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Glutathione S-transferase polymorphisms may be associated with risk of oedematous severe childhood malnutrition

Published online by Cambridge University Press:  08 March 2007

Kwesi G Marshall
Affiliation:
Tropical Metabolism Research Unit, University of the West Indies, Mona, Jamaica
Sharon Howell
Affiliation:
Tropical Metabolism Research Unit, University of the West Indies, Mona, Jamaica
Marvin Reid
Affiliation:
Sickle Cell Unit, Tropical Medicine Research Institute, University of the West Indies,Mona, Jamaica
Asha Badaloo
Affiliation:
Tropical Metabolism Research Unit, University of the West Indies, Mona, Jamaica
Martin Farrall
Affiliation:
Department of Cardiovascular Medicine, University of Oxford, Wellcome Trust Centre for Human Genetics, Oxford, UK
Terrence Forrester
Affiliation:
Tropical Metabolism Research Unit, University of the West Indies, Mona, Jamaica
Colin A. McKenzie*
Affiliation:
Tropical Metabolism Research Unit, University of the West Indies, Mona, Jamaica
*
*Corresponding author: Dr Colin A. McKenzie, fax +1 876 977 0632, email colin.mckenzie02@uwimona.edu.jm
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Abstract

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It has been estimated that more than 50% of deaths before the age of 5 years have undernutrition as an underlying cause. Severe childhood malnutrition, an extreme form of undernutrition, occurs as oedematous and non-oedematous syndromes. The reasons why only some children develop oedematous severe childhood malnutrition (OSCM) have remained elusive, but the heterogeneity of clinical appearances among children from relatively homogeneous backgrounds suggests that interindividual variation in susceptibility to OSCM may exist. We investigated variants of four glutathione S-transferase (GST) genes in a retrospective study among subjects (n136) previously admitted to the Tropical Metabolism Research Unit, Jamaica, for the treatment of either OSCM (cases) or non-oedematous severe childhood malnutrition (controls). We found that GSTP1 Val105 homozygotes were significantly more common among the cases (odds ratio (OR) 3·5; 95% CI 1·1, 10·8). We also found an association of borderline significance between non-deletion GSTT1 genotypes (i.e. +/+ or +/0) and OSCM (OR 2·4; 95% CI 1·0, 5·9). There was no significant association between OSCM and any of the other GST variants. These preliminary findings suggest that genetic variation within the GST superfamily may contribute to the risk of OSCM. Additional, larger data sets and studies of variants in other candidate genes are required in order to properly assess the true contribution, if any, of genetic variation to risk of OSCM. Such studies may improve our understanding of the causes of clinical heterogeneity in malnutrition.

Type
Research Article
Copyright
Copyright © The Nutrition Society 2006

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