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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Shear stress is a potential cause of erythrocyte fragmentation and hemolysis in flowing blood. In this study, the response of abnormal human erythrocytes to shear stress in virto was evaluated using a concentric cylinder viscometer. Compared to normal red cells, deoxygenated erythrocytes from persons with sicle cell anemia were particularly susceptible to fragmentation and hemolysis by shear stress. Oxygenation of sicke cell blood improved the resistance of those red cells to shear stress; they remain, however, more susceptible to shear stress than normal erythrocytes. Erythrocytes from patients with iron deficiency, thalassemia minor, and erythrocyte pyruvate kinase deficiency showed fragmentation and hemolysis at threshold shear stresses intermediate between those ovserved for blood from patients with sickle cell anemia and normal persons. Blood samples from patients with hereditary spherocytosis were more resistant to shear stress than normal blood. These results indicate that there are important differences in the response of various red cells to shear stress.
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PMID:Fragility of abnormal erythrocytes evaluated by response to shear stress. 114 31

The basic ferritin level in red cells was examined in 60 healthy volunteers and in 110 patients with various diseases of the red cell series. From samples of heparinized whole blood first leucocytes were removed and then they were haemolyzed. After subsequent centrifuging in the supernatant the basic ferritin content was assessed by means of an Amersham Ferritin RIA kit (Amersham, Great Britain). Normal values in healthy volunteers varied between 3.2 and 30.2 ag/ery. In patients with iron deficiency the values were significantly reduced, in patients with pernicious anaemia, beta-thalassemia minor, hereditary spherocytosis and glucose-6-phosphate dehydrogenase deficiency or pyruvate kinase deficiency the levels of red cell ferritin were significantly elevated, as compared with the control group. The red cell ferritin level depends on the iron supply to cells of the red cell series and the amount needed for erythropoiesis. A reduced supply in sideropenia leads to a reduced level of red cell ferritin, in haemolytic anaemia its level depends on the generally elevated iron supply in the organism and possibly impaired haemoglobin synthesis, on the one hand, and concurrent elevated iron requirements in case of hyperplasia of red cell formation, on the other hand. Assessment of red cell ferritin is important not only for accurate estimation of the amount of iron available in the cell for haeme formation but also to elucidate the pathogenesis of some changes of iron metabolism in diseases of the red cell series.
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PMID:[The importance of determination of ferritin levels in erythrocytes]. 224 33

Iron overload has been reported with pyruvate kinase deficiency. Erythropoietin (EPO) may lead to iron deficiency; thus, patients who are unable to be phlebotomized due to anemia may benefit from EPO as a treatment of iron overload.
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PMID:Erythropoietin in the treatment of iron overload in a patient with hemolytic anemia and pyruvate kinase deficiency. 797 18

Possible causes for a normocytic hyperregeneratory anemia are beside an incomplete treatment of iron deficiency, vitamin B12 deficiency or folic acid deficiency notably a hemolysis. After exclusion of other causes of hemolysis like immune hemolytic anemias, microangiopathic hemolytic anemias and hemoglobinopathies, an enzyme deficiency of erythrocytes should be considered. By far the most common form worldwide is the Glucose-6-phosphate deficiency. In the most frequent variants of this disease hemolysis occurs only during stress, imposed for example by infection, "oxidative" drugs or after ingestion of fava beans. The most serious clinical complication of the Glucose-6-phosphate deficiency is the rarely observed neonatal icterus. Some enzyme variants can cause chronic hemolysis which is described as chronic nonsperocytic hemolytic anemia. This form of chronic anemia can also be caused by other enzyme deficiencies, most frequently by the Pyruvate kinase deficiency. All other deficiencies of glycolytic enzymes are even rarer. It should be noted that in some of these very rare forms neurological rather than hematological symptoms predominate the clinical syndrome. If there is suspicion, on the basis of clinical symptoms and/or familial history, diagnosis of an enzyme deficiency can be achieved relatively easy by measurement of the enzyme activity. Accurate diagnosis might be helpful in therapeutic decisions (e.g. splenectomy in certain forms) and it is essential for genetic counseling, since certain deficiencies are transmitted as autosomal recessive disorders (e.g. pyruvate kinase deficiency), while the most common form, the glucose-6-phosphate dehydrogenase deficiency is linked to the X-chromosome.
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PMID:[Hereditary enzyme defects of erythrocytes: glucose-6-phosphate dehydrogenase deficiency and pyruvate kinase deficiency]. 1645 Jul 34

No satisfactory explanation has been offered, to date, to account for the prevalence of the haemochromatosis genes in the European population and yet relative paucity of the gene in the tropics. Traditional wisdom suggests that, in antiquity, the haemochromatosis gene, which promotes iron absorption, would have protected ancient man from iron loss resulting from injury either during hunting or through war. However, such an advantage would be equally desirable for other populations where the incidence of the alleles is negligible. Others have tackled the polemic from the another view, postulating that the paucity of the haemochromatosis alleles in populations outside of Europe may be explained by the fact that iron load predisposes to infection and that iron deficiency anaemia is protective against this by limiting parasitic access to host stores of iron. This explanation alone is equally unsatisfactory as European populations are exposed to pathogens and would benefit from any protection afforded by mild anaemia. Others have mooted genetic drift as another alternative explanation. Yet this would be unexpected for a gene which is deleterious. We propose here that the driving force for the propagation of the haemochromatosis alleles was not infection per se but the nature of the parasitic fauna which sojourned with mankind. The tropics are inhabited with multicellular parasitic and highly pathogenic organisms, which consequently have a high demand for iron. The organisms have developed aggressive means of iron extraction from their hosts. Where there is iron in abundance such organisms would have a licence to multiply in an unbridled fashion at the expense of the host. Such a host, due to their increased iron load, would be able to harbour a high parasitic load which would be harmful to the population as a whole, not just the individual with the haemochromatosis allele. As man migrated from the tropics many of the larger pathogens disappeared and man had only to contend with traditional unicellular adversaries. Iron is a critical micronutrient that the host attempts to withhold for invading pathogens. We also advance the theory that the tropical anaemias including sickle cell trait, thalassaemia, glucose-6-phosphate dehydrogenase deficiency, and pyruvate kinase deficiency are an ingenious evolutionary means by the host of withholding iron from tropical pathogens while simultaneously avoiding the deleterious effects of frank iron deficiency and/or iron deficiency anaemia. The mechanism is essentially an immunological passive aggressive orchestrated by man kind.
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PMID:The distribution of the parasitic fauna dictates the distribution of the haemochromatosis genes. 2070 39