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

The protoporphyrinemia of iron deficiency is well recognized. Clinically, information on the protoporphyrin/heme molar ratio in whole blood offers certain advantages over protoporphyrin measurement alone. A procedure for determining this ratio is reported. Protoporphyrin is extracted, solubilized, and measured fluorometrically. Heme (as hemin chloride) is precipitated with the blood proteins, the precipitate is dissolved in an alkaline/pyridine solvent, and the resulting bispyridine ferriprotoporphyrin is measured spectrophotometrically. The molar ratio of these two metabolites correlates well with values for plasma ferritin, plasma iron, transferrin saturation, hemoglobin, and hematocrit. In some cases the ratio increases detectably while the other variables, especially hematocrit and hemoglobin, remain normal. Evidently it is a more sensitive index to iron status. For healthy men and women, the mean ratio is 16.0 (SD, 5.3). The mean + 3 SD, or a ratio of 32, is distinctly abnormal, as shown by a confirmatory test. We validated the test by surveying routine blood specimens obtained from several population groups.
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PMID:Erythrocyte protoporphyrin/heme ratio in the assessment of iron status. 76 86

The currently accepted concept of iron absorption proposes first the entry of iron into the intestinal mucosal cell through the brush border membrane. It is a relatively slow process. In the cell, the iron may be transferred to plasma or become sequestered by ferritin. The latter becomes unavailable for transfer to plasma and is exfoliated and excreted. In iron deficiency and idiopathic hemochromatosis, the rate of iron uptake into the intestinal mucosal cell is increased and entry into ferritin is decreased, whereas the rate of transfer to plasma remains constant. The reverse occurs in case of secondary iron overload. It is currently accepted that a transferrin, whose levels increase in iron deficiency, enters the intestinal lumen from the liver via bile, where it may sequester iron and bring it into the cells by the process of endocytosis. Iron presented as inorganic ferric or ferrous salts may also be absorbed, though the more soluble ferrous salts are adsorbed much more rapidly. Heme iron is absorbed very effectively, though it is not subject to regulation by the individual's iron status to the same extent as is inorganic iron absorption. Brush border membranes apparently contain saturable iron receptors for inorganic iron, but whether or not the absorption process requires energy is an open question. Absorption of iron may also be affected by its availability; different food components affect iron absorbability to a different extent.
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PMID:Biochemistry of nonheme iron in man. II. Absorption of iron. 266 38

We sought to determine whether chloramphenicol would worsen or mitigate the anemia associated with Haemophilus influenzae type b meningitis if administered in doses which produce 'therapeutic' serum concentrations. Seventy-four cases of H. influenzae meningitis were stratified by chloramphenicol cumulative doses (mg/kg body weight) of less than 300 and greater than 300. There was no significant difference in the decrease in blood hemoglobin concentration or in the increase in the FEP:Heme ratio between the two study groups. Plasma iron and transferrin saturation values indicated iron deficiency at days 1 and 5 of hospitalization; by day 10 mean values were within the normal range. These data suggest that H. influenzae type b meningitis, not chloramphenicol therapy in the presence of monitoring is causing the observed anemia.
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PMID:Anemia during Haemophilus influenzae type b meningitis: lack of an effect of chloramphenicol. 276 22

