Na. Le et al., Evidence for the in vivo generation of oxidatively modified epitopes in patients with atherosclerotic endothelium, METABOLISM, 49(10), 2000, pp. 1271-1277
There is increasing evidence that autoantibodies (AAbs) against oxidatively
modified low-density lipoprotein (LDL) are present in humans and may be de
tected in fasting plasma. Using a standardized immunoassay for the detectio
n of circulating revels of AAbs against malondialdehyde (MDA)-modified LDL,
we examined the acute changes in AAb levels during postprandial lipemia in
a group of men and women without (n = 28) and with (n = 17) normal endothe
lium. The presence of atherosclerotic vessel is documented by clinical evid
ence of coronary artery disease (CAD). In response to the oxidative stress
associated with postprandial lipemia, statistically significant reductions
in AAb levels were demonstrated at 2 and 4 hours postprandially by paired t
test. In patients with atherosclerotic arterial wall, the mean AAb level w
as reduced to 90.8% of fasting levels (P < .001) after 2 hours and to 90% a
fter 4 hours (P < .01). This acute reduction in AAbs against MDA-LDL appear
s to be unique to atherosclerotic patients and could not be demonstrated in
young controls with healthy blood vessels. In nonatherosclerotic controls,
the mean normalized levels during postprandial lipemia were not statistica
lly different from baseline (104.5% at 2 hours and 104.6% at 4 hours). The
transient reduction in AAb levels with postprandial lipemia in atherosclero
tic patients could be reproduced in a subset of the CAD patients after sign
ificant improvement in the lipid profile with weight loss. In patients with
atherosclerotic disease, the transient reduction in the level of circulati
ng AAbs reflects either an increased propensity to generate oxidatively mod
ified epitopes or a reduced capacity to remove excess modified epitopes. Th
ese data are the first in vivo demonstration of an acute change in the oxid
ative process during postprandial lipemia. Copyright (C) 2000 by W.B. Saund
ers Company.