Type 2 diabetes mellitus is a well-established risk factor for cardiovascular disease (CVD). New therapeutic approaches have been developed recently based on the incretin phenomenon, such as the degradation-resistant incretin mimetic exenatide and the glucagon-like peptide-1 (GLP-1) analogue liraglutide, as well as the dipeptidyl dipeptidase (DPP)-4 inhibitors, such as sitagliptin, vildagliptin, saxagliptin, which increase the circulating bioactive GLP-1. GLP-1 exerts its glucose-regulatory action via stimulation of insulin secretion and glucagon suppression by a glucose-dependent way, as well as by weight loss via inhibition of gastric emptying and reduction of appetite and food intake. These actions are mediated through GLP-1 receptors (GLP-1Rs), although GLP-1R-independent pathways have been reported. Except for the pancreatic islets, GLP-1Rs are also present in several other tissues including central and peripheral nervous systems, gastrointestinal tract, heart and vasculature, suggesting a pleiotropic activity of GLP-1. Indeed, accumulating data from both animal and human studies suggest a beneficial effect of GLP-1 and its metabolites on myocardium, endothelium and vasculature, as well as potential anti-inflammatory and antiatherogenic actions. Growing lines of evidence have also confirmed these actions for exenatide and to a lesser extent for liraglutide and DPP-4 inhibitors compared with placebo or standard diabetes therapies. This suggests a potential cardioprotective effect beyond glucose control and weight loss. Whether these agents actually decrease CVD outcomes remains to be confirmed by large randomized placebo-controlled trials. This review discusses the role of GLP-1 on the cardiovascular system and addresses the impact of GLP-1-based therapies on CVD outcomes.

Antithyroid drugs (ATDs) remain the first-line therapy in patients with Graves' disease (GD), despite a high relapse rate. The purpose of this study was to identify the predictors of remission in patients with GD treated with ATDs-retrospective study at an endocrine referral service in Northern Greece. Two-hundred and eleven patients met the study's criteria. Females (p = 0.049), non-smokers (p = 0.017), patients without ophthalmopathy (p = 0.033), and those developing pharmaceutical hypothyroidism (p = 0.018) experienced longer duration of remission. Duration of remission was positively associated with therapy duration (r s = 0.151, p = 0.030), maximum TSH levels during (r s = 0.241, p = 0.001), at the end (r s = 0.280, p < 0.001) and 3 months after therapy (r s = 0.341, p = 0.003). There was a negative association with free T4 (FT4) (r s = -0.426, p < 0.001) and free triiodothyronine (FT3) (r s = -0.467, p = 0.038) levels at 6 months after ATDs discontinuation. In multiple-regression analysis, only duration of the first ATDs course for more than 24 months independently predicted duration of remission. Female gender, non-smoking, the absence of orbitopathy, treatment duration, pharmaceutical hypothyroidism, higher TSH levels during, at the end and 3 months after ATDs discontinuation, and lower FT4 and FT3 levels 6 months after therapy were associated with longer duration of remission. However, only duration of ATDs therapy for more than 24 months independently predicted predict long-term remission in GD.

The majority of NFPAs not selected for surgery at diagnosis remained stable in size. Pituitary dysfunction and visual defects at diagnosis were common. Surgical debulking led to clinical improvement, but relapse occurred in 2/3 of the cases.

Majority of PIs are non-functioning adenomas that remain stable in size. Relapse in size and hypopituitarism postoperatively are common. PIs, for which conservative management was initially considered appropriate, did not progress in size.

Rosuvastatin compared with atorvastatin resulted in significant improvements in IS indices. No significant changes in adiponectin, leptin or hsCRP levels were observed at 4 and 12 weeks of treatment with either statin.