AimsTo determine the global extent of hypoglycaemia experienced by patients with diabetes using insulin, as there is a lack of data on the prevalence of hypoglycaemia in developed and developing countries.MethodsThis non‐interventional, multicentre, 6‐month retrospective and 4‐week prospective study using self‐assessment questionnaire and patient diaries included 27 585 patients, aged ≥18 years, with type 1 diabetes (T1D; n = 8022) or type 2 diabetes (T2D; n = 19 563) treated with insulin for >12 months, at 2004 sites in 24 countries worldwide. The primary endpoint was the proportion of patients experiencing at least one hypoglycaemic event during the observational period.ResultsDuring the prospective period, 83.0% of patients with T1D and 46.5% of patients with T2D reported hypoglycaemia. Rates of any, nocturnal and severe hypoglycaemia were 73.3 [95% confidence interval (CI) 72.6–74.0], 11.3 (95% CI 11.0–11.6) and 4.9 (95% CI 4.7–5.1) events/patient‐year for T1D and 19.3 (95% CI 19.1–19.6), 3.7 (95% CI 3.6–3.8) and 2.5 events/patient‐year (95% CI 2.4–2.5) for T2D, respectively. The highest rates of any hypoglycaemia were observed in Latin America for T1D and Russia for T2D. Glycated haemoglobin level was not a significant predictor of hypoglycaemia.ConclusionsWe report hypoglycaemia rates in a global population, including those in countries without previous data. Overall hypoglycaemia rates were high, with large variations between geographical regions. Further investigation into these differences may help to optimize therapy and reduce the risk of hypoglycaemia.

Hypoglycaemia has a major impact on patients and their behaviour. These global data for the first time reveal regional variations in response to hypoglycaemia and highlight the importance of patient education and management strategies.

Background: It is still debatable whether psoriasis increases cardiovascular risk indirectly since it is associated with metabolic syndrome or is an independent cardiovascular risk factor. The aim of this study was to evaluate psoriasis severity as an independent predictor of insulin resistance (IR) irrespective of the presence of metabolic syndrome (MetS). Methods: This was a case control study including 128 patients stratified into two groups: patients with psoriasis and metabolic syndrome vs. patients with psoriasis and no metabolic syndrome. MetS was diagnosed according to ATP III criteria with homeostatic model assessment of insulin resistance (HOMA-IR), as well as a homeostatic model assessment of beta cell function (HOMA-β) were calculated. Results: Compared to subjects without metabolic syndrome, patients with metabolic