scholarly journals Studies on Copper Metabolisn

Blood ◽  
1952 ◽  
Vol 7 (11) ◽  
pp. 1053-1074 ◽  
Author(s):  
M. E. LAHEY ◽  
C. J. GUBLER ◽  
M. S. CHASE ◽  
G. E. CARTWRIGHT ◽  
M. M. WINTROBE

Abstract 1. A total of 70 swine were fed a diet consisting only of evaporated cow’s milk. Copper and iron were added to the diet of 10 of the pigs. Iron only was added to the diet of 46 of the pigs. Copper only was added to the diet of 10 of the pigs. Four pigs received neither iron or copper. 2. The animals deficient in copper developed skeletal abnormalities, microcytic hypochromic anemia, leukopenia, neutropenia, normoblastic hyperplasia of the bone marrow, hypoferremia, an increase in the iron-binding capacity of the plasma, hypocupremia and reduced erythrocyte copper as well as tissue copper. No abnormality in porphyrin metabolism was observed and tissue as well as erythrocyte catalase activity was not significantly reduced. Following the administration of copper, the blood of the animals was rapidly and completely restored to normal. 3. The animals deficient in iron developed a severe microcytic, hypochromic anemia, normoblastic hyperplasia of the bone marrow, hypoferremia and an increase in the total iron-binding capacity of the plasma. No abnormality in copper or porphyrin metabolism was observed in these animals except for a slight elevation in the plasma copper level and a marked increase in liver copper. 4. The animals deficient in both copper and iron developed all of the manifestations noted in the copper-deficient pigs. These changes occurred more rapidly and to a greater degree than in the swine with a deficiency of either element alone. 5. The morphologic and biochemical similarities between anemia due to copper deficiency and anemia due to iron deficiency suggest that in copper-deficient swine there is an abnormality in the metabolism of iron and that, furthermore, the anemia may be the consequence of this abnormality.

1966 ◽  
Vol 4 (3) ◽  
pp. 9-11

We have discussed iron preparations for adults in earlier articles;1 much of the information applies equally to children. Iron is not a ‘tonic’ and should be given only to prevent or correct iron deficiency. Estimation of the haemoglobin and inspection of a blood smear are the minimum investigations necessary before iron is prescribed in therapy. When deficiency is suspected in the absence of hypochromic anaemia, plasma iron and iron-binding capacity should be estimated and/or the bone marrow examined for haemosiderin crystals which disappear when iron stores are depleted.


Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 5397-5397
Author(s):  
Ankit Mangla ◽  
Sriman Swarup ◽  
Muhammad Umair Mushtaq ◽  
Hussein Hamad ◽  
Sharad Khurana ◽  
...  

