scholarly journals Effect of transfused reticulocytes on iron exchange

Blood ◽  
1982 ◽  
Vol 59 (2) ◽  
pp. 364-369 ◽  
Author(s):  
CA Finch ◽  
H Huebers ◽  
M Eng ◽  
L Miller

Abstract A animal model was developed whereby reticulocyte-rich blood was introduced into normal rats by exchange transfusion. Measurements of plasma iron turnover was made at similar plasma iron concentrations before and after exchange transfusions. High reticulocyte blood obtained from animals rendered iron deficient by diet or by treatment with phenylhydrazine resulted in a mean increase of 86% in internal iron exchange, while the plasma iron turnover was unaffected by exchange with normal red cells. Since iron input from reticuloendothelial cells could have increased due to breakdown of transfused cells, iron absorption was also measured. Within 1 hr and for a least 6 hr after exchange with high reticulocyte blood, mean absorption in six groups of animals was increased over control animals by 50%-130%. The increased plasma iron turnover and absorption was not mediated by a decrease in plasma iron or an increase in unsaturated iron-binding capacity. Indeed, a higher plasma iron and transferrin saturation augmented the movement of iron into the plasma from iron- donating tissues. It is proposed that the donation of iron by transferrin in some way immediately facilitates the procurement of more iron by transferrin.

Blood ◽  
1982 ◽  
Vol 59 (2) ◽  
pp. 364-369
Author(s):  
CA Finch ◽  
H Huebers ◽  
M Eng ◽  
L Miller

A animal model was developed whereby reticulocyte-rich blood was introduced into normal rats by exchange transfusion. Measurements of plasma iron turnover was made at similar plasma iron concentrations before and after exchange transfusions. High reticulocyte blood obtained from animals rendered iron deficient by diet or by treatment with phenylhydrazine resulted in a mean increase of 86% in internal iron exchange, while the plasma iron turnover was unaffected by exchange with normal red cells. Since iron input from reticuloendothelial cells could have increased due to breakdown of transfused cells, iron absorption was also measured. Within 1 hr and for a least 6 hr after exchange with high reticulocyte blood, mean absorption in six groups of animals was increased over control animals by 50%-130%. The increased plasma iron turnover and absorption was not mediated by a decrease in plasma iron or an increase in unsaturated iron-binding capacity. Indeed, a higher plasma iron and transferrin saturation augmented the movement of iron into the plasma from iron- donating tissues. It is proposed that the donation of iron by transferrin in some way immediately facilitates the procurement of more iron by transferrin.


1987 ◽  
Vol 33 (2) ◽  
pp. 273-277 ◽  
Author(s):  
H A Huebers ◽  
M J Eng ◽  
B M Josephson ◽  
N Ekpoom ◽  
R L Rettmer ◽  
...  

Abstract We evaluated plasma iron (PI) and total iron-binding capacity (TIBC) or transferrin in normal individuals and in patients with iron imbalance. The standard colorimetric measurements of PI and TIBC and the standard isotope-dilution measurement of TIBC were compared with an immunoprecipitation method and also with immunoelectrophoresis of transferrin. PI concentrations as measured by the standard and immunoprecipitation methods agreed closely for all individuals except those with saturated transferrin, where nontransferrin iron increased the results in the standard assay. This excess iron in saturated plasma may be derived from either free iron or iron-bearing ferritin. There were also differences in TIBC between the two methods. Iron-deficient sera gave higher values for transferrin when measured by immunoelectrophoresis. Unsaturated iron-binding capacity was increased in the isotope-dilution method in some iron-saturated plasma, compounding errors when added to erroneously high PI values to compute TIBC. Perhaps some exchange of iron occurred between added iron and transferrin iron in the isotope-dilution method. These measurements confirm the accuracy of the standard colorimetric method of measuring PI and TIBC except in iron-saturated plasma. However, the greater specificity of a polyclonal immunoprecipitation method of measuring PI and TIBC makes it particularly useful in differentiating transferrin-bound iron from nontransferrin iron.


1981 ◽  
Vol 27 (2) ◽  
pp. 276-279 ◽  
Author(s):  
F Peter ◽  
S Wang

Abstract Ferritin values for 250 selected sera were compared with values for iron, total iron-binding capacity (TIBC), and transferrin saturation, to assess the potential of the ferritin assay for the detection of latent iron deficiency. The specimens were grouped (50 in each group) according to their values for iron and TIBC. In Group 1 (low iron, high TIBC) the saturation and ferritin values both indicated iron deficiency in all but one. In the 100 specimens of Groups 2 (normal iron, high TIBC) and 4 (normal iron, high normal TIBC), the saturation values revealed 16 iron-deficient cases, the ferritin test 55. For Groups 3 (low iron, normal TIBC) and 5 (low iron, low TIBC), the ferritin test revealed fewer cases of iron deficiency than did the saturation values (37 cases vs 51 cases, in the 100 specimens). Evidently the ferritin test detects iron deficiency in many cases for whom the serum iron and TIBC tests are not positively indicative. The correlation of serum ferritin with iron, TIBC, and transferrin saturation in the five groups was good only in the case of specimens for which the TIBC was normal; if it was abnormal the correlation was very poor.


