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| Year : 1981 | Volume
: 27
| Issue : 1 | Page : 12-5 |
Effect of malnutrition on iron metabolism -- a study of 45 children.
Agarwal MB, Mehta BC, Mhaiskar UM, Kumta NB, Shah MD
How to cite this article:
Agarwal M B, Mehta B C, Mhaiskar U M, Kumta N B, Shah M D. Effect of malnutrition on iron metabolism -- a study of 45 children. J Postgrad Med 1981;27:12 |
How to cite this URL:
Agarwal M B, Mehta B C, Mhaiskar U M, Kumta N B, Shah M D. Effect of malnutrition on iron metabolism -- a study of 45 children. J Postgrad Med [serial online] 1981 [cited 2023 Oct 2];27:12. Available from: https://www.jpgmonline.com/text.asp?1981/27/1/12/5670 |
Iron deficiency (ID) is widely prevalent in India. Its diagnosis is commonly confirmed by a low serum iron together with a transferrin saturation (TS) of under 16%.[2] Transferrin is an iron binding protein and it is commonly expressed in terms of its iron binding capacity. The fall in serum iron is not diagnostic of ID as it also occurs in inflammatory disorder[5], [12] and malignancies.[3] Similarly, although the total serum iron binding capacity (TIBC) is usually raised in III, it may remain normal or even low.[15] Even in such cases, the TS is rarely above 16% and hence this level is considered to indicate normal iron status.[15] But any condition which leads to a severe transferrin deficiency, could result in its higher saturation with iron despite iron deficiency. Such conditions include hereditary atransferrinemia,[9] nephrotic syndrome,[8] undernutrition, malabsorption and protein losing enteropathy.[8] In the present study, we have investigated 45 children with protein energy malnutrition to see the effect of such malnutrition on iron binding capacity and indirectly on transferrin saturation.
Forty-five unrelated children with a mean age of 3.8 years (1.5-8 years) were studied. These were cases of protein energy malnutrition admitted in the Pediatric Units of our hospital. The cases were divided into three groups i.e. (1) kwashiorkor-10 cases, (2) marasmic kwashiorkor-20 cases and (3) marasmus-15 cases, as per "Wellcome Classification" shown in [Table 1]. 14 Cases with evidence of active infection on history, clinical examination, chest radiography or urine examination were excluded. None had proteinuria while renal chemistry (blood urea nitrogen and creatinine) was normal in all.
Fifteen children referred for iron deficiency anemia without any clinical evidence of protein energy malnutrition with a mean age of 4.1 years (1.5-8 years) formed the control group. Standard haematological techniques were used as described by Dacie and Lewis.[6] Iron studies were done by using Ramsay's method.[13] Protein electrophoresis was carried out in each case. Patients were said to have iron deficiency anemia if the Hb could be shown to rise with iron therapy.[8], [15]
Thirty-one patients out of 45 could be said to have iron deficiency anemia on the basis that their Hb improved with iron therapy. Distribution of these 31 cases between the different groups is shown in [Table 2]. Out of these 31 cases, only 15 had a transferrin saturation of less than 16% [Table 2]. The incidence of iron deficiency together with a diagnostic fall in transferrin saturation in individual groups is also shown in [Table 2].
[Table 3] shows the results of serum iron, iron binding capacity and serum albumin in the different groups.
Transferrin is a pink glycoprotein with an electrophoretic mobility of betaglobulin.[4] It is synthesised in various tissues but mainly in the liver.[10] Its plasma concentration is about 230 mg/dl,[8] and its half disappearance time is about 10 days.[10] Transferrin is more commonly quantitated in terms of the amount of iron it can bind i.e. TIBC.[13] The normal TIBC is about 300 ug/dl. Only about one-third of the available sites are occupied by iron and thus the transferrin saturation is about 33% (16-45%).[8] In iron deficiency, the serum iron level and the transferrin saturation (TS) are lowered.[8] The TS of less than 16% is required before a confident diagnosis of iron deficiency can be made in a case of anemia.[8], [15] If the transferrin level fails to rise or if it falls, the usefulness of the transferrin saturation in the diagnosis of iron deficiency is lost. Of the various factors that reduce the transferrin level, infections, inflammation and proteinuric conditions were carefully ruled out in the present study and hence undernutrition appeared to be the chief cause of lowered TIBC.
