Changes in plasma
lipoprotein levels and platelet reactivity were evaluated during sequential treatments with
clofibrate and
tiadenol, two
hypolipidemic agents with apparently different mechanisms, in 27 hyperlipoproteinemic patients. The objective of the study was to determine the pattern of plasma
lipoprotein variations, induced by a
drug mainly affecting
lipoprotein catabolism (
clofibrate) and by a
drug affecting biosynthesis (
tiadenol), and to single out-patients specifically responding to either treatment. Both drugs proved significantly active in type IIA and IV
hyperlipoproteinemias, not in type IIB.
Clofibrate significantly lowered
very low density lipoprotein (VLDL) associated
cholesterol in all three
hyperlipoproteinemia phenotypes, and it also lowered VLDL
triglycerides in type IV, while increasing
high density lipoprotein (
HDL) cholesterol in type IIA patients.
Low density lipoprotein (
LDL) cholesterol levels were minimally reduced by
clofibrate in type IIA (-4%), and increased in types IIB (+ 14.2%) and IV (+ 6.1%) patients. Conversely,
tiadenol lowered
VLDL cholesterol and
triglycerides to a lesser extent, but it did significantly reduce
LDL cholesterolemia in type IIA (-17.6%), while increasing
HDL cholesterol in type IIB. Statistical evaluation of the results did not permit identification of parameters associated with the response to either
drug, although individuals specifically responding to one or the other agent, or to both, were detected in all three phenotypes. The sensitivity to the major platelet aggregating factors,
ADP,
adrenaline and
collagen, was not significantly altered after
drug treatments. Evaluation of the hypolipidemic response to agents with different mechanisms may be of help in selecting the best treatment for individual patients.