Abstract Introduction Iron plays a critical role in patients with multiple myeloma (MM). The limited availability of iron to the developing erythroid precursors results in the characteristic anemia so frequently seen in these patients. Moreover, iron is also a determinant in growth of the malignant plasma cells that makes it one of the critical factors in progression of the disease. Iron is a key component in success of erythropoietin (EPO) therapy that is often used to maintain hemoglobin (Hb) level of >10g/dL in patients with MM. International Myeloma working group (2011) advised transfusing IV iron to aid in success of EPO therapy. However, apart from determining the iron stores on bone marraow aspirate, there is hardly any reliable clinical or lab indicator of the iron stores in the body. The utility of various iron indices in determining the bone marrow iron stores remains anecdotal. In this study we aim to determine the relation between iron indices and iron level in the bone marrow of patients diagnosed with multiple myeloma. Methods A total of 268 multiple myeloma patients, diagnosed from 2004 to 2015, were identified from tumor registry of John H. Stroger Jr. Hospital of Cook County, Chicago. Accuracy of ferritin, iron level, total iron binding capacity (TIBC), unsaturated iron binding capacity (UIBC) and transferrin saturation (TSAT) was evaluated using receiver operating characteristic curves (ROC). Out of sampled patients, 167 patients had a concurrent bone marrow biopsy and aspirate, serum ferritin and iron panel, and were included in ROC analyses. Results The study population consisted of 57% African-Americans, 18% Caucasians and 16% Hispanics. Median age was 61 years and 51% were females. Past history was significant for hypertension (48%), diabetes (31%), co-existing inflammatory conditions (18%), smoking (25%), alcohol abuse (17%) and illicit drug abuse (8%). Median hemoglobin, mean corpuscular volume (MCV), leukocytes and platelets were 10g/dL, 90.3fL, 6,200/mcL and 219,500/mcL respectively. Bone marrow aspirates for iron were rated as absent (37%), mild/moderate (18%) and adequate/normal (45%). Anemia was found in 79% of males (Hb <12.9g/dL) and 76% of females (Hb<11.7 g/dL). Of the patients with anemia, 36% of males and 39% of females had absent iron stores (determined by prussian blue staining method) on bone marrow aspirate. MCV was not significantly related with iron deficiency. Iron level, TIBC, UIBC and TSAT were not significantly associated with bone marrow iron (P>0.05). Only ferritin was significant predictor of iron deficiency and presence of iron in bone marrow (AUC 0.64, 95%CI 0.55-0.74, P=0.002). Ferritin levels of ≤15mcg/L (positive LR 3.77, sensitivity 3.4%, specificity 99.1%), ≤30mcg/L (positive LR 2.59, sensitivity 11.9%, specificity 95.4%) and ≤50mcg/L (positive LR 4.35, sensitivity 32.2%, specificity 92.6%) predicted iron deficiency. Ferritin levels of ≥100mcg/L (positive LR 1.47, sensitivity 76.9%, specificity 47.5%), ≥200mcg/L (positive LR 1.46, sensitivity 54.6%, specificity 62.7%) and ≥500mcg/L (positive LR 1.94, sensitivity 23.1%, specificity 88.1%) ruled out iron deficiency. Conclusion Of all the indices predicting iron deficiency, only ferritin was significantly associated with absent iron in bone marrow aspirates. In MM patients, iron supplementation should be considered with ferritin levels of ≤50mcg/L and can be deferred with ferritin levels of ≥500mcg/L. Further studies are needed to explore the association. Disclosures No relevant conflicts of interest to declare.


1988 ◽  
Vol 40 (4) ◽  
pp. 576-583 ◽  
Author(s):  
R. B. Harvey ◽  
D. E. Clark ◽  
W. E. Huff ◽  
L. F. Kubena ◽  
D. E. Corrier ◽  
...  

