| |
|
|
|
|
|
|
|||
|
EM Sloand, HG Klein, KB Pastakia, P Pierce and KN Prodouz
National Heart, Lung, and Blood Institute, National Institutes of Health,
Bethesda, MD 20892.
Platelet aggregation and bleeding time abnormalities are reported in
patients receiving beta-lactam antibiotics (beta LAs), although clinical
bleeding most frequently occurs in chronically ill, malnourished patients.
Although most beta LAs bind to serum albumin, the relative influence of
bound versus unbound beta LAs on platelet function is unknown. We examined
the effect of beta LAs on the aggregation of gel-filtered platelets from
normal subjects and on platelet-rich plasma (PRP) from hypoalbuminemic
patients. Therapeutic concentrations of five beta LAs were added to normal
platelets at different albumin concentrations (1.5 to 4.5 g/dL). Inhibition
of aggregation by the beta LAs was inversely proportional to the albumin
concentration, and most antibiotic-treated samples showed more than 50%
inhibition at albumin levels below 2.0 g/dL. When PRPs from hypoalbuminemic
patients were incubated with cephalothin, aggregation was completely
inhibited, in contrast to samples from patients with normal albumin levels,
and this decreased platelet aggregation was partially restored (25% to 75%)
by increasing the albumin concentration above 4.0 g/dL. Specific binding of
[35S]-benzylpenicillin to normal platelets decreased proportionately as the
albumin concentration increased in the range of 1.0 to 5.0 g/dL. The
inhibitory effects of beta LAs on platelets in vitro appear to be
influenced by albumin concentration. Plasma albumin concentration may
influence bleeding in patients receiving beta LAs.
This article has been cited by other articles:
| |||||||||||
| Copyright © 1992 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||