Key result
Adrenocortical steroid therapy was associated with increased plasma levels of cholesterol and triglyceride, increased plasma insulin response to glucose, and increased pre-β-lipoprotein turnover.
Why the study?
Does adrenocortical steroid therapy increase plasma lipid levels in patients with rheumatic diseases?
Observational
Does adrenocortical steroid therapy increase plasma lipid levels in patients with rheumatic diseases?
Adrenocortical steroid therapy in rheumatic diseases is associated with adverse metabolic changes, including elevated cholesterol, triglycerides, and hyperinsulinemia driven by diminished glucose tolerance.
May warrant lipid/glucose monitoring with adrenocortical steroids; leaves open causal confirmation in randomized trials.
For a three-month period, all patients attending an immunology clinic were screened for disorders of lipid metabolism in order to study the relationship between plasma lipids and adrenocortical steroid therapy. Among women, significantly higher cholesterol and triglyceride levels were found in treated patients than in untreated patients. The number of men screened was insufficient for statistical analysis. A prospective study was therefore carried out that indicated corticoid treatment led to increased plasma levels of cholesterol and triglyceride, and also to an increased plasma insulin response to orally given glucose and to increased pre-β-lipoprotein turnover. These metabolic changes are compatible with the following scheme: diminished glucose tolerance stimulates compensatory hyperinsulinemia, and the latter stimulates increased hepatic production of pre-β-lipoprotein, which leads to elevated plasma levels of this lipoprotein.
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Michael P. Stern (1973) conducted an observational in Rheumatic Diseases. Adrenocortical steroid therapy vs. Untreated patients was evaluated on Plasma levels of cholesterol and triglyceride. Adrenocortical steroid therapy was associated with increased plasma levels of cholesterol and triglyceride, increased plasma insulin response to glucose, and increased pre-β-lipoprotein turnover.
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