• Lipid Disorders
• Diabetes & Endocrinology Clinical Trials
• Diabetes Mellitus

Atorvastatin therapy may delay the loss of beta-cell function in patients with recent-onset type 1 diabetes mellitus (T1DM). In rheumatoid arthritis patients, atorvastatin diminishes immune-mediated disease activity, but little is known about the systemic immune response that is associated with atorvastatin in patients with newly diagnosed T1DM. Hubert Kolb, PhD, Heinrich-Heine University, Dusseldorf, Germany, presented a study that investigated this issue.

The multicenter, randomized, placebo-controlled Diabetes and Atorvastatin (DIATOR) trial included 89 patients aged 18 to 39 years with newly diagnosed T1DM and islet autoantibodies. Patients were randomized to receive either atorvastatin (40 mg daily for 4 weeks followed by 80 mg daily; n=46) or placebo (n=43) for a total of 18 months. At 12 months, 33 patients in the atorvastatin group and 35 patients in the placebo group were included in the analysis. The final analysis at 18 months included 29 patients from the atorvastatin group and 34 patients from the placebo group. The groups were well matched at baseline. The primary endpoint was change in serum C-peptide levels from baseline to 12 and 18 months. C-peptide levels were assessed before and 90 minutes after patients received a standardized liquid mixed meal (Boost HP).

At 18 months, the median stimulated C-peptide and fasting C-peptide concentrations were higher in the atorvastatin group than in the placebo group (48% and 50%, respectively). Due to the high interindividual variation, this difference was not significant. Secondary analyses indicated partial preservation of beta-cell function in the atorvastatin but not the placebo group. Median fasting C-peptide levels within the atorvastatin group remained stable throughout the duration of the study. However, median fasting C-peptide levels in the placebo group decreased from baseline to 12 months and again at 18 months (p<0.001). There was a significant decline in median stimulated C-peptide concentrations for both groups from baseline to Month 12 (0.88 to 0.73 nmol/l for atorvastatin and 0.89 to 0.71 nmol/l for placebo; p<0.01 for both). This decline continued in the placebo group at Month 18 (p=0.047) but did not occur in the atorvastatin group.

The course of metabolic control was similar between the two groups. However, at 12 months, insulin doses varied between the two groups (p=0.007). An increase in HbA1C levels was observed in the placebo group from 12 to 18 months, but this was not the case in the atorvastatin group. Those who were treated with atorvastatin demonstrated decreases in systemic levels of C-reactive protein, total and low-density lipoprotein cholesterol, and triglycerides (p<0.001 for all). Additionally, the course of the chemokine MCP-1 differed between the two groups, as a decrease was observed in the placebo group but not in the atorvastatin group (p=0.009). The course of the other 14 immune mediators appeared to be similar for atorvastatin and placebo. There did not appear to be covariates that were associated with atorvastatin and C-peptide secretion such as age, body mass index, or baseline serum C-peptide concentrations.

Atorvastatin may delay the loss of residual beta-cell function in patients with newly diagnosed T1DM and merits further investigation in a larger clinical trial.

• © 2010 MD Conference Express