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

In order to examine the effects of mild iron deficiency on physical work capacity, 40 prelatent iron-deficient female endurance runners were studied before and after 8 wk of supplementation with either oral iron (320 mg ferrous sulfate) or a matching placebo. Subjects underwent the following physical work capacity tests: the Wingate cycle ergometer test, the anaerobic speed test, the ventilatory threshold, VO2max, and maximal treadmill velocity during the VO2max test. Muscle biopsy samples pre- and post-treatment were obtained from 17 of the subjects, and these were assayed for citrate synthase and cytoplasmic alpha-glycerophosphate dehydrogenase activity. Subjects were randomly assigned to one of the treatment groups, and a double-blind method of administration of the supplements was used. The differences in improvement scores between the two groups on the work capacity and enzyme activity variables were statistically nonsignificant (P greater than 0.05). Serum ferritin values rose from a mean of 12.4 +/- 4.5 to 37.7 +/- 19.7 ng.ml-1 for the experimental group and from 12.2 +/- 4.3 to 17.2 +/- 8.9 ng.ml-1 for the controls (P = 0.0025), whereas hemoglobin levels remained fairly constant for both groups (P = 0.6). Eight weeks of iron supplementation to prelatent/latent iron-deficient, physically active females did not significantly enhance work capacity. Within the limitations of this study, the presence of a serum ferritin below 20 ng.ml-1 does not pose a significant handicap to physical work capacity.
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PMID:The effects of prelatent/latent iron deficiency on physical work capacity. 273 74

Treatment with recombinant human erythropoietin (r-HuEPO; EPOGEN [epoetin alfa], AMGEN Inc, Thousand Oaks, CA) rapidly corrects the anemia associated with end-stage renal disease during the acute phase of therapy and supports hematocrit levels throughout the maintenance phase. However, during the acute phase of therapy, iron deficiency will develop in most patients; it is therefore initially essential to monitor body iron stores monthly. A plasma ferritin level of less than 30 ng/mL or a transferrin saturation level of less than 20% confirms the diagnosis of iron deficiency. Microcytic, hypochromic red cell morphology appears only after prolonged iron deficiency due to inadequate monitoring and insufficient iron supplementation; alternatively, microcytosis in the presence of adequate iron stores suggests aluminum toxicity. In all patients except those with transfusional iron overload, prophylactic supplementation with ferrous sulfate (325 mg up to three times daily) is recommended. When oral supplements, which are poorly tolerated at high doses, are insufficient to meet the extraordinary needs resulting from r-HuEPO-induced erythropoiesis, intravenous iron dextran (500 to 1,000 mg administered in five to ten doses) may be required. During the maintenance phase of therapy, it may be necessary to continue iron supplementation to counteract ongoing loss of iron associated with blood loss through dialyzers and gastrointestinal bleeding. At the other extreme of iron balance, iron overload in transfusion-dependent patients, recent studies suggest that the ability of r-HuEPO to mobilize iron stores can be harnessed with therapeutic phlebotomy to reverse transfusional iron overload.
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PMID:Iron management during recombinant human erythropoietin therapy. 275 26

Nutritional iron deficiency induced in rats causes a significant reduction in level of brain nonheme iron and is accompanied by selective reduction of dopamine D2 receptor Bmax. Our previous studies have clearly demonstrated that these alterations can be restored to normal by supplementation with ferrous sulfate; however, neither brain nonheme iron level nor dopamine D2 receptor Bmax can be increased beyond control values even after long-term iron therapy. The possibility that iron deficiency can induce the breakdown of the blood-brain barrier (BBB) was examined. A 70 and 100% increase in brain uptake index (BUI) for L-glucose and insulin, respectively, were noted in iron-deficient rats. However, the BUI for valine was decreased by 40%, and those for L-norepinephrine and glycine were unchanged. In addition, it was demonstrated that in normal rats insulin is transported into the brain. The data show that iron deficiency selectively affects the integrity of the BBB for insulin, glucose, and valine transport. Whether the effect of iron deficiency on the BBB is at the level of the capillary endothelial cell tight junction is not yet known. However, this study has shown that an important nutritional disorder (iron-deficiency anemia) has a profound effect on the BBB and brain function.
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PMID:Selective alteration in blood-brain barrier and insulin transport in iron-deficient rats. 296 35

