|Badaloo, Asha - UNIV WEST INDIES, JAMAICA|
|Reid, Marvin - UNIV WEST INDIES, JAMAICA|
|Forrester, Terrence - UNIV WEST INDIES, JAMAICA|
Submitted to: Book Chapter
Publication Type: Book / Chapter
Publication Acceptance Date: February 14, 2006
Publication Date: June 19, 2006
Citation: Jahoor, F., Badaloo, A., Reid, M., Forrester, T. 2006. Unique metabolic characteristics of the major syndromes of severe childhood malnutrition. In: Picou, D., Forrester, T., Walker, S.P., editors. The Tropical Metabolism Research Unit, the University of the West Indies Jamaica 1956-2006. The House that John Built. Kingston: Ian Randle Publishers. p. 25-60. Technical Abstract: The major clinical syndromes of severe childhood malnutrition (SCM) are marasmus, kwashiorkor and marasmic-kwashiorkor. Whereas treatment of marasmus is straightforward and the associated mortality is low, kwashiorkor and marasmic-kwashiorkor are difficult to treat and have high morbidity and mortality rates. While wasting characterizes all syndromes of SCM, kwashiorkor and marasmic-kwashiorkor are characterized additionally by oedema, anorexia, dermatitis, hypopigmented skin and hair, neurological abnormalities (lethargy and irritability), and a higher incidence of hepatic steatosis. These additional signs and symptoms of oedematous SCM are associated with numerous physiological/pathological differences between the two syndromes. For example, the oedematous syndromes have increased Na/KATPase activity, lower plasma concentrations of amino acids and the nutrient transport proteins, and more impaired immune and antioxidant capacities. These observations suggest that similar differences may exist in macronutrient metabolism between these two syndromes of SCM. For example, the observation that children with kwashiorkor have lower plasma cortisol, a primary mediator of protein breakdown, lower plasma amino acids and plasma protein concentrations suggest that there are marked differences in protein metabolism between these two types of SCM. Also, the higher incidence of hepatic steatosis in children with the oedematous forms of SCM is indicative of profound differences in lipid metabolism between the two syndromes. Finally, although our colleagues had shown in earlier studies that children with oedamatous SCM, but not marasmus, had markedly depleted erythrocyte pools of the ubiquitous antioxidant/detoxicant glutathione (GSH), the metabolic mechanism responsible for GSH depletion has remained unknown. The main aim of our recent work presented in this chapter has been to uncover possible metabolic differences between the oedematous and nonoedematous syndromes of SCM and thus to better understand their divergent clinical courses and outcomes. A major interest has been to understand how malnutrition and infection act separately and together to alter amino acid and lipid metabolism. During hospitalization, the children were managed according to a standard treatment protocol that is based upon an understanding of the metabolic state at different stages of treatment.