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At least 19 recordsLinked to original sources
PubMed1977

[Frequency of iron deficiency and iron deficiency anaemia in infancy and childhood (author's transl)].

266 children with iron deficiency were treated over a period of 2 years. The incidence rate and age distribution did not deviate much compared with former results. A different incidence of iron deficiency was found when 120 healthy children from 2 socially and economically different groups were examined. In both groups together the incidence rate of iron deficiency was 19%. But while in the socially higher standing group only 5% were afflicted, the other group showed 33%. This difference questions the value of generally iron medication and favours the opinion that iron deficiency indicates that children have not been looked after properly.

Adolescent↗
PubMed1978

Ferritin in bone marrow and serum in iron deficiency and iron overload.

Nonheme iron and ferritin in the bone marrow and serum ferritin was investigated in patients with iron deficiency anaemia or iron overload. As controls served patients without any disturbance of the iron metabolism. There is a precise correlation between the nonheme iron and ferritin in the bone marrow of patients with and without disturbance of iron metabolism. A correlation was also found between the ferritin in the bone marrow and the serum. Nonheme iron and ferritin in the bone marrow and serum ferritin was decreased in patients with iron deficiency anaemia. Conversely, the same parameters were increased in patients with iron overload.

Anemia, Hypochromic↗
PubMed1979

Transferrin binding and iron transport in iron-deficient and iron-replete rat reticulocytes.

Three aspects of iron metabolism were studies in reticulocytes from iron-deficient, phlebotomized, and phenylhydrazine-treated rats: (1) the number of transferrin binding sites; (2) the uptake of 59Fe-transferrin; and (3) the ability of cytosol to mobilize 59Fe from 59Fe-labeled reticulocyte plasma membrane. The number of transferrin binding sites, assayed by measuring the binding of 125I-labeled transferrin to reticulocytes, were similar in iron-deficient and phlebotomy-induced reticulocytes, 66,000 and 75,000 binding sites/cell, respectively, but were about doubled, 120,000 binding sites/cell, in phenylhydrazine-induced reticulocytes. Uptake of 59Fe into iron-deficient reticulocytes was about one-half that for phlebotomy-induced reticulocytes and one-quarter that for phenylhydrazine-induced reticulocytes, the rates of uptake being measured as 21,540, 41,233, and 79,600 molecules of 59Fe per minute per cell, respectively. The mobilizing activity of cytosol free iron-deficient reticulocytes was also about one-half that of cytosol from phlebotomy-induced reticulocytes and about one-quarter that of cytosol from phenylhydrazine-induced reticulocytes. These results indicate that instead of a compensatory increase in these aspects of iron metabolism, the iron-deficient reticulocyte had a decreased ability to transport iron.

Anemia, Hypochromic↗
PubMed1975

Utilization of dietary calcium by iron-deficient rats.

Iron deficiency causes cytological and enzymic changes in the gastrointestinal mucosa of animals and man that can be expected to impair the digestion and absorption of other nutrients. In experiment 1, healthy, weanling, female rats were grouped into pair-mates and pair-fed either an iron-deficient or an iron-supplemented diet for 19 weeks. In experiment 2, iron-deficient offspring reared by iron-deficient females were grouped into pair-mates and pair-fed either an iron-deficient or an iron-supplemented diet for 15 weeks. In experiment 1, apparent absorption of calcium was significantly depressed in week 9 (p less than 0.001) and slightly depressed in weeks 10 and 11. In experiment 2, the apparent absorption of calcium was significantly (p less than 0.001) depressed in weeks 6, 13, and 14. Absorption was not measured in other weeks in these experiments. The concentrations of calcium and magnesium were consistently higher in the fecal dry matter of the iron deficient rats in both experiments. It was concluded that any defects in digestion and absorption by the iron-deficient rats was confined primarily to the mineral nutrients because in both experiments apparent absorption of dry matter was consistently higher in these animals compared to their iron-supplemented pair-mates.

Animals↗
PubMed1979

Lactic acidosis as a result of iron deficiency.

