INTRODUCTION: Thiazolidinediones significantly reduce fasting plasma glucose and HbA (1c). These effects are due to improved insulin sensitivity by activating the nuclear PPAR-gamma (peroxisomal proliferator-activated receptors-gamma) and affection of different intracellular functions. The objective of this review was to analyse recently published studies and meta-analyses about thiazolidinediones, which suggested a significant cardiovascular risk associated with rosiglitazone therapy. Therefore clinicians have been left uncertain as to whether rosiglitazone should still be considered for the treatment of type-2-diabetes. DISCUSSION: An important side-effect of thiazolidinediones is fluid retention and edema. Therefore, heart failure NYHA I-IV is a contraindication for treatment with Thiazolidinediones. Pioglitazone shows favourable changes in lipid parameters like decrease of serum-triglycerides and increase of HDL-cholesterol, while Rosiglitazone temporarily increases LDL-cholesterol. In patients with type-2-diabetes mellitus and a high cardiovascular risk the PROactive study did not show a significant effect on the primary endpoint but significantly reduced the predefined secondary combined endpoint of total mortality, nonfatal myocardial infarction and stroke. Conversely, recently published meta-analyses suggested an increased cardiovascular risk and myocardial infarction rate associated with rosiglitazone therapy. CONCLUSION: Treatment with Rosiglitazone should be reconsidered because of a potential cardiovascular risk. In high risk patients without heart failure pioglitazone may be favoured for treatment of type 2 diabetes mellitus.
INTRODUCTION:Thiazolidinediones significantly reduce fasting plasma glucose and HbA (1c). These effects are due to improved insulin sensitivity by activating the nuclear PPAR-gamma (peroxisomal proliferator-activated receptors-gamma) and affection of different intracellular functions. The objective of this review was to analyse recently published studies and meta-analyses about thiazolidinediones, which suggested a significant cardiovascular risk associated with rosiglitazone therapy. Therefore clinicians have been left uncertain as to whether rosiglitazone should still be considered for the treatment of type-2-diabetes. DISCUSSION: An important side-effect of thiazolidinediones is fluid retention and edema. Therefore, heart failure NYHA I-IV is a contraindication for treatment with Thiazolidinediones. Pioglitazone shows favourable changes in lipid parameters like decrease of serum-triglycerides and increase of HDL-cholesterol, while Rosiglitazone temporarily increases LDL-cholesterol. In patients with type-2-diabetes mellitus and a high cardiovascular risk the PROactive study did not show a significant effect on the primary endpoint but significantly reduced the predefined secondary combined endpoint of total mortality, nonfatal myocardial infarction and stroke. Conversely, recently published meta-analyses suggested an increased cardiovascular risk and myocardial infarction rate associated with rosiglitazone therapy. CONCLUSION: Treatment with Rosiglitazone should be reconsidered because of a potential cardiovascular risk. In high risk patients without heart failurepioglitazone may be favoured for treatment of type 2 diabetes mellitus.