Cases with kwashiorkor had the maximum decrease in the iron binding capacity while those with marasmus had the minimum [Table 3]. The lowest TIBC (57 ug%) was also seen in a patient with kwashiorkor. This could be correlated with the degree of fall in the serum albumin level which was also maximum in the kwashiorkor group [Table 3]. Despite these variations, all the three groups had significantly low TIBC as compared to the control group with pure iron deficiency and normal serum albumin [Table 3].
It is important to realise that the absolute value of TIBC is very often used to differentiate between iron deficiency anemia and anemia of chronic systemic disorders as TIBC is increased in iron deficiency while it is invariably decreased in chronic disorders.[2] The present report highlights the effect of hypoproteinemia in obscuring such differentiation.
The importance of transferrin in iron deficiency anaemia can be realised if its role in iron metabolism can be reviewed. The transferrin mediated delivery of iron to red cell precursors imparts direction to the flow of iron.[7] Unbound iron is not oriented towards red marrow. Instead it leaves plasma rapidly and gets distributed into many tissues.[7] Such biological importance of transferrin is classically seen in congenital atransferrinemia,[9] where tissues are loaded with iron but red cells have morphological stigmata of iron deficiency with no iron in the marrow.[9] This highlights that merely giving iron to such undernourished hypoproteinemic individuals is not adequate. The protein supply to correct the transferrin deficiency and hence to direct the iron towards the marrow is also equally important. Lastly, Antia et al[l] have shown that transferrin may be a better index of malnutrition than albumin. McFarlane et al[11] have considered that transferrin has a bactericidal action and in its absence, free iron may favour bacterial multiplication. Giving iron therapy to such patients without replacing proteins could thus be positively harmful.
| 1. | Antia, A. U., McFarlane, H. and Soothill, .T.. F.: Serum siderophilin in kwashiorkor. Arch. Dis. Childhood, 43: 459463, 1968.  |
| 2. | Bainton, D. F. and Finch, C. A.: The diagnosis of iron deficiency anemia. Amer. J. Med., 37: 62-70, 1964. |
| 3. | Banerjee, R. N. and Naming, R. M.: Hematological changes in malignancy. Brit. J. Hematol. 13: 829-843, 1967. |
| 4. | Brown, E. S.: Transferrin: Physiology and Function in Iron Transport. In, "Iron Metabolism". Ciba Foundation Symposium. 51 (New Series), Elsevier, Netherland, 1977, p. 125-143. |
| 5. | Cartwright, G. E.: The anemia of chronic disorders. Semin. Hematol., 3: 351-355, 1966. |
| 6. | Dacie, J. V. and Lewis, S. M.: "Practical Hematology." 5th ed., Churchill, Livingstone, Edinburgh and London, 1975. |
| 7. | Eldor, A., Manhy, N. and Izak, G.: The effect of transferrin-free serum on the utilisation of iron by rabbit reticulocytes. Blood, 36: 233-238, 1970. |
| 8. | Fairbanks, V. F. and I3eutler, E.: Iron deficiency. In, "Hematology" ed. by William, W. J., Beutlisr, E., Erslev, A. J. and Rundles, R. W. 2nd Ed., McGraw-Hill, London and New York, N.Y. 1977, 13. 363-387. |
| 9. | Goya, N., Miyazaki, S., Kodate, S. and Ushio, B.: A family of congenital atransferrinemia. Blood 40: 239-245, 1972. |
| 10. | Kartz, J. N.: Transferrin and its functions in the regulation of iron metabolism. In "Regulation of Hematopoiesis", ed. A. S. Gordon, N.Y., Appleton-Century-Crafts, New York, 1970, p. 539-551. |
| 11. | McFarlane, H., Ggbeide, M. I., Reddy, S., Adcock, K. J., Adeshina, H., Gurney, J. M., Cooke, A., Taylor, G. O. and Moodie, J. A.: Biochemical assessment of protein calorie malnutrition. Lancet, 1: 392-394, 1969. |
| 12. | Moe, P. J.: The diagnosis of iron deficiency anemia in children. Acta Paediatr. Scand., 58: 141-146 1969. |
| 13. | Ramsay, W. N. M.: "Plasma Iron". Advances in Clinical Chemistry, 1: 1-18, 1958. |
| 14. | Wellcome Trust Working Party: Classification of Infantile Malnutrition. Lancet, 2: 302-303, 1970. |
| 15. | Wintrobe, M. M.: "Clinical Hematology", 7th ed. Lea & Febiger, Philadelphia 1974, p. 154. |
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