Two patients with iron deficiency experienced rapid decreases in their platelet levels following initiation of replacement therapy with oral ferrous sulfate or ferrous gluconate. The first patient, whose pretreatment platelet count was 168,000 per mm3, developed marked thrombocytopenia (platelet count, 21,000 per mm3) on the sixth day of iron repletion. The second patient's platelet level fell from 725,000 to 105,000 per mm3 on the tenth day of therapy. In both instances, platelet levels gradually returned to normal levels. The data suggest that the administration of oral iron resulted in an acute reduction in platelet production. The mechanism(s), prevalence, and clinical significance of thrombocytopenia following iron repletion in patients with iron deficiency anemia remain unknown.
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PMID:Thrombocytopenia associated with repletion of iron in iron-deficiency anemia. 333 37

Iron-deficiency anemia impairs exercise capacity, but whether nonanemic iron depletion decreases endurance performance is unclear. In 14 iron-deficient (serum ferritin level, less than 20 micrograms/L [less than 20 ng/L])nonanemic runners, hematologic and treadmill running values were followed up during a competitive season. Following a four-week control period, runners were treated for one month in a double-blind protocol with ferrous sulfate (975 mg/d) or placebo. During treatment, the mean ferritin level rose from 8.7 to 26.6 micrograms/L (8.7 to 26.6 ng/mL) in those patients taking iron and fell from 10.6 to 8.6 micrograms/L (10.7 to 8.6 ng/mL) in the placebo group. Treadmill endurance times improved significantly in the iron-treated runners compared with controls. Endurance time declined in all seven controls (range, 0.07 to 1.30 minutes), while six of seven iron-treated subjects improved their performance (range, 0.03 to 1.92 minutes). No significant differences in maximal or submaximal oxygen consumption, ventilation, or heart rate were observed between the groups except for a 4% increase in maximum oxygen consumption during placebo treatment. These data indicate that nonanemic iron deficiency impairs exercise performance but does not influence gas exchange or cardiac measures.
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PMID:The effect of iron therapy on the exercise capacity of nonanemic iron-deficient adolescent runners. 334 17

Volunteers attending blood donor sessions who fail the copper sulfate screening test merit an explanation of why they are considered ineligible to donate. During a 30-month period, 0.24 percent of men and 2.8 percent of women attending blood donor sessions in the northern region of England failed this test. Their hematologic status was determined by performing complete blood counts on a venous blood specimen and measuring ferritin as an indication of iron stores in a representative sample of approximately 10 percent. Normal blood counts were found in some donors, while others had severe degrees of anemia, and such discrepancies could be clarified only by hemoglobin determinations. Iron deficiency was very common in deferred donors, including 36 of the 88 with normal blood counts in whom ferritin assays were performed. Microcytic blood cells, a hallmark of iron deficiency, were found to be a relatively insensitive measure of low iron stores, except at low levels of hemoglobin. By a check of a venous sample, the hematologic status of most volunteers failing the copper sulfate screening test can be ascertained, and appropriate review, investigation, and treatment can be undertaken.
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PMID:Volunteer blood donors who fail the copper sulfate screening test. What does failure mean, and what should be done? 342 Jun 76