Hemoglobin and myoglobin are a major source of dietary iron in man. Heme, separated from these hemoproteins by intraluminal proteolysis, is absorbed intact by the intestinal mucosa. The absorbed heme is cleaved in the mucosal cell releasing inorganic iron. Although this mucosal heme-splitting activity initially was ascribed to xanthine oxidase, we investigated the possibility that it is catalyzed by microsomal heme oxygenase, an enzyme which converts heme to bilirubin, CO, and inorganic iron. Microsomes prepared from rat intestinal mucosa contain enzymatic activity similar to that of heme oxygenase in liver and spleen. The intestinal enzyme requires NADPH; is completely inhibited by 50% CO; and produces bilirubin IX-alpha, identified spectrophotometrically and chromatographically. Moreover, duodenal heme oxygenase was shown to release inorganic (55)Fe from (55)Fe-heme. Along the intestinal tract, enzyme activity was found to be highest in the duodenum where hemoglobin iron absorption is reported to be most active. Furthermore, when rats were made iron deficient, duodenal heme oxygenase activity and hemoglobin-iron absorption rose to a comparable extent. Upon iron repletion of iron-deficient animals, duodenal enzyme activity returned towards control values. In contrast to heme oxygenase, duodenal xanthine oxidase activity fell sharply in iron deficiency and rose towards base line upon iron repletion. Our findings suggest that mucosal heme oxygenase catalyzes the cleavage of heme absorbed in the intestinal mucosa and thus plays an important role in the absorption of hemoglobin iron. The mechanisms controlling this intestinal enzyme activity and the enzyme's role in the overall regulation of hemoglobin-iron absorption remain to be defined.
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PMID:Intestinal absorption of hemoglobin iron-heme cleavage by mucosal heme oxygenase. 443 36

Iron in food is classified as belonging to the haem pool, the nonhaem pool, and extraneous sources. Haem iron is derived from vegetable and animal sources with varying bioavailability. Hookworm infestation of the intestinal tract affects 450 million people in the tropics. Schistosoma mansoni caused blood loss in 7 Egyptian patients of 7.5- 25.9 ml/day which is equivalent to a daily loss of iron of .6-7.3 mg daily urinary loss of iron in 9 Egyptian patients. Trichuris trichiura infestation by whipworm is widespread in children with blood loss of 5 ml/day/worm. The etiology of anemia in children besides iron deficiency includes malaria, bacterial or viral infections, folate deficiency and sickle-cell disease. Severe infections cause profound iron-deficiency anemia in children in central American and Malaysia. Plasmodium falciparum malaria-induced anaemia in tropical Africa lowers the mean haemoglobin concentration in the population by 2 g/dI, causing profound anaemia in some. The increased risk of premature delivery, low birthweight, fetal abnormalities, and fetal death is directly related to the degree of maternal anemia. Perinatal mortality was reduced from 38 to 4% in treated anemic mothers. Mental performance was significantly lower in anemic school children and improved after they received iron. Supplements of iron, soy-protein, calcium, and vitamins given to villagers with widespread malnutrition, iron deficiency, and hookworm infestation in Colombia reduced enteric infections in children. Severe iron-deficiency anemia was treated in adults in northern Nigeria by daily in Ferastral 10 ml, which is equivalent to 500 mg of iron per day. Choloroquine, folic acid, rephenium hydroxynaphthoate, and tetrachlorethylene treat adults with severe iron deficiency from hookworm infestation in rural tropical Africa. Blood transfusion is indicated if the patient is dying of anaemia or is pregnant with a haemoglobin concentration 6 gm/dl. In South East Asia, mg per day prevented iron-deficiency anaemia in pregnancy. Field-trials on nutritional iron deficiency include an acidified milk formula plus ferrous sulphate for infants; biscuits with added bovine hemoglobin for children in Chile; sugar plus sodium ferric EDTA in Guatemala; salt with ferric orthophosphate and sodium acid sulphate in India; and Salt with ferrous sulphate plus sodium hexametaphosphate.
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PMID:Iron deficiency in the tropics. 704 57

Ineffective erythropoiesis was assessed in a series of 32 patients with rheumatoid arthritis by means of a new in-vitro method which measures the release of haem from a labelled cohort of erythroblasts in culture. Haem release was significantly increased in patients with the anaemia of chronic disorders but was normal in those who were not anaemic or who had an iron-deficiency anaemia. In 2 patients with anaemia of chronic disorders haem release returned to normal after successful antirheumatic therapy. The increased ineffective erythropoiesis in patients with rheumatoid arthritis and anaemia of chronic disorders appeared to be unrelated to functional iron deficiency and was not attributable to a serum factor.
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PMID:In-vitro studies of ineffective erythropoiesis in rheumatoid arthritis. 712 19

