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Red cell survival

Increased nonconjugated (indirect) bilirubin Shortened red cell survival time as measured by injection of autologous Cr-labeled red cells... [Pg.620]

Impaired production Impaired production Shortened red cell survival... [Pg.730]

Within days following splenectomy, jaundice fades, the hemoglobin concentration rises, and red cell survival usually returns to near normal. Although the number of peripheral blood microspherocytes remains unchanged, the morphological features of accelerated ery-thropoiesis are not observed. Blood transfusion is rarely indicated except during aplastic crisis. At such times, red cell replacement may be lifesaving. [Pg.74]

Lundh B, CavaUin-Stahl E, Mercke C. Heme catabo-hsm, carbon monoxide production and red cell survival in anaemia. Acta Med Scand 1975 197 161-71. [Pg.1361]

Traditionally, red cell survival has been the main criterion of the quality of stored blood. However, cell survival does not necessarily correspond to maintenance of adequate organic phosphate levels. Studies on the composition of the storage medium needed to prevent this metabolic loss of organic phosphates show the following ... [Pg.655]

A pharmacological role for vitamin E may exist in claudication arising from peripheral vascular disease. Studies with small numbers of patients having cystic fibrosis, glucose-6-phosphate dehydrogenase deficiency, and sickle cell anemia conditions associated with decreased erythrocyte half-lives showed that many had chemical evidence of vitamin E deficiency. Administration of vitamin E supplements (400-800 lU/d) significantly increased red cell survival time. Claims that doses of vitamin E 10-20 times the RDA are beneficial for treatment of skin disorders, fibrocystic breast disease, sexual dysfunction, cancer, baldness, and other disorders have not been substantiated. [Pg.914]

A severe decrease in P-globin levels leads to the precipitation of the a-chain, which in turn causes a defect in the maturation of the erythroid precursor, and erythropoiesis thus reducing red cell survival. The profound anemia in the affected individual stimulates the production of erythropoietin leading to the expansion of bone marrow and subsequent skeletal deformities. The hyperplasia of the bone marrow induces increased iron absorption leading to the deposition of iron in tissues. If the concentration of iron in the tissues becomes too high, it can lead to organ failure and death if appropriate therapeutic steps are not taken. [Pg.114]

Most patients who require dialysis have a normocytic normochronic anemia and a hypoproliferative bone marrow. As erythropoiesis decreases with advancing renal disease, iron shifts from circulating red cells to the reticuloendothelial system, leading to high serum ferritin levels. Repeated blood transfusion is also a common cause of iron overload and hyperferritinemia. Clearly the most important cause of the anemia of chronic renal failure is decreased erythropoietin production by the kidneys uremic patients have much lower plasma erythropoietin levels than comparably anemic patients with normal renal function (E8). Less important causes are shortened red cell survival, iron or folate deficiency, aluminum intoxication, and osteitis fibrosa cystica (E8). Uremic retention products such as methylguanidine (G10) and spermidine (R2) may also have an adverse effect on erythropoiesis. [Pg.87]

Richards et al. (1957), however, could find no correlation between the degree of peroxide hemolysis and the intensity of physiological jaundice in the newborn, and Goldbloom (1960) found normal red cell survival in tocopherol-deficient rats and in a 2-year-old boy with fibrocystic disease of the pancreas and persistently low serum tocopherol levels. [Pg.589]

The study of erythrokinetics in man requires the use of appropriate isotopes to evaluate red cell production and destruction. Red cell production is generally investigated through studies of iron kinetics and Fe is the chosen isotope. Red cell destruction is cammonly evaluated through labelled red cell survival studies, and Cr is the most extensively employed label. These isotopes can be simultaneously. [Pg.517]

One of the eventual results of lead - induced inhibition of enzymes in the heme synthesis pathway is anemia which can be asymptomatic if mild but associated with a wide array of symptoms including dizziness, fatigue, and tachycardia when more severe. Studies have indicated that lead levels as low as 50 xg/dl can be associated with a definite decreased hemoglobin, although most cases of lead - induced anemia, as well as shortened red-cell survival times, occur at lead levels exceeding 80 xg/dl. Inhibited hemoglobin synthesis is more common in chronic cases whereas shortened erythrocyte life span is more common in acute cases. [Pg.259]

Hernberg, S., Nurminen, M., Hasan, J., 1967. Nonrandom shortening of red cell survival times in men exposed to lead. Environ. Res. 1, 247 —261. [Pg.629]

Other findings suggestive of increased hemolysis are an elevated stercobilinogen content of the stool, reticulocytosis, lack or deficiency of serum haptoglobin, and erythroid hyperplasia of the bone marrow (Sobrevilla et al. 1964 Wolff et al. 1965). In contrast to the latter finding, Mier et al. (1960) saw significant reduction of erythropoesis, suggestive of hypoplastic anemia. Red cell survival, as measured with Cr, was found to be shortened in three cases so studied (Mier et al. 1960 Druez 1959 Ways et al. 1963). In the case of Ways et al. (1963) the half-life of red cells was approximately 22 days (normal 26—27 days). [Pg.388]

Anemia is also an independent risk factor for progression of chronic renal failure. The anemia of CKD is, in most patients, normocytic and normochromic, and is due primarily to reduced production of erythropoietin (EPO) by the kidney (a presumed reflection of the reduction in functioning renal mass), low iron stores and shortened red cell survival. In 40%, it could be corrected by iron replacement. Early initiation of EPO therapy in patients with CKD and mild to moderate anemia significantly slowed down the progression of renal disease and delayed the need for renal replacement therapy. The target level of hemoglobin is llOg/1 [10],... [Pg.28]

Chromimn-51, a positron emitter, is used in research to study red cell survival. It is delivered as a solution of sodium chromate. Write the nuclear equation for the decay of Cr-51. [Pg.586]


See other pages where Red cell survival is mentioned: [Pg.732]    [Pg.1229]    [Pg.154]    [Pg.154]    [Pg.1381]    [Pg.373]    [Pg.130]    [Pg.599]    [Pg.1051]    [Pg.625]    [Pg.1184]    [Pg.1696]    [Pg.263]    [Pg.50]    [Pg.53]    [Pg.71]    [Pg.156]    [Pg.58]    [Pg.795]    [Pg.564]    [Pg.385]    [Pg.65]    [Pg.348]    [Pg.65]    [Pg.612]   
See also in sourсe #XX -- [ Pg.655 ]




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