Trial design was
similar to that described above and lasted 12 to 24 weeks. Patients with diabetes showed a statistically significant mean percentage increase in walking distance (51.4%) when compared to placebo (32.6%). No statistical difference was found between the percentage change in maximal walking distance in the diabetic patients (51.4%) when compared to the non-diabetic patients (60.6%) treated with cilostazol. The authors examined the response to cilostazol based on baseline absolute claudication distance (ACD); they found that the response in non-diabetic patients was linear with greater response in those with better baseline function. However, this pattern was not seen in the diabetic cohort. Diabetic patients in the first quartile (ACD <96m) responded best to cilostazol with a 34.4% (95% CI 6.68–62.16%) improvement from baseline PS-341 order (n=59), in the second quartile (ACD 97–141m)
5.5% (95% CI -30.91–41.93%), in the third quartile (ACD 142–233m) 23% (95% CI -7.82–53.82%), and in the fourth quartile (ACD >233m) a 17.2% (95% CI -16.33–50.69%) change from baseline was seen. The adverse event profile was similar in the diabetic and non-diabetic patients. A recent randomised, double-blinded trial assessed the vascular and biochemical effects of cilostazol compared to mTOR inhibitor placebo in diabetic patients with peripheral arterial disease.4 They recruited 26 patients between the ages of 30 and 90 years with type 2 diabetes and intermittent claudication. Twelve patients were randomised to receive cilostazol 100mg twice daily and 14 to placebo. The groups were assessed at baseline, six and 24 weeks. Walking assessment was matched at baseline and there was a non-significant trend for improvement in the cilostazol group at 24 weeks with the initial claudication distance improving by 21.1% compared to -4.4% in the placebo group. Lipid profiles were not significantly different between groups at baseline. However, in the cilostazol group there was a significant reduction in serum cholesterol (p=0.007) and triglycerides many (p=0.005), and a significant increase in HDL
cholesterol (p=0.047) at 24 weeks when compared to baseline. There was no significant difference between ankle-brachial indices, arterial compliance or HbA1c in the cilostazol compared to the placebo group at baseline, six or 24 weeks. Cilostazol improves walking distance in patients with intermittent claudication and has desirable effects on lipid profiles. Diabetic patients with intermittent claudication have a higher risk of the complications of PAD and of cardiovascular events. The overall response to cilostazol in diabetic patients was not significantly different compared to non-diabetic patients but, interestingly, there appears to be a different pattern of response with the most severely affected diabetic patients gaining most benefit.