Toxic damage to the respiratory epithelium induces acute phase changes in vitamin A metabolism without depleting retinol stores of South African children.
Whereas there is much information concerning the effects of vitamin A status on response to infectious challenge, the effects of infection or trauma on vitamin A metabolism and status are less well documented. These relationships need to be understood to optimize clinical and public health programs to improve vitamin A status and health of children in less-developed countries. We measured acute changes in retinol and retinol-binding protein in 57 young South African children hospitalized following respiratory epithelial damage resulting from accidental ingestion of kerosene. In addition, vitamin A status, as measured by the modified relative dose response test, of these children 3 mo later was compared with that of neighborhood control children to determine whether their illness had depleted retinol stores. Plasma retinol was already significantly below control levels when children were admitted [geometric mean (95% CI): 0.57 micromol/L (0.48-0.67) compared with 1.15 micromol/L (1.02-1.30) for controls] and decreased further the following morning [0.38 micromol/L (0.31-0.46)]. Significant differences in retinol-binding protein were not detected until the next morning [5.99 mg/L (4.70-7.63) compared with 14.0 mg/L (11.8-16.6) for controls] and were not as large as the relative differences in retinol. This dissociation between changes in retinol and its binding protein suggests that there may be increased retinol uptake by certain tissues during the acute phase response. The proportion of case children (37/46, 80%) with inadequate liver retinol stores 3 mo after the illness was slightly, but not significantly (chi2 = 2.16, P = 0.14), greater than the proportion of control children (28/42, 67%). Acute respiratory illness therefore did not further deplete retinol stores in this population in which stores were already frequently inadequate.
Willumsen
J F
JF
Centre for International Child Health, Institute of Child Health, London, WC1N 1EH, United Kingdom.
Simmank
K
K
Filteau
S M
SM
Wagstaff
L A
LA
Tomkins
A M
AM
D000209:Acute-Phase Proteins / Q000032:analysis / Q000378:metabolism; D000210:Acute-Phase Reaction / Q000139:chemically induced* / Q000378:metabolism*; D000375:Aging / Q000378:metabolism; D016022:Case-Control Studies; D002675:Child, Preschool; D004848:Epithelium / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D005527:Food, Fortified; D006801:Humans; D007223:Infant; D007648:Kerosene / Q000009:adverse effects*; D008297:Male; D012137:Respiratory System / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D012177:Retinol-Binding Proteins / Q000032:analysis / Q000378:metabolism; D054839:Retinol-Binding Proteins, Plasma; D013019:South Africa; D014801:Vitamin A / Q000008:administration & dosage / Q000097:blood / Q000378:metabolism*
D000209:Acute-Phase Proteins; D007648:Kerosene; D012177:Retinol-Binding Proteins; D054839:Retinol-Binding Proteins, Plasma; D014801:Vitamin A