In a nutshell
This study investigated the link between glucocorticoid (for example Deltasone, Orasone) use in patients with rheumatoid arthritis and changes in levels of good and bad cholesterol.
Some background
Atherosclerosis is the buildup of fatty substances on the inner walls of the arteries. In particular, low-density lipoprotein (the “bad” cholesterol) and triglycerides are fatty substances that can build up inside arteries. This reduces blood flow and increase the risk of strokes and heart attacks.
Another fatty substance, high-density lipoprotein, is known as the “good” cholesterol. This is because higher levels can actually decrease the risk of atherosclerosis. The effect of glucocorticoids on the balance between good and bad cholesterol is unknown. However, this is very important as patients with rheumatoid arthritis already have higher levels of heart attacks and strokes.
Methods & findings
This study included 202 rheumatoid arthritis patients who had taken glucocorticoids by mouth or injection for at least 3 months. 436 rheumatoid arthritis patients who had not taken any glucocorticoids were also included for comparison. Levels of different fatty substances in patient blood samples were measured before and after glucocorticoid use.
Patients who received more than 7.5 mg of glucocorticoids every day had the biggest increase in levels of “good” cholesterol, 6.0 mg/dL. This was significantly more than patients who had not taken glucocorticoids (2.4 mg/dL increase) and patients who had received less than 7.5 mg of glucocorticoids every day (3.1 mg/dL increase).
Glucocorticoid use had no significant affect on any of the other fatty substances measured in these patients.
The bottom line
These results suggest that this glucocorticoid dose is not associated with increases in fatty substances that cause atherosclerosis. They suggest that this finding is especially important for rheumatoid arthritis patients, as they have a higher risk of heart problems and stroke.
Published By :
Rheumatology International
Date :
Dec 28, 2014
