Lipoprotein(a) has been strongly suggested to be a risk factor for atherosclerosis. However, its metabolism and/or regulation by drug treatment still remain unknown.Wetherefore studied the effects of glucocorticoid therapy on serum lipoprotein(a) in rheumatic diseases. Although the glucocorticoid treatment increased the total serum cholesterol, high-density lipoprotein cholesterol and apolipoprotein B concentrations, it reduced the serum lipoprotein(a) concentration (mean, 40%) in a dose-dependent manner in 9 patients with rheumatic diseases without nephrotic syndrome. Similar results were observed in 2 patients who did have nephrotic syndrome. It is assumed that the increase of total cholesterol and apolipoprotein B in serum levels are atherogenic, whereas the increase of high-density lipoprotein cholesterol and the decrease of lipoprotein(a) are protective for atherosclerosis. The clinical outcome of the concomitant results in lipid metabolism in the development of atherosclerosis remains to be studied.
(Internal Medicine 32: 382-386, 1993)