Blood ◽  
1965 ◽  
Vol 26 (4) ◽  
pp. 421-432 ◽  
Author(s):  
S. K. SOOD ◽  
M. G. DEO ◽  
V. RAMALINGASWAMI

Abstract 1. This investigation deals with a study of the anemia of protein deficiency in Rhesus monkeys. 2. Protein deficiency was induced in 17 rhesus monkeys. Seven animals, given a protein-rich diet, served as controls. The diets of both the groups were identical in all respects, except protein. All animals were tube-fed to ensure adequate caloric intake. Hematocrit, hemoglobin, erythroctye count, serum iron, serum iron binding capacity, plasma iron tolerance curves, and iron absorption using the Fe59 fecal recovery method were studied before and at intervals of the experiment in both deficient and control groups. Protein-deficient monkeys consistently developed normocytic normochromic anemia of moderate severity. A striking fall in serum iron binding capacity, total proteins and albumin with a rise in gamma globulin was observed in all deficient animals. A significant and comparable fall in serum iron was also observed. The Fe59 absorption was depressed and there was flattening of plasma iron tolerance curves. Two deficient animals, refed a high protein diet, showed reversal of all these changes. The control animals did not show any of these changes. The mechanism of anemia and decreased iron absorption observed in the protein-deficient animals and the relevance of these findings to those in Kwashiorkor are discussed.


2017 ◽  
Vol 40 (2) ◽  
pp. 42-47
Author(s):  
Al-Hadithy H. AH.

     The study was conducted on 150 healthy and 102 diagnosed iron deficient anemic camels to determine serum iron, total iron binding capacity, unbound iron binding capacity, transferrin saturation, copper and cobalt concentrations. The normal (81 males and 69 females) and anemic (48 males and 54 females) groups both aged between 1-15 years in Najaf governorate- Iraq. Blood samples were collected from the jugular veins into plain tubes during the period November 2014 until May 2015, and the separated sera were used for the measurement of studied parameters. Results showed that the ranges and means ± SE in normal and anemic camels were as follows; Serum iron concentration was 7.37-19.48 μmol/L and 12±0.22 μmol/L, 1.52-15.70 μmol/L and 8.43±0.21 μmol/L, respectively, TIBC 73.80-108.47 μmol/L and 89.19±0.7 μmol/L, 93.12-135.32 μmol/L and 111.28±1.02 μmol/L, respectively, UIBC 57.5-95.25 μmol/L and 76.5±0.74 μmol/L, 83.27-125.69 μmol/L and 102±1.06 μmol/L, respectively, TS% 7.80- 24.04 %  and 14.3 ±0.27%, 1.22-14.79% and 7.6±0.21%, respectively, serum copper 6.28-16.5 μmol/L and 11±0.2 μmol/L, 3.67-12.40 μmol/L and 7±0.19 μmol/L, respectively and serum cobalt 0.84-6.78 μmol/L and 3±0.13 μmol/L, 0.42-6.42 μmol/L and 2.67±0.16 μmol/L, respectively. However, There was a significant (P<0.05) decrease in serum iron, TS% and copper. While, there was a significant (P<0.05) increase in serum TIBC and UIBC of anemic camels in comparison with normal control. The cobalt concentrations were almost similar in both groups. The present data recorded reference ranges and mean values of specific biochemical parameters in clinically normal and anemic camels with significant differences between them.


The Lancet ◽  
1975 ◽  
Vol 305 (7919) ◽  
pp. 1293
Author(s):  
Terry Hamblin

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 ◽  
1961 ◽  
Vol 18 (1) ◽  
pp. 61-72 ◽  
Author(s):  
MIGUEL LAYRISSE ◽  
ALFREDO PAZ ◽  
NORMA BLUMENFELD ◽  
MARCEL ROCHE ◽  
Iris Dugarte ◽  
...  

Abstract Iron metabolism, balance of red cell production and destruction and iron absorption from hemoglobin were determined in 11 patients with heavy hookworm infection and severe anemia. The plasma iron, total iron binding capacity, bone marrow hemosiderin and plasma Fe59 clearance are in agreement with the idea that the anemia associated with hookworm infection is of the iron deficiency type. The rate of red cell production measured by the E/M ratio, absolute reticulocyte count and plasma iron turnover showed an increase to about twice normal, while the rate of destruction estimated by the T ½ erythrocyte survival showed a destruction about 5 times normal. This unbalance between production and destruction could explain the severity of the anemia. The increase of fecal urobilinogen output to twice normal was interpreted as due to the metabolism of the hemoglobin lost into the intestine rather than to an increase of hemolysis. The estimation of fecal blood loss in the patients whose red cells were tagged with Cr51 and Fe59, showed that the radioactivity counted with Fe59 was only about 63 per cent of the radioactivity counted with Cr51. This difference was interpreted as due to iron absorption from the hemoglobin lost into the intestine. The mean daily fecal excretion of iron reaches 4.7 mg. Since the iron metabolism in these patients is in equilibrium, we have concluded that the iron loss is replaced by the iron from food; this is in addition to the 3 mg. hemoglobin iron which is reabsorbed from the blood lost into the gut.


The Lancet ◽  
1975 ◽  
Vol 305 (7917) ◽  
pp. 1191
Author(s):  
Adam Turnbull ◽  
JoanF Zilva

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