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Chemical composition of organs of children who died from malnutrition

Published online by Cambridge University Press:  09 March 2007

G. A. O. Alleyne
Affiliation:
Medical Research Council, Tropical Metabolism Research Unit, University of the West Indies, Kingston, Jamaica
D. Halliday
Affiliation:
Medical Research Council, Tropical Metabolism Research Unit, University of the West Indies, Kingston, Jamaica
J. C. Waterlow
Affiliation:
Medical Research Council, Tropical Metabolism Research Unit, University of the West Indies, Kingston, Jamaica
B. L. Nichols
Affiliation:
Bay lor College of Medicine, and Texas Children's Hospital, Houston, Texas
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Abstract

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1. Chemical analysis was carried out on samples of brain, liver, skeletal muscle, heart and kidney obtained from children who died of malnutrition. Total body potassium was measured before autopsy by the ‘whole body counting’ technique.

2. There was a marked increase in liver fat, and the brain contributed a higher percentage of the body-weight in the more severely malnourished children.

3. All the organs had approximately the same concentrations of non-collagen nitrogen. The proportion of collagen was highest in muscle.

4. All organs were depleted of potassium, but the muscle was most severely affected. Brain potassium as a percentage of total body potassium was higher than normal in the most severely potassium depleted children.

5. Measurements of tissue magnesium showed that there was no difference in magnesium content of tissues when expressed in terms of non-collagen nitrogen. When compared with normal values, muscle was magnesium depleted. The potassium to magnesium ratio was lowest in muscle.

Type
Research Article
Copyright
Copyright © The Nutrition Society 1969

References

Alleyne, G. A. O. (1968). Clin. Sci. 34, 199.Google Scholar
Forbes, G. B. & Lewis, A. M. (1956). J. clin. Invest. 35, 596.CrossRefGoogle Scholar
Garrow, J. S. ( 1965 a). W. Indian med. J. 14, 73.Google Scholar
Garrow, J. S. (1965 b). Lancet ii, 455.CrossRefGoogle Scholar
Garrow, J. S. (1967). Lancet ii, 643.CrossRefGoogle Scholar
Garrow, J. S., Fletcher, K. & Halliday, D. (1965). J. clin. Invest. 44, 417.CrossRefGoogle Scholar
Halliday, D. (1966). Body composition in severe infantile protein malnutrition. PhD Thesis, University of London.Google Scholar
Halliday, D. (1968). Clin. Sci. 33, 365.Google Scholar
Hansen, J. D. L. (1956). S. Afr. J. Lab. clin. Med. 2, 206.Google Scholar
MacArthur, C. G. & Doisy, E. A. (1919). J. comp. Neurol. 30, 445.CrossRefGoogle Scholar
Montgomery, R. D. (1960). Lancet ii, 74.CrossRefGoogle Scholar
Nelson, W. E. (1957). Textbook of Pediatrics, 7th ed.Philadelphia: Saunders.Google Scholar
Neuman, R. E. & Logan, M. A. (1950). J. biol. Chem. 184, 299.CrossRefGoogle Scholar
Nichols, B. L., Alleyne, G. A. O., Hazlewood, C., Barnes, D. J. & Waterlow, J. C. (1967). Fedn Proc. Fedn Am. Socs exp. Biol. 26, 304.Google Scholar
Picou, D., Halliday, D. & Garrow, J. S. (1966). Clin. Sci. 30, 345.Google Scholar
Smith, R. (1960). Clin. Sci. 19, 275.Google Scholar
Waterlow, J. C. (1948). Spec. Rep. Ser. med. Res. Coun. no. 263.Google Scholar
Waterlow, J. C. & Mendes, C. B. (1957). Nature, Lond. 180, 1361.CrossRefGoogle Scholar
Waterlow, J. C. & Weisz, T. (1956). J. clin. Invest. 35, 346.CrossRefGoogle Scholar
Whang, R. & Welt, L. G. (1963). J. clin. Invest. 42, 305.CrossRefGoogle Scholar
Widdowson, E. M. & Dickerson, J. W. T. (1964). In Mineral Metabolism. Vol. 2, Part A, p. 1. [Comar, C. L. and Bronner, F., editors.] New York and London: Academic Press Inc.Google Scholar