating effects of alcohol are well known, they usually result in an indolent course. This is the first report of recurrent severe polycythemia and multi-organ failure following acute alcohol consumption.

Adult↗

Splenic rupture complicating periinterventional glycoprotein IIb/IIIa antagonist therapy for myocardial infarction in polycythemia vera.

Polycythemia vera is a myeloproliferative disorder predisposing to thromboembolic and bleeding complications. We report the case of a patient with polyglobuly, leukocytosis, and thrombocytosis, who suffered from acute ST-segment elevation myocardial infarction due to thrombotic high-grade pre-stent stenosis two months after percutaneous coronary intervention for complex coronary one vessel disease. Following re-PTCA and stent implantation in conjunction with periinterventional GP IIb/IIIa antagonist treatment, the patient was initially symptom free for about two hours before rapidly developing signs of a hemorrhagic shock. An abdominal CT scan showed splenic rupture with massive intraabdominal hemorrhage as a consequence of secondary bleeding into multiple pre-existing splenic infarctions. The patient's condition stabilized after emergency splenectomy. Subsequent bone marrow biopsy revealed the presence of polycythemia vera. Post-operatively, the patient was treated with the anti-platelet agents aspirin and clopidogrel to prevent subacute stent thrombosis. Additionally, cyto-reductive therapy with hydroxyurea was initiated because of a further increase in the platelet count. In patients with polycythemia vera, the indication for treatment with GP IIb/IIIa antagonists should be carefully weighed against the potentially serious bleeding complications. Should treatment be established, a risk stratification using abdominal sonography and bleeding time testing is recommended, while during treatment red blood count, platelet count, coagulation tests, and hemodynamic parameters should be closely monitored.

Abciximab↗

Successful surgical treatment for spontaneous retroperitoneal hematoma in polycythemia vera: report of a case.

Bleeding is a common complication of such myeloproliferative disorders as polycythemia vera, and it usually occurs in either the skin or mucosa. We experienced a case of a massive retroperitoneal hematoma with no history of trauma in association with polycythemia vera. A 68-year-old man was referred to our hospital as a case of acute abdomen, and was diagnosed as having a retroperitoneal hematoma and polycythemia vera based on radiological and hematological examinations. Because the mass effect of the hematoma caused a progressive deterioration of his respiratory condition, surgical drainage was necessitated and successfully undertaken. Although conservative treatment is reportedly sufficient and uncontrollable intraoperative bleeding may occur, especially in cases of myeloproliferative disorders, our experience suggests that an operation may nevertheless be occasionally advisable for this rare condition.

Aged↗

Fetal polycythemia and hyperviscosity: effect on umbilical blood flow and fetal oxygen consumption.

To evaluate the effect of fetal polycythemia and hyperviscosity on fetal oxygen transport, we induced those conditions in eight chronically instrumented fetal lambs by isovolemic exchange transfusion with packed red cells obtained from a donor ewe. This procedure resulted in polycythemia and hyperviscosity without altering fetal arterial blood oxygen content. The fetuses were studied at 1 and 48 hours after polycythemia and hyperviscosity. In spite of decreased oxygen delivery to the fetus, the fetal oxygen consumption was unchanged because of an increase in oxygen extraction by the fetus.

Animals↗

Polycythemia vera.

Polycythemia vera (PV) is one of the myeloproliferative diseases, and, as such, is an example of clonal hematopoiesis. The progeny of a single, abnormal, hematopoietic stem cell gain a growth advantage over their normal counterparts resulting in overproduction of red cells generally accompanied by overproduction of granulocytes and platelets as well. There are a variety of nonspecific symptoms at onset related to the increased red cell mass and hematocrit accompanied by the more specific manifestations of pruritus, erythromelalgia, and hepatic, portal, and mesenteric vein thrombosis. Splenomegaly and hypertension are common. The laboratory hallmark is an increased red cell mass. There is also often an increase in white cell count, platelet count, and leukocyte alkaline phosphatase along with other findings reflecting the increased rate of turnover of hematopoietic cells. The bone marrow biopsy generally displays hypercellularity involving all three cell lines and absent iron stores. The diagnosis of PV depends on excluding spurious polycythemia in which there is a high hematocrit but a normal red cell mass and secondary polycythemia in which there is an increased red cell mass in response to tissue hypoxia or the inappropriate production of erythropoietin, generally by a tumor. In addition, one should try to establish the diagnosis in a positive fashion by a combination of studies of the blood and bone marrow. Phlebotomy and occasionally plateletpheresis should be used as acute therapy. Chronic therapy is guided by the knowledge that patients treated with phlebotomy alone have an increased rate of thrombotic complications particularly in older patients and those with previous thrombotic disease. Myelosuppressive therapy can reduce the incidence of these complications, but is commonly associated with an increased incidence of second malignancies, particularly acute leukemia. At present, hydroxyurea is the myelosuppressive agent of choice. Antiplatelet agents have a limited role except in the palliation of the syndrome of erythromelalgia. Median survival is approximately 10 years. As implied above, the causes of morbidity and mortality vary with the mode of chronic therapy which has been employed, leukemia being more common after myelosuppressive therapy and thrombotic complications being more common after therapy with phlebotomy alone. Ten percent to 50% of patients move into a spent phase followed by postpolycythemic myeloid metaplasia, irrespective of previous therapy employed. Eventually, the major problems may be cytopenias and massive splenomegaly.

Humans↗

Hydronephrosis and polycythemia.

Polycythemia is consistently produced in animals undergoing experimental hydronephrosis. This hematologic response is thought to be mediated by a microcirculatory insult and a more accelerated elaboration of erythropoietin by the hydronephrotic kidney. While an association between hydronephrosis and polycythemia has been reported in humans, it is a relatively rare event. Further studies are necessary to explain why this should be so, as well as to confirm that the polycythemia in humans is secondary to an increased production of erythropoietin.

Adult↗

Polycythemia.

Plethora ('a morbid condition due to excess of red corpuscles') has been recognized since antiquity as a manifestation of disease. The use of leeches and blood letting, which was for centuries the mainstay of therapy in many clinical situations, reflected the importance then attached to having too much blood. Greater knowledge has achieved greater precision, so that measurement of packed cell volume (PCV) or hematocrit now defines polycythemia (> 0.51 in men and > 0.48 in women, when blood is sampled without venous occlusion). Clinical and laboratory investigations, mainly in the last 30 years, have enabled the subdivision of polycythemia into different subtypes of radically different etiology which will be described in this Chapter. The last decade, however, has seen the advancing edge of research in this field passing from clinical and routine laboratory testing to studies of cellular proliferation at the molecular level. Detailed understanding is, however, as always elusive, with each new finding revealing deeper layers which in turn need elucidation. The field of polycythemia is nevertheless moving slowly into the molecular era.

Bone Marrow↗