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Selasa, 07 Januari 2014

Infection-induced depression of serum retinol—a component of the acute phase response or a consequence?

This issue of the Journal contains closely linked articles by
Mitra et al (1, 2) about acute (but transient) depression of serum
retinol and retinol losses in the urine of children suffering from
dysenteries caused chiefly by
Shigella
species. Whereas these
articles provide new information about pathophysiologic mecha-
nisms that contribute to these infection-induced changes in
retinol metabolism, they also raise important questions about
how these new data are to be interpreted.
The 1968 monograph by Scrimshaw et al (3) reviewed
instances in which severe infections were followed by an abrupt
development of xerophthalmia or other optical manifestations of
vitamin A deficiency. It thus seemed evident that infectious dis-
eases could deplete vitamin A stores by accelerating metabolic
losses, impairing intestinal absorption, or both (3, 4). The con-
cept that infections could deplete hepatic stores of retinol was
strengthened further by Stephensen et al (5), who showed that
vitamin A was lost via the urine in patients with pneumonia or
sepsis. New estimates (2) suggest that urinary losses in children
with severe infection could deplete marginal stores of hepatic
retinol within 1 or 2 wk. But these new data (1, 2) also indicate
that infectious illnesses influence retinol metabolism in ways far
more complex than the simple depletion of vitamin A stores.
Infection-related declines in serum vitamin A have been noted
since the 1950s, with numerous reports this decade (1–4, 6). The
experimental design of Mitra et al’s study (1) was strengthened
by important variables included in their patient population. The
90 children with dysentery ranged in age from 5 mo to 5 y and
had different degrees of preexisting malnutrition and severities
of illness. Dysentery varied with etiology, ie, 66 children (73%)
had
Shigella
infections, and of these, 49 (54%) were infected
with highly virulent
S. dysenteriae
type l strains.
Type 1 strain
Shigella
infections were manifested by high
fevers, higher white cell counts, more prominent acute phase
serum protein responses, more bloody diarrhea, and longer ill-
nesses than those caused by other strains and species of bacteria
(1). In addition, severity of type 1
S. dysenteriae
infections cor-
related with larger depressions in serum retinol, urinary losses of
retinol, and more preexisting malnutrition (as estimated by sev-
eral anthropometric indexes) (1)
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