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

Young chicks were fed diets deficient in proteins, iron, niacin or thiamin to study the effects on various parameters of mineral metabolism in the duodenal mucosa. None of the treatments affected mucosal alkaline phosphatase activity; however, a five-day deprivation of protein reduced the inorganic phosphate content of mucosal cell nuclei. Iron deficiency reduced mucosal Ca, Zn, Fe and phosphate content, while niacin deficiency decreased mucosal Ca and phosphate. Thiamin deficiency reduced only the phosphate centent of intestinal mucosa. Duodenal phosphatase activity was positively correlated with tissue Ca and Fe and negatively with Zn.
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PMID:Relationship of dietary protein, iron, niacin or thiamin to intestinal mineral metabolism. 60 17

The onset of postpolycythemic myeoloid metaplasia or spent polycythemia has been recognized for many years. As the result of many different series, the development of postpolycythemic myeolid metaplasia might be expected in from 15%-20% of patients with postpolycythemia vera. It appears that an etiologic role for sodium phosphate 32P may exist in this evolutionary pattern. About 70% of patients with PPMM will have symptoms with the onset of the syndrome. The major mechanisms producing symptoms result from (1) anemia, (2) pressure from massive splenomegaly, and (3) bleeding problems. Iron deficiency is a frequent cause of anemia in patients with PPMM. The major mechanism of anemia in these patients, however, relates to ineffective erythropoiesis and shortened red cell survival. Androgen trials for ineffective erythropoiesis seem worthwhile, although data on this point is too limited to draw any firm conclusions. A steroid trial for those patients with major hemolytic episodes is indicated. In those patients in whom adrenal steroid therapy fails to control major hemolysis, a consideration for splenectomy exists. Pressure-related manifestations secondary to massive splenomegaly have been treated with radiation therapy and oral alkylators. Although there is data to document amelioration of painful symptoms with associated shrinking of the spleen, long-term control of this problem has not been forthcoming. Again, patients who are medical failures in control of pressure-related manifestations may be considered for splenectomy. Bleeding problems may arise with PPMM secondary to thrombocytopenia, thrombocythemia, or qualitative platelet dysfunction. Adrenal steroids have met with some success in improving platelet counts in patients with life-threatening thrombocytopenia. Those patients who are medical failures with adrenal steroids in terms of thrombocytopenia might be candidates for splenectomy. Control of thrombocythemia has been observed with oral alkylator therapy and chlorambucil may have a special role in managing this complication. Qualitative platelet defects leading to severe bleeding are best managed with fresh platelet transfusions. Patients with PPMM in contrast to patients with agnogenic myeoloid metaplasia have a more lethal syndrome and shortened survivorship. Causes of death in patients with PPMM include cardiac problems, transition to acute leukemia, hemorrhage, and infection.
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PMID:The evolution into and the treatment of late stage polycythemia vera. 125 Dec 24

A modified silver stain is described for the demonstration of ringed sideroblasts in bone marrow. It is more sensitive than Perls' reaction for that purpose, especially when iron stores of marrow are low or absent. Ringed sideroblasts may still be demonstrable by silver stain in cases of sideroblastic anemia without ringed sideroblasts, for which severe iron deficiency prevents detection of the abnormal sideroblasts by Perls' reaction. As iron has been reported to be present in mitochondria of ringed sideroblasts in the form of ferric phosphate, it is possible that the silver stain demonstrates the phosphate moiety and not the iron, thus explaining its greater sensitivity in iron deficiency as compared to Perls' reaction. Further study is necessary to confirm the staining mechanism, to elucidate the composition of iron deposits, and to explain the pathophysiology of sideroblastic anemia.
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PMID:Silver stain for ringed sideroblasts. A sensitive method that differs from Perls' reaction in mechanism and clinical application. 169 93

Anaerobic threshold (AT) has been advocated as an objective method of evaluating exercise capacity in patients with chronic congestive heart failure. The factors that determine AT, however, remain still unclear. To assess the influence of oxygen transport capacity on AT, patients with iron deficiency anemia were studied before and after treatment with iron. Twenty-nine female subjects were studied. They were divided into the following 3 groups: 1) iron deficiency anemia (group IDA: Hgb less than 11 g/dl and ferritin less than 10 ng/ml) consisting of 4 athletes and 6 non-athletes, 2) latent iron deficiency (group Lat-ID: Hgb greater than or equal to 11 g/dl and ferritin less than 10 ng/ml) consisting of 4 athletes, and normal (group Nor: Hgb greater than or equal to 11 g/dl and ferritin greater than or equal to 10 ng/ml) consisting of 15 athletes and 6 non-athletes. By bicycle ergometer using ramp protocol, peak oxygen uptake (peak VO2) and AT were measured in each group. Following the 1st exercise testing, groups IDA and Lat-ID were treated by oral iron for 1-1.5 months. The 2nd exercise testing was then performed. Furthermore, to investigate whether muscle cell energy metabolism itself is altered by iron deficiency, P magnetic resonance spectroscopy (MRS) was performed in 2 relatively severe anemic patients during forearm exercise while assessing the changes in phosphocreatine and inorganic phosphate. Peak VO2 and AT in non-athletes were significantly lower in IDA group than Nor group (peak VO2 (ml/min/kg): 23.7 +/- 5.1 vs 33.3 +/- 3.8, p less than 0.01, AT (ml/min/kg): 15.9 +/- 3.3 vs 21.3 +/- 1.3, p less than 0.01). After iron administration, Hgb was increased significantly in IDA group (from 9.0 +/- 1.8 to 12.1 +/- 0.8 g/dl, p less than 0.01) accompanied by an improvement in peak VO2 and AT (peak VO2 (ml/min/kg): from 34.2 +/- 12.4 to 40.0 + 13.0, p less than 0.001, AT (ml/min/kg): from 20.9 +/- 6.3 to 25.0 +/- 8.0, p less than 0.001). Lat-ID and Nor groups showed no changes. MRS indices of cell energy metabolism of the 2 severely anemic patients did not differ from those of normal controls, and no changes were observed after iron treatment. It is concluded from these results in iron deficiency anemia that oxygen transport is a determinant of anaerobic threshold.
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PMID:[Effect of blood hemoglobin concentration on anaerobic threshold]. 191 24

Adult rats raised on 90% iron deficient diet for 6 weeks showed a decrease in the levels of brain phosphatidylinositol (60%), phosphatidylinositol 4-phosphate (25%) and phosphatidylinositol 4,5-bisphosphate (30%), the precursors for the second messengers, diacylglycerol and inositol phosphates. Rehabilitation to normal diet for 24 days was found to restore the levels to control values. The data suggests that iron deficiency could lead to alterations in the functions related to phosphoinositide-linked receptor system(s).
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PMID:Effect of iron deficiency on phosphoinositide levels in rat brain. 217 35

Therapy with recombinant human erythropoietin (rHuEPO) can reverse anemia and improve the quality of life in anemic hemodialysis patients. However, therapy is costly and must be used efficiently. An initial rHuEPO dose less than 50 U/kg intravenously three times weekly may be adequate to achieve a hematocrit of 30-33% in many patients. Acquired iron deficiency is a common problem during rHuEPO therapy and must be prevented with oral and parenteral iron replacement to maintain the efficacy of rHuEPO. Patients should be monitored carefully for additional problems including: an increase in blood pressure; onset of seizures or headaches; increased blood potassium, phosphate, and creatinine concentrations; enhanced coagulability resulting in dialyzer and vascular access clotting; and myalgias with a 'flu-like' syndrome.
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PMID:Practical approach to initiation of recombinant human erythropoietin therapy and prevention and management of adverse effects. 226 Jun 19

Four groups of weanling male rats were fed one of three iron-deficient diets (6, 18 and 23 mg iron/kg diet) or a normal iron-containing diet (41 mg iron/kg diet) for 30 d. The effects of the diets on various iron status parameters were determined and four enzymes were assayed: cytochrome P450 (P450) and NADPH cytochrome P450 reductase (P450-RED) in liver and intestine microsomes, and glucose-6-phosphate dehydrogenase (G6P-DH) and 6-phosphogluconate dehydrogenase (6PG-DH) in liver, intestine and erythrocyte cytosol. Rats fed 6 mg iron/kg diet were severely anemic, whereas rats fed 18 or 23 mg iron/kg diet were moderately or mildly iron-deficient, as shown by their hemoglobin levels, hematocrit, red blood cell parameters, erythrocyte protoporphyrin and liver iron stores. P450 concentration and P450-RED activity in liver were unaffected by iron deficiency, but P450 concentration was markedly lower in the intestine of the three iron-deficient groups than in the controls. Activities of G6P-DH and 6PG-DH were not impaired in liver or intestine, except that liver 6PG-DH activity of severely anemic rats was less than that of control rats. However, severe and moderate iron deprivation resulted in a stimulation of G6P-DH and 6PG-DH activities per million erythrocytes. These results demonstrate that even moderate iron deficiency may alter fundamental enzymatic systems intervening in drug metabolism and in the pentose phosphate pathway.
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PMID:Effects of different degrees of iron deficiency on cytochrome P450 complex and pentose phosphate pathway dehydrogenases in the rat. 249 36

Young rats maintained on an iron-deficient diet developed severe anemia and had large decreases in the levels of the iron-containing flavoproteins and cytochromes of the mitochondrial respiratory chain in skeletal muscle. In contrast, the levels of a number of mitochondrial matrix marker enzymes, including citrate synthase, isocitrate dehydrogenase, 3-hydroxyacyl-CoA dehydrogenase, 3-ketoacid-CoA transferase, and aspartate aminotransferase, increased in red skeletal muscle but not in white muscle. Phosphocreatine concentration was decreased and inorganic phosphate concentration was increased in soleus muscle frozen in situ. We hypothesize that the increase in mitochondrial matrix enzymes reflects a stimulus to mitochondrial biogenesis in posture-maintaining and weight-bearing red muscle fibers in severely iron-deficient rats. It is our working hypothesis that this stimulus to mitochondrial biogenesis arises from mild activity of the red fibers and is due to the same perturbation in cellular homeostasis that is normally caused by vigorous exercise or hypoxia. In iron deficiency, the stimulus to mitochondrial biogenesis can induce an increase in only those enzymes not prevented from increasing by iron deficiency, resulting in formation of mitochondria of grossly abnormal composition.
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PMID:Induction of an increase in mitochondrial matrix enzymes in muscle of iron-deficient rats. 347 8

Cultures of Streptomyces griseus grown under phosphate-limiting conditions produced a complex of green products. Three of these were separated from the mixture and characterized. One was identified as viridomycin A, the ferrous chelate of 4-hydroxy-3-nitrosobenzaldehyde; the second (actinoviridin A) was the corresponding carboxylic acid chelate and the third (viridomycin E) was a hybrid chelate containing both the aldehyde and acid ligands. Only two out of nine strains of S. griseus examined produced viridomycins and the ligands were biosynthesized only in media from which phosphate had been exhausted. Optimization of the production medium showed that fructose and alanine were the most favorable carbon and nitrogen sources and that relatively high concentrations of ferrous ions were necessary. The results suggest that viridomycins are not produced by S. griseus as iron scavengers in response to iron deficiency but as secondary metabolites that are stabilized adventitiously in the broth by metal ion chelation.
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PMID:Characterization of new viridomycins and requirements for production in cultures of Streptomyces griseus. 368 25

The effects of chronic iron deficiency anemia on brain (cortex) metabolism were estimated by 31P-nuclear magnetic resonance spectroscopy and biochemical analyses in male Wistar rats. Iron deficiency anemia was induced by supplying diet containing either approximately 2 or approximately 6 ppm Fe. Control diet was supplemented with 100 ppm Fe as ferric citrate. After 8-9 weeks, blood hemoglobin levels were approximately 13, 5, and 3 g/100 ml in the 100 ppm, 6 ppm, and 2 ppm Fe group, respectively. The blood lactate levels at rest in these groups were approximately 3, 5, and 6 mM. The blood glucose concentration also tended to be elevated in iron-deficient rats. The high-energy phosphate contents in brain were not affected by iron deficiency. The activities of succinate dehydrogenase and cytochrome oxidase per unit protein in the 2 ppm Fe group were significantly less than in the 100 ppm Fe group, but those activities were not significantly affected by feeding diet with 6 ppm Fe. The activities of lactate dehydrogenase in iron-deficient group tended to be elevated but not significantly. The activities of non-iron containing mitochondrial enzymes, citrate synthase and beta-hydroxyacyl CoA dehydrogenase, were unchanged. It is suggested that the brain has a higher tolerance to iron deficiency than skeletal muscle in terms of the metabolic characteristics, although this may be associated with a lower level of neural activity.
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PMID:Effects of chronic iron deficiency anemia on brain metabolism. 756 62


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