Episodes of acute infection are thought to deplete body stores of vita
min A. The mechanism by which this might occur is not known, but incre
ased metabolic requirements are presumed to play a role. We have found
, however, that significant amounts of retinol and retinol-binding pro
tein (RBP) were excreted in the urine during serious infections, where
as only trace amounts were found in the urine of healthy control subje
cts. The geometric mean excretion rate in 29 subjects with pneumonia a
nd sepsis was 0.78 mu mol retinol/d. Subjects with fever (temperature
greater than or equal to 38.3 degrees C) excreted significantly more r
etinol (geometric ($) over bar chi = 1.67 mu mol/d) than did those wit
hout fever (0.18 mu mol/d; t = 3.53, P < 0.0015). Aminoglycoside admin
istration and low glomerular filtration rates (< 35 mL/min) were also
associated with higher rates of urinary retinol excretion. Thirty-four
percent of patients excreted > 1.75 mu mol retinol/d, equivalent to 5
0% of the US recommended dietary allowance. These data show that vitam
in A requirements are substantially increased during serious infection
s because of excretion of retinol in the urine, and suggest that these
losses are due to pathologic changes associated with the febrile resp
onse.