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

Iron is an essential trace element. In its heme-form as well as in its non heme-form it is a part of enzymes and hemoproteins. For a safe and adequate dietary intake 10-18 mg of iron are recommended daily. Frequently, this quantity is not available: approximately 20% of the world population is iron-deficient. In this state the enteral transfer capacity for toxic metals, e.g., Cd and Pb, is increased and the adaptation to physical strain as well as the immunological responses are depressed. Alterations of body iron-stores are almost exclusively balanced by adequate adaptation of the enteral iron-transfer capacity. The mechanism of this adaptation process can neither be satisfactorily explained by the "mucosal block hypothesis", nor by the "mucosal transferrin hypothesis". When the time-course of iron storage and its relation to intestinal iron transfer was investigated after i.v. iron administration to iron-deficient rats, the results indicated that the process of adaptation is located in the intestinal mucosa. Intestinal iron loading is decreased in iron deficiency, whereas the iron transfer into the organism is increased. Further investigation is necessary to find out by which mechanism the iron manages to bypass existing mucosal storage capacity in this situation. The geographical distribution of iron deficiency is influenced by a variety of local factors. Still, the paramount causes of iron-deficiency are unbalanced iron losses and the lack of bioavailable iron in the diet. The bioavailability of non heme iron is influenced by the composition of the diet. The effect of promotors of iron absorption, such as meat, amino acids, polycarbonic acids and ascorbate is opposed by the influence of inhibitors, such as bran, soya products, vegetables and egg-dishes. Iron losses are mainly due to blood losses. Thus, the wide distribution of hookworm diseases in tropical areas contributes significantly to the endemic iron-deficiency in these regions. A more physiological loss of iron is caused by menstruation and pregnancy. In small infants the iron-demand of the organism is increased by rapid growth, which in turn increases the intestinal iron transfer. An increased iron-demand can be balanced by an iron-supplemented diet or by pharmaceutical iron compounds. Acute intoxications can be caused by an overdose of such preparations. The pathophysiology and symptoms of acute iron intoxication are summarized. Their frequency has markedly decreased since "childproof" packaging has been introduced for iron-preparations. To meet the increased iron demand of young children, commercial infant formulas are frequently fortified with iron, preferentially with heme-iron.(ABSTRACT TRUNCATED AT 400 WORDS)
Z Ernahrungswiss 1989 Dec
PMID:[The role of iron as a deficient element]. 269 40

Cognitive function. There is reasonably good evidence that mental and motor developmental test scores are lower among infants with iron deficiency anemia. Although the research on cognitive function in iron deficient older children and adults is sparse and diverse, it suggests that there may be alterations in attentional processes associated with iron deficiency. Iron therapy has not yet been shown effective in completely correcting many of the observed disturbances. Although some aspects of cognitive function seem to change with iron therapy, lower developmental. I.Q., and achievement test scores have still been noted after treatment. The behavioral effects of iron-deficiency anemia may be due to changes in neurotransmission. However, the biochemical bases are not yet completely understood. Noncognitive disturbances. A variety of noncognitive alterations during infant developmental testing has also been observed, including failure to respond to test stimuli, short attention span, unhappiness, increased fearfulness, withdrawal from the examiner, and increased body tension. Exploratory analyses suggest that such behavioral abnormalities may account for poor developmental test performance in infants with iron deficiency anemia. These studies indicate the fruitfulness of examining noncognitive aspects of behavior such as affect, attention, and activity, in addition to specific cognitive processes. Activity and work capacity: There has been a steady accumulation of evidence that iron-deficiency anemia limits maximal physical performance, submaximal endurance, and spontaneous activity in the adult, resulting in diminished work productivity with attendant economic losses. The relative importance of central and peripheral mechanisms underlying these effects, the extent to which anemia or iron deficiency separate from anemia is responsible, and the counterpart in infants and children remain to be established. This essay has examined recent evidence from research on central nervous system biochemistry and from human studies that iron deficiency adversely affects behavior by impairing cognitive function, producing noncognitive disturbances, and limiting activity and work capacity. The body of research taken as a whole provides increasingly persuasive arguments for intensifying efforts to prevent and treat iron deficiency anemia.
Bull N Y Acad Med 1989 Dec
PMID:Iron and learning potential in childhood. 269 45

Protein and fat deficiency diet produced significant reduction of Giardia cysts in rats, while vitamin A, D and iron deficiency diet had no effect on cyst count. On the other hand pathological changes due to Giardia infection encountered in small intestine and liver were aggravated by the diet deficiency induced.
J Egypt Soc Parasitol 1989 Dec
PMID:Effect of diet on experimental giardiasis. 276 61

Most of the previous studies on the effects of iron deficiency on skeletal muscle respiratory capacity and work performance have been investigated in severe or moderate iron-deficiency anemia. We report here that even in mild iron deficiency where the hemoglobin concentration was 10 g/dl and the iron stores in livers and spleen were not completely depleted, a marked reduction in succinate dehydrogenase was observed in skeletal muscles but not in heart. Similarly, cytochrome oxidase activities were reduced. Although no significant change in glycerophosphate dehydrogenase was detected in the iron-deficient rats, exposure to cold in this group greatly reduced this enzyme activity. As cold acclimatization accelerates marrow erythropoiesis (20) which in turn, demands more iron, it seems that in the iron-insufficient state, this iron demand for marrow activity may persist at the expense of the tissue iron pool, resulting in a marked reduction in glycerophosphate dehydrogenase activities. Since succinate dehydrogenase plays a significant role in the impairment of mitochondrial function and early fatigue of iron-deficient muscle (11), the present study shows that even in mild iron deficiency, some loss of muscle functions could result as succinate dehydrogenase activities were greatly reduced.
Biochem Med 1985 Dec
PMID:Biochemical effects of mild iron deficiency and cold acclimatization on rat skeletal muscle. 300 73

