[Lipid profile and cardiovascular risk in patients with rheumatoid arthritis: Effect of the disease and of drug therapy].
The increased mortality in patients with rheumathoid arthritis (RA) is mainly due to high incidence of cardiovascular (CV) disease. CV morbidity and mortality in RA can be explained by several mechanisms: (1) chronic inflammation, (2) enhanced prevalence of traditional CV risk factors including atherogenic dyslipoproteinemia, (3) a lower use of evidence-based therapy such as statins and (4) chronic treatment for RA such as glucocorticoids. It is difficult to distinguish between the role of pharmacological treatment per se and the severity or duration of the disease since these two parameters are closely interrelated. RA likely influences lipoprotein metabolism leading to quantitative and qualitative alteration of low-density lipoproteins (LDL) and of high-density lipoproteins. Glucocorticoids alter carbohydrate and lipid metabolism. However, by reducing the inflammation level, the net effect on lipid parameters and on the CV risk may be favorable. Data from open follow-up studies would suggest that methotrexate use is associated with a beneficial effect on lipid parameters and with a reduction in the incidence of CV disease. Anti-TNF agents increase LDL-cholesterol in some but not all studies; however the use of anti-TNF agents likely reduce CV risk in patients with RA. The influence of recently developed compounds, anti-CD20, CTLA-4 Ig or anti-IL6 is not well documented. Anti-IL6 seem to increase total and LDL-cholesterol; however these changes are associated with an improvement in the TC/HDL-C ratio.
Hansel
B
B
Service d'endocrinologie-métabolisme et de prévention cardiovasculaire, hôpital de la Pitié-Salpêtrière, 47-83, boulevard de l'Hôpital, 75013 Paris, France. boris.hansel@psl.aphp.fr
Bruckert
E
E
D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000188:drug therapy* / Q000401:mortality*; D050197:Atherosclerosis / Q000139:chemically induced / Q000188:drug therapy; D002318:Cardiovascular Diseases / Q000097:blood / Q000188:drug therapy* / Q000401:mortality*; D002908:Chronic Disease; D050171:Dyslipidemias / Q000139:chemically induced / Q000188:drug therapy; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007249:Inflammation / Q000139:chemically induced / Q000188:drug therapy; D050356:Lipid Metabolism / Q000187:drug effects; D008055:Lipids / Q000097:blood*; D008074:Lipoproteins / Q000378:metabolism; D008297:Male; D008727:Methotrexate / Q000627:therapeutic use; D012307:Risk Factors; D000093242:Interleukin-6 Inhibitors
D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D005938:Glucocorticoids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D008074:Lipoproteins; D008727:Methotrexate; D000093242:Interleukin-6 Inhibitors; C502936:tocilizumab