PEDIATRICS ◽  
1956 ◽  
Vol 18 (2) ◽  
pp. 267-298
Author(s):  
Phillip Sturgeon

The infant has no route or organ for the physiologic excretion of iron. Clinically insignificant quantities are lost through the skin and gastrointestinal tract. Assimilation of iron by the adult does not exceed 10 per cent of that ingested in the food; natural foods have a relatively low content of iron. There is evidence from balance studies that at least some infants may have a greater capacity to absorb iron than adults; confirmatory studies using isotopic labeled iron in naturally occurring food, especially milk, would be most helpful in considering and re-evaluating this phase of iron nutrition in the infant. The intestinal mucosa tends to act as a barrier to the rapid entrance of iron into the circulation (mucosal block). Iron in serum is transported bound to a serum globulin (siderophilin); the latter is present in a two- to threefold excess of the concentration of iron in the serum (this represents the serum iron-binding capacity). Relative to adults, many normal infants have a reduced concentration of serum iron and increased iron-binding capacity. Similar changes are seen in iron deficiency states. Storage iron is found primarily in the liver and spleen in 2 chemical forms. One, ferritin, is detectable only by chemical means, and the other, hemosiderin, is visible microscopically and takes iron stains. The content of the latter in bone marrow is reduced in iron deficiency states. Also, hemosiderin is not found in the bone marrow of normal infants. The time required for the assimilation of iron, including metabolic transport across the intestinal mucosa, through the serum iron pool, into the bone marrow and out into the circulating erythrocytes, is very short; as little as 4 hours. The vast majority of iron metabolized internally comes from the daily breakdown of hemoglobin and, to a lesser extent, from other iron compounds such as myoglobin, cytochrome and ferritin. The dietary iron assimilated constitutes only a small percentage of the daily total iron turnover. Studies of iron turnover rates (ferro-kinetics) have not been performed in infants; the magnitude and significance of the additional factor created by rapid growth in such considerations is not known at present. The phyisologic anemia of late infancy is associated with evidence of depletion of iron in the various iron compartments: hemoglobin, serum iron, iron-binding capacity and iron stores. In view of recent data on the blood volume and concentration of hemoglobin of the newborn infant, considerable reduction in estimates of the total amount of iron present at birth are in order: A mean value of 200 mg. for a 3-kg. infant is consistent with these data, and is also consistent with studies of total iron content of stillborn fetuses over 3 kg. A relatively wide range in values, 120 to 320 mg. for total body iron are well within the limit's of normal. Calculations are presented to show that those infants endowed with the smaller quantities of iron at birth and a relatively rapid growth factor will have to assimilate iron at 3 times the rate of other normal infants. In the normal infant with reduced iron content at birth, the drain of iron from hemoglobin by growth of muscle and myoglobin mass may constitute a significant factor contributing to a profound degree of anemia. Preliminary studies on the prophylactic use of intramuscular iron indicate that many of the manifestations of iron deficiency in normal infancy can be altered. A statistically significant higher mean concentration of hemoglobin (0.7 gm./100 ml.) was achieved. Infants, so treated, with values for hemoglobin less than 11.0 gm./ 100 ml. were not observed, whereas 20 per cent of normal infants at 1 year of age had values for hemoglobin ranging from 9.4 to 11 gm./100 ml. Highly significant reductions in the total iron-binding capacity, serum copper and free erythrocyte protoporphyrin were achieved. Increases in the concentration of serum iron and mean erythrocyte hemoglobin concentration were also significant. The average mean corpuscular volume in the treated group was 78.9 µm.; this was not significantly different from the value of 77.2 in the control group. In previous studies using oral iron in large doses, the only one of the above manifestations of iron deficiency which was altered significantly was the concentration of hemoglobin. Except for staining of the skin, the intramuscular iron preparation employed gave no reactions. The iron requirement for the first year of life was given in 3 injections of 1 to 2 ml. without difficulty.


1958 ◽  
Vol 192 (3) ◽  
pp. 560-562 ◽  
Author(s):  
Thomas J. Haley ◽  
Anna M. Flesher ◽  
Nathan Komesu

Acute whole body-x-irradiation produced a hyperferremia in rabbits. This effect reached its peak on the 4th day, at which time the iron-binding globulins were almost completely saturated. The radiation dose did not affect the iron-binding mechanism even when the globulins were saturated prior to irradiation because the saturation resulted in a prolongation of the period of irradiation hyperferremia. The results support the theory that irradiation hyperferremia is a result of decreased iron utilization by the bone marrow. There does not appear to be any relationship between radiation lethality and hyperferremia.


1980 ◽  
Vol 19 (06) ◽  
pp. 274-277 ◽  
Author(s):  
Ursula Scheffel ◽  
Min-Fu Tsan

SummaryThe effect of serum unbound iron-binding capacity (UIBC) on the blood clearance and tissue distribution in abscessbearing rabbits was studied. In rabbits with low serum UIBC (95 ± 28 μg/dl), the blood clearance of 67Ga was much faster than that of rabbits with high serum UIBC (306 ± 27 μg/dl). The 67Ga uptake by the liver, spleen, kidney, muscle, bone marrow or abscess 24 hrs after injection was also much lower in rabbits with low serum UIBC. In contrast, the 67Ga deposition in bone was much higher in rabbits with low serum UIBC. Since the amounts of 67Ga in muscle and blood were disproportionally lower than that in the abscess, the abscess-to-muscle or abscess-to-blood ratio was much higher in rabbits with low serum UIBC than that of rabbits with high serum UIBC.


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