The overwhelming majority of nutritional deficiencies that affect the bone marrow and blood are due to the lack of vitamin B12, folic acid, or iron or combinations thereof. The two vitamins are closely related in DNA synthesis, whereas iron is the most abundant heavy metal in the body and is chiefly utilized for hemoglobin synthesis. Concomitant conditions of vitamin B12 and/or folate deficiency along with iron deficiency are not infrequent, and one type of anemia may mask the other. It is important to establish the correct diagnoses, as therapy directed at the wrong deficiency may hide the real deficiency with disastrous results. Specific diagnostic tests are now available to determine definitive diagnoses, and specific therapy is readily available to restore and maintain a normal nutrient status.
Hematol Oncol Clin North Am 1988 Dec
PMID:The bone marrow in nutritional deficiencies. 306 18

A number of nutritional complications occur after total gastrectomy, such as protein malnutrition, dumping syndrome, diarrhoea, weight loss, iron deficiency and osteomalacia. Lack of appetite, absence of the sensation of hunger, oesophagitis, dysphagia and the limited capacity for food in most cases are the causes of suboptimal dietary intake after total gastrectomy. To avoid underweight and symptoms after gastrectomy it is necessary that all patients are seen soon after operation and at regular intervals thereafter not only by physicians but by dietitians additionally.
Leber Magen Darm 1987 Dec
PMID:[Dietary treatment following gastrectomy]. 332 49

A significant proportion of the world's population suffers from iron deficiency or iron overload. These disorders arise primarily from defects in the gastrointestinal absorption of iron. The intestinal mucosal cell plays a key role in this process because it lies at the interface between the gastrointestinal lumen which supplies its iron and body compartments which control its behaviour. The concentration of mucosal ferritin is closely linked to absorption, but it is still not clear whether it plays an active or a passive role. Transferrin also has been detected in the mucosal cell, but firm evidence that it participates in the absorptive process is lacking. Deficiencies in the luminal phase are responsible for the high global prevalence of iron deficiency which is predominantly dietary in origin. Much information has accumulated in recent years on dietary factors that enhance or impair iron absorption but their quantitative importance as determinants of iron status remains to be determined.
Blood Rev 1987 Dec
PMID:Intestinal regulation of body iron. 333 11

Healthy term infants were given a low-fat powdered milk fortified with 15 mg/100g of iron, as ferrous sulphate, for one year, starting at three months of age. The control group received non-fortified milk. A total of 510 infants entered the study, and 314 could be studied at the age of 15 months. Consumption of the fortified formulas was monitored through iron determinations in stools. Groups had a comparable hemoglobin concentration at the age of three months. Hemoglobin was higher in the fortified group at nine months (11.7 +/- 1.0 vs 11.4 +/- 1.1 g/dl, p less than 0.02), and 15 months (12.0 +/- 1.1 vs 11.4 +/- 1.2, p less than 0.001). The percentage of subjects with anemia (Hb less than 11.0 g/dl) was lower in the fortified group: 14.8% vs 27.7% of the controls at nine months and 7.0% vs 35.3% at 15 months. Percentages of subjects with iron deficiency (Fe/TIBC less than 9%) were lower in the fortified group: 28.0% vs 49.1% of the controls at nine months, and 20.0% vs 41.8% at 15 months. Although the fortified milk markedly improved iron nutrition, deficiency of this mineral was still high in the group receiving it. This was probably due to the low bioavailability of iron when administered with non-modified milks.
Arch Latinoam Nutr 1986 Dec
PMID:[Prevention of iron deficiency in infants by fortified milk. Field study of a low-fat milk]. 343 15

In this report we rate a new, third-generation automated hematology system (Technicon Instruments H-1) that can furnish a full range of values, including erythrocyte parameters and a leukocyte differential count. Particular attention is focused on erythrocyte morphometric parameters, including measurement of cell size and hemoglobin content on a cell-by-cell basis. We assess the usefulness of new parameters derived from these measurements, such as mean corpuscular volume and red blood cell distribution width, which characterize cell size, and mean corpuscular hemoglobin concentration, and hemoglobin distribution width, which characterize cell hemoglobinization in evaluating normal and abnormal subjects. The value of these parameters in classifying anemias is assessed in our patient population that includes those with iron deficiency anemias and thalassemias, as well as other forms of anemia.
Arch Pathol Lab Med 1987 Dec
PMID:New parameters in erythrocyte counting. Value of histograms. 367 51

Concern for the concomitant occurrence of iron deficiency and elevated blood lead in children is raised by animal studies documenting increased gastrointestinal lead absorption in the presence of iron deficiency. An elevation in free erythrocyte protoporphyrin (FEP) above 35 mg/dl is seen with both iron deficiency and lead toxicity. To determine whether the degree of elevation in FEP is useful in predicting which children with elevated blood lead levels have concomitant iron deficiency, 109 children suspected of having an elevated lead burden were studied. A complete blood count, reticulocyte count, FEP, lead, and ferritin were measured on each child. The effect of the independent variables, lead and iron status, both alone and in combination, on the dependent variable, FEP, was analyzed through a linear regression model. Lead status alone accounted for 42 percent of the explained variance in FEP, and the lead-iron interaction increased the explained variance by only an additional 1 percent. Screening for iron deficiency in children with elevated blood lead should continue to be based on dietary and socioeconomic risk factors and not on degree of elevation in FEP.
Clin Pediatr (Phila) 1987 Dec
PMID:Combined iron deficiency and lead poisoning in children. Effect on FEP levels. 367 34


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