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

Five smokers had erythrocyte masses sufficiently larger than normal to pose a problem in the differential diagnosis of polycythemia. Evaluation excluded lung disease, shunt physiology, hemoglobin with increased oxygen affinity, erythropoietin-producing tumor, renal disease, or polycythemia rubra vera as the primary cause of erythrocytosis in these patients. All were found to have levels of carboxyhemoglobin sufficient to cause clinically significant hypoxemia and to account for the increased erythrocyte masses. In two patients the erythrocytosis improved when they stopped smoking. Heavy smoking is a reversible cause of polycythemia and should be considered in the differential diagnosis of this problem.
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PMID:Smoking as a cause of erythrocytosis. 23 31

The absolute polycythaemias include all patients who have a raised red cell mass. They may be divided by clinical and laboratory investigation into: primary proliferative polycythaemia (polycythaemia rubra vera), secondary polycythaemias, and idiopathic erythrocytosis. In vitro, the PCV is the single most important determinant of whole blood viscosity with the most marked effects at low shear rates. Yield stress is also dominantly influenced by PCV. Thus in the absolute polycythaemias, from whatever cause, whole blood viscosity and yield stress are high. However, flow conditions in vivo are much more complex than those usually used in in-vitro measurements. Under normal physiological conditions, whole blood viscosity probably does not determine flow in vivo. The observed in-vitro changes are only of relevance in vivo when local or general abnormalities of flow occur. In primary proliferative polycythaemia (PPP) and idiopathic erythrocytosis, presentation with ischaemia or thrombosis (either arterial or venous) is common, and the cerebral circulation is at particular risk. The incidence of vascular occlusion is positively correlated with the PCV. There is an inverse correlation between PCV and cerebral blood flow (CBF), with untreated patients having low CBF values. This is probably a 'physiological' change related to the increased oxygen carrying capacity at high PCV values. However, in many patients, cerebral oxygen carriage actually increases on reduction of the PCV to normal. This explains the improvement in cerebral ischaemic symptoms and mental performance which may be observed following treatment. Platelet contact and adhesion to the vessel wall are increased at high PCV values and, combined with the lower blood flow in both the arteries and veins, tend to favour thrombus formation. Ischaemia causes vessel dilatation but when this is maximal the high whole-blood viscosity demonstrated in vitro is a major determinant of flow. Hence in man and experimental animals, as demonstrated in the brain, the area of ischaemia or non-perfusion following arterial occlusion is greatest at high PCV values. Patients with polycythaemia due to hypoxic lung disease have a poor prognosis. The hypoxic pulmonary vasoconstriction combined with the high blood viscosity causes an increase in pulmonary vessel resistance. PCV reduction of 0.50-0.52 leads to an improvement in work performance and mental alertness, and reduction in pulmonary vascular resistance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Rheology of the absolute polycythaemias. 332 60

n vitro, rheological studies establish that whole blood viscosity and yield stress are high in patients with an erythrocytosis. However, a number of factors ensure that these patients, under physiological conditions, do not show the clinical features observed in other hyperviscosity states. These include red cell axial migration in flowing blood and "plug flow" in the largest vessels. In addition, a small increase in vessel diameter leads to large increases in blood flow, and generally high blood flows produce the lowest blood viscosity values. The increased hemoglobin levels and the increase in oxygen-carrying capacity at high hematocrit values compensate for the tissue hypoxia. In the "non-hypoxemic" erythrocytoses (polycythemia vera, idiopathic and apparent erythrocytosis), there is an increased incidence of vascular occlusion in untreated patients. The reasons for this include reduced peripheral blood flow, increased platelet-vessel wall interactions, and the demonstrated in vitro hyperviscosity which comes into play with abnormally low flow, seen in vivo under pathological conditions. In the erythrocytosis of hypoxemic lung disease and its associated hypoxemia, pulmonary vasoconstriction enhances susceptibility to hyperviscosity effects in particular. Moreover, the vasoconstriction caused by the hypoxemia prevents the normal adaptive changes of increased vessel diameter. Microcytic hypochromic red cell changes of iron deficiency do not cause a higher viscosity value at any given hematocrit value compared with normal red cells. However, in hypoxemic states oxygen-carrying capacity should be maximized, since the hemoglobin value is disproportionately lower at any given hematocrit in the presence of microcytic hypochromic cells compared with normal red cells.
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PMID:Hemorheology in the erythrocytoses. 1137 90