Iron deficiency is an important nutritional problem in third world countries because it diminishes work performance. In meat-eating countries, iron excess may be more important than iron deficiency. Heme iron is more efficiently absorbed from the diet than inorganic iron, and iron excess can produce cellular oxidation in association with superoxide dismutase. Metal ion catalysis is linked to aging, coronary artery disease, stroke, carcinogenesis, neurodegenerative disorders, and inflammatory disorders. Prudence is advised in the excessive consumption of meat and iron supplementation of the diet until this process is more thoroughly investigated.
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PMID:Ironic catastrophes: one's food--another's poison. 819 51

Although body iron status modulates whole body retention of heme derived iron, it is not known with certainty whether modulation occurs by regulation of mucosal uptake of heme. In vivo uptake from perfused intestine of heme labeled with 14C in the porphyrin ring was studied in groups of rats of differing iron status ranging from fully replete to markedly iron deficient. Heme extraction from infusate and mucosal heme uptake were significantly different between test groups (P < 0.005 and 0.001, respectively). Marked iron deficiency induced a 4.8-fold rise in heme extraction relative to iron-replete animals; rats with latent iron deficiency showed a smaller but still significant rise. Heme extraction correlated negatively with indicators of iron status: hemoglobin (r = -0.76, P < 0.001) and serum iron (r = -0.56, P < 0.05). The specific binding of [14C]heme to purified brush borders from iron-replete and iron-deficient rats was 1.4-fold higher in deficient rats when expressed per milligram of protein (P = 0.046) and 3.3-fold higher when expressed relative to alkaline phosphatase activity (P = 0.014). Thus mucosal uptake of heme in iron deficiency is increased because of an increase in its binding to the brush border.
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PMID:Modulation of uptake of heme by rat small intestinal mucosa in iron deficiency. 823 54

The assessment of the iron (Fe) status is very important because its deficiency is one of the most common in both developing and industrialized countries, being particularly prevalent among infants and young children. Diagnosis is difficult in the presence of other conditions which interfere with the interpretation of laboratory tests, such as hemoglobin (Hb), hematocrit (Hct), serum iron, transferrin saturation percentage and serum ferritin. Free erythrocyte protoporphyrin (FEP) is a precursor of Heme and normally occurs in very low concentration in red blood cells (RBC); elevated values indicate early impaired iron nutritional status, providing information about gradual changes in the iron supply to the marrow. This laboratory test is a practical and convenient method because it needs a small blood sample easily preserved. Although the Second National Health and Nutritional Examination Survey (NHANES II) of USA has provided a good opportunity to define more precisely the cut-off points, it is doubtful whether the age-related differences in children represent normal development or the effects of iron deficiency. In order to provide information about these aspects the present experimental model was performed: weanling Wistar rats were fed until 95 days of age (t 95) with an isocaloric diet containing 20 or 30 g/100 g. of protein (casein) (N 20 and N 30, respectively), allowing the highest growth and erythropoiesis rates and covering the requirements of all the nutrients (Table 1). Body weight and food intake were recorded three times/week.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Free erythrocyte protoporphyrin as a function of age in growing rats]. 824 30

The relative intestinal absorption of heme- and non heme-iron in connection with a standardized test meal was studied in a group of fertile women given 16 mg Fe in the form of FeSO4 and 2 mg Fe in the form of hemoglobin. Both in normal subjects and in women with iron deficiency, the heme-iron was significantly better absorbed (16.13% +/- S.D. 8.0 vs 4.59 +/- 3.4, p < 0.01 and 22.03 +/- 8.9 vs 9.45 +/- 7.8, p < 0.05). For targeted prophylaxis of iron deficiency with small, side-effect-free doses, heme-iron is thus a valuable component which increases the absorption by about 40%. Heme-iron does not cause high concentrations in the intestinal lumen of free radical inducing, possibly harmful ferric iron.
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PMID:Comparative absorption of ferrous and heme-iron with meals in normal and iron deficient subjects. 848 71


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