cosyntropin and Hyperlipidemias

The mechanisms behind secondary hyperlipidemia in patients with various chronic inflammatory diseases are not known in detail. We have recently demonstrated that ACTH exerts strong hypolipidemic effects in healthy volunteers. To test the clinical relevance of this finding, we administrated ACTH during three weeks to nine hyperlipidemic steroid-treated patients with kidney disease. Before administration of ACTH 1-24, plasma ACTH concentrations were low. Treatment with ACTH led to 20 to 50% reductions in serum concentrations of triglycerides, cholesterol, LDL cholesterol and Apo B as well as of Lp(a). HDL cholesterol and Apo A1 concentrations increased by 10 to 25%. HL activity in postheparin plasma decreased by about 40% and LPL activity, which was initially low, increased by about 140%. The effects of ACTH were similar in kidney transplant recipients and in patients with inflammatory kidney disease. Our results indicate that hyperlipidemia in steroid treated patients with kidney disease may at least partly be due to iatrogenic ACTH deficiency.

Topics: Adrenocorticotropic Hormone; Adult; Cosyntropin; Humans; Hyperlipidemias; Hypolipidemic Agents; Kidney Diseases; Lipids; Lipoproteins; Male; Middle Aged; Steroids; Time Factors

In hyperlipaemic rabbits (fat supply), perirenal adipose tissue lipolysis does not vary with one in vitro clofibride dose. After a 16 days pretreatment, one in vitro clofibride dose reduces the basal lipolysis and the lipolytic action of synacthene, and increases the antilipolytic effect of insulin. The reduction of the lipolysis of adipose tissue could explain, in part, the hypolipaemic action of clofibride.

Topics: Adipose Tissue; Animals; Clofibrate; Cosyntropin; Female; Hyperlipidemias; Hypolipidemic Agents; Insulin; Kinetics; Lipolysis; Rabbits