Diabetes PubMed

In this community-based cohort, 30 months of therapy with rosiglitazone treatment was associated with increased risk of congestive heart failure (CHF) but was not associated with increased risk of acute myocardial infarction (AMI), acute coronary syndrome (ACS), coronary revascularization, or all-cause mortality.

Rosiglitazone may protect against cognitive decline in older persons with type 2 diabetes and mild cognitive impairment (MCI).

Disclosure rates for financial conflicts of interest were unexpectedly low, and there was a clear and strong link between the orientation of authors' expressed views on the rosiglitazone controversy and their financial conflicts of interest with pharmaceutical companies.

While regular monitoring of liver enzymes is still recommended and more long term data are desirable, current evidence from clinical trials and postmarketing experience in the US supports the conclusion that rosiglitazone and pioglitazone do not share the hepatotoxic profile of troglitazone.

Analysis of these cases and of the experimental troglitazone toxicity data points to mitochondrial toxicity as a central factor.

Thiazolidinediones are usually well tolerated; however, their use may be associated with several adverse effects. The first TZD, troglitazone, was withdrawn from the market owing to serious hepatotoxicity.

In conclusion, our study demonstrated for the first time that TGZS (Troglitazone sulfo-conjugated metabolite) has direct toxicity effect on human liver cells and may be partially responsible for the hepatotoxicity of TGZ (Troglitazone).

Pioglitazone is the preferred thiazolidinedione to reduce cardiovascular risk in people with type 2 diabetes.

This suggests that a 24-week treatment with pioglitazone or bed-time insulin has a similar impact on intra-abdominal fat mass and systemic low-grade inflammation.

These findings strongly suggest that pioglitazone has an important place in the management of type 2 diabetes.

To the best of our knowledge this is the first reported case of pancytopenia induced by pioglitazone therapy.

These results indicate that pioglitazone may enhance the efficiency of glucose metabolism in the brain.

Thus, the combination of pioglitazone with candesartan is potentially a promising therapeutic strategy for type 2 diabetes.

Pioglitazone may offer a novel strategy for the treatment of AD.

The advantages and disadvantages of adding pioglitazone instead of adding basal insulin should be assessed further.

Pioglitazone appears to play an anti-inflammatory role in atherosclerosis process.

We conclude that, in type 2 diabetes mellitus patients, pioglitazone-but not rosiglitazone-significantly raised sRAGE, which may contribute to its antiatherogenic effects.

Pioglitazone also had a favourable risk profile compared with rosiglitazone; although this requires replication in other studies, it may have implications for prescribing within this class of drugs.

Pioglitazone improves glucose metabolism and insulin-resistance compared to acarbose in type 2 diabetic patients already treated with metformin and sulphonilureas.

The efficacy and safety of adding pioglitazone to either metformin monotherapy or sulphonylurea monotherapy were good.