[Secondary hyperlipoproteinemia induced by diuretic therapy (author's transl)].
In order to study the degree and pathogenic aspects of the secondary hyperlipoproteinemia in patients under diuretic therapy we measured serum lipids, lipoproteins and the apoproteins A1, A2 and B in 12 adults after a 4 weeks placebo period and 6 weeks of treatment with chlorthalidon. There was a significant increase in atherogenic low density lipoproteins (LDL), (18%, P less than 0.05) whereas the high density lipoprotein-cholesterol Apo A1 and A2 levels were not significantly altered. The same was true for the total serum triglyceride- and the very low density lipoprotein- and LDL-triglyceride levels. The activity of lipoprotein lipase and hepatic triglyceride lipase was slightly but not significantly increased. A delayed LDL-catabolism seems to be the most probable pathogenic mechanism underlying the Chlorthalidon-induced hyperlipoproteinemia.
D000293:Adolescent; D000328:Adult; D001059:Apoproteins / Q000097:blood; D002752:Chlorthalidone / Q000009:adverse effects*; D005260:Female; D006801:Humans; D006951:Hyperlipoproteinemias / Q000139:chemically induced*; D008071:Lipoprotein Lipase / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D010919:Placebos; D014280:Triglycerides / Q000097:blood
D001059:Apoproteins; D008077:Lipoproteins, LDL; D010919:Placebos; D014280:Triglycerides; D008071:Lipoprotein Lipase; D002752:Chlorthalidone
Zur Pathogenese der Diuretika-induzierten Hyperlipoproteinämie.