Iron-deficient rats have an impaired work performance, even when their anemia is corrected by exchange transfusion. Muscle activity is associated with a higher blood lactate concentration than is observed in iron-replete animals. The accumulation of lactate is a result of excessive production as lactate clearance from the blood was shown to be unaffected. By adjusting the work load to a lower level, it was possible to divide iron-deficient animals into two groups, one capable of continued treadmill running and another in which animals stopped before 20 min. In the former, blood lactate concentration reached a plateau at moderate levels, whereas it continued to increase in the latter until the animal stopped running. Levels of alpha-glycerophosphate oxidase in skeletal muscle mitochondria were found to be much lower in the second group (P < 0.001). Lactate infusion into normal animals was shown to interfere with work performance, and maintenance of a normal pH in iron-deficient and iron-replete animals did not prevent the impairment in work associated with high blood lactate concentrations. Additional evidence was obtained that energy substrate (blood glucose and free fatty acids, muscle glycogen) was adequate in irondeficient animals. Oxygen tension in their vena caval blood was higher than in controls. Furthermore, the in situ behavior of electrically stimulated gastroenemius and soleus muscles appeared similar to that of control animals. Because the stimulation of the single muscle in the iron-deficient animal did not result in appreciable elevation of blood lactate and did not show impaired contractility further supported the hypothesis that the elevation of blood lactate caused the decreased work performance. It is concluded that iron deficiency by a depletion in the iron-containing mitochondrial enzyme, alpha-glycerophosphate oxidase, impairs glycolysis, resulting in excess lactate formation, which at high levels leads to cessation of physical activity.

Acidosis↗
PubMed1978

[The treatment of anemia due to iron-deficiency with iron combined with vitamins (author's transl)].

The effect of combined iron-vitamin therapy and iron therapy only was studied in 14 respectively 14 children with hypochromic anemia. Pyridoxalphosphate in serum, activity of red cell glutamic oxaloacetic transaminase and excretion of 4-pyridoxic acid were measured as indices of vitamin B6 nutriture before therapy was started, four and seven days under therapy once more. Erythrocytes, reticulocytes, concentration of hemoglobin were simultaneously counted, whereas serum iron and transferrin have been measured before and after therapy. A group of 22 hematologically healthy children was studied as controls. After iron therapy a decrease of vitamin B6 body pool came off as a consequence of increased requirement of pyridoxalphosphate for heme synthesis. Additional dosage of vitamins compensated the biochemical B6 deficit and had an accelerating effect on heme synthesis.

Anemia, Hypochromic↗
PubMed1979

Catecholamine elevation in iron deficiency.

Iron-deficient rats have increased blood and urinary catecholamines regardless of whether anemia is or is not present. The catecholamine response in both iron-deficient and control animals is largely temperature dependent, showing little difference at the isothermic temperature of 30 degrees C but a two- to threefold increase in iron-deficient animals over controls at lower temperatures. The iron-deficient rat is unable to maintain body temperature at 4 degrees C and this is independent of anemia or of food intake. When animals are run on the treadmill for 4 h, body temperatures increase but the difference observed at 4 degrees C between iron-deficient and control animals persists. The underlying abnormality in temperature regulation and in catecholamine response disappeared after 6 days of iron therapy.

Animals↗
PubMed1977

Iron-deficiency anaemia in pregnancy: (biochemical investigations of iron-deficiency and nutritional status).

Biochemical investigations on iron deficiency and nutritional status were carried out in a group of 130 women in the second or third trimesters of pregnancy and in 42 control non-pregnant women. The important findings were: 1. Anaemia was present in 46.1% of pregnant women in comparison with 19% in non-pregnant women. It was found to be more prevalent in the third trimester of pregnancy. 2. Iron deficiency with and without anaemia, as judged from serum transferrin saturation (%) was evident in 59.2% of pregnant women with an incidence of 70.3% in the third trimester of pregnancy. 3. Serum albumin, gamma globulin and A/G ratio were found to be decreased in pregnancy whereas serum levels of alpha-2 and beta globulins were elevated. The results have been discussed.

Adult↗
PubMed1979

[Serum ferritin and cytochemical storage iron in erythropoiesis and the R.E.S. in iron deficiency and faulty iron metabolism].

In 60 patients with iron deficiency anemia of chronic disorders serum iron, an iron absorption test, serum transferrin, serumferritin and stainable non-heme iron in erythropoiesis and reticuloendothelial system, were evaluated. Intercorrelations of these parameters were studied in different diagnostic groups. Pathogenetic principles and the clinical value of the applied diagnostic methods are discussed.

Adult↗
PubMed1976

Posthaemorrhagic iron deficiency. Clinical course, 59Fe whole-body iron losses, and oral iron supplementation.

Clinical and laboratory data characterizing post-haemorrhagic anaemia with still normal iron stores and posthaemorrhagic iron deficiency in the manifest, latent or prelatent stage are presented. Initially, increased 59Fe whole-body iron losses (greater than 0.1-3.6%/day) returned to normal range (less than 0.1%/day) after haemostasis. Subsequently, slow increase of haemoglobin and repletion of iron stores occurred under normal diets. Manifest, latent, and prelatent iron deficiencies were corrected much more rapidly by total doses of 12.0, 10.5 and 8.0 g iron (Fe2+ sulfate), respectively, when 2 X 50 mg/day were given in quick-release capsules apart from meals.

Adult↗