Urinary vanillyl-mandelic acid (VMA) excretion by chronically anaemic children.

Hypoxia has been regarded as one of the many factors stimulating augmented catecholamine biosynthesis (Vogt, 1960). Plasma levels of epinephrine and norepinephrine were found to be increased in newborns with the respiratory distress syndrome or placental insufficiency (Cheek, Malinek, and Fraillon, 1963). Infants with severe heart failure eliminate in the urine twice as much metanephrine, normetanephrine, and 3-methoxy-4-hydroxymandelic acid (VMA) as do normal infants (Lees, 1966), and it has been suggested that increased catecholamine production may contribute to the relative hypermetabolism observed in some infants with congenital heart disease and undernutrition (Lees et al., 1965). Reports about the effects of heart failure on the urinary excretion of catecholamines or their metabolites in adults have been conflicting. They have included inconsistent changes (Raab and Gigee, 1954; Pekkarinen et al., 1960), important increases in norepinephrine and epinephrine (Tomatsu et al., 1963), or in norepinephrine, but not in epinephrine or in VMA (Chidsey, Braunwald, and Morrow, 1965). An increase in the urinary output of VMA has been demonstrated in some patients with severe pulmonary insufficiency (Gitlow et al., 1961), but a normal urinary VMA has been reported in children with various conditions which may cause hypoxia, such as lobar pneumonia, atelectasis, acute asthmatic attack, or cyanotic heart disease (Young et al., 1963). The urinary excretion of catecholamines or their metabolites in patients with chronic anaemia has not been studied, and the present report deals with the daily urinary excretion of VMA, the major final product of catecholamine metabolism (Armstrong,