Soy products have been reported to inhibit absorption of nonheme food iron and fortification iron. Iron bioavailability from a soy formula (Prosobee-PP 710) (iron added as ferrous sulfate: 12 mg/L; ascorbic acid: 54 mg/L) was examined in 16 adult women using the extrinsic radioactive tag method. The geometric mean absorption from the soy formula was only 1.7%. The effect of this formula on iron nutrition in infants was studied in 47 healthy term infants weaned spontaneously before 2 months of age and who received the formula ad libitum until 9 months of age. For control, 45 infants received a cow's milk formula fortified with ferrous sulfate (iron: 15 mg/L; ascorbic acid: 100 mg/L), which has been shown to be effective in preventing iron deficiency, and 49 additional breast-fed infants were also followed. All babies received solid foods (vegetables and meat) starting at 4 months of age. Iron nutritional status was determined at 9 months. Infants fed soy formula and iron-fortified cow's milk had similar mean values of hemoglobin, mean corpuscular volume, transferrin saturation, free erythrocyte protoporphyrin, and serum ferritin; both formula groups differed significantly (P less than .05) from the breast-fed group in all measurements except free erythrocyte protoporphyrin. Anemia (hemoglobin less than 11 g/dL) was present in only 4.3% and 2.2% of infants receiving the soy and the fortified formulas, respectively, v 27.3% in the breast-fed group. These results indicate that soy formula, in spite of the lower iron bioavailability when measured in adults, is essentially as effective as iron-fortified cow's milk in preventing iron deficiency in infants.
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PMID:Bioavailability of iron in soy-based formula and its effect on iron nutriture in infancy. 376 74

Phagocytosis and bactericidal capacity of neutrophils were measured in 10 iron-deficient infants age 6-23 mo. All infants had hemoglobins less than 11 mg/dL with low saturation of transferrin and serum ferritin but were otherwise in good health. Neutrophil function and iron status were assessed at 0, 3-5, 15, 30, and 90 days of oral iron therapy. Phagocytosis was unaffected in iron deficiency and remained unchanged during therapy. Bactericidal capacity was severely impaired prior to treatment. After 3-5 days of ferrous sulfate administration, there was no significant improvement. At day 15 it returned to normal ranges and remained so at days 30 and 90. The sequence of events suggests that iron does not have a direct effect upon circulating neutrophils but, rather, that it is required during the development of neutrophils in the bone marrow.
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PMID:Effect of iron therapy on phagocytosis and bactericidal activity in neutrophils of iron-deficient infants. 378 34

An evaluation was made of 278 healthy-appearing 1-year-old infants who were tested for iron deficiency to determine the relative frequency of adverse side effects attributable to oral iron treatment. After obtaining parental informed consent, laboratory tests of iron status were performed on venous blood and infants with hemoglobin level greater than 10.5 g/dL were randomly chosen to receive 1.2 mL of ferrous sulfate (FeSO4) drops (about 3 mg of iron per kilogram per day) or equal volume of placebo for 3 months. After 3 months of treatment, infants were to return to the clinic for repeat blood testing, compliance estimation, and evaluation for possible adverse side effects. There was no significant difference (P greater than .50) in the frequency of vomiting, diarrhea, or fussiness in iron-treated infants (6%) compared with placebo-treated infants (9%). Constipation was slightly more frequently reported (P = .03) in placebo-treated infants (9%) than in iron-treated infants (1%). Compliance with therapy was confirmed in 179 completely evaluated infants by the lack of remaining medication at 3 months, the higher incidence (P less than .0001) of dark stools reported among iron-treated infants, and the changes in laboratory tests of iron status. No parents reported dark stools as an adverse effect of therapy. It is concluded that once daily, moderate-dose FeSO4 therapy given to fasting 1-year-old infants results in no more gastrointestinal side effects than placebo therapy.
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PMID:Lack of adverse side effects of oral ferrous sulfate therapy in 1-year-old infants. 396 39

Iron supplements are commonly administered to infants in order to prevent iron deficiency. We wished to determine whether iron administration could compromise zinc nutrition as might be suspected from previous studies. Measures of iron nutrition, serum zinc, and serum copper were measured before and after randomization of 291 healthy 1-yr-old infants to a 3 mo course of placebo or iron treatment (30 mg iron as ferrous sulfate given before a meal). There was no significant difference in serum zinc or copper in the two groups before or after treatment; thus iron administration did not result in any evidence of zinc deficiency in a healthy, well-nourished group of T-yr-old infants.
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PMID:Does iron supplementation compromise zinc nutrition in healthy infants? 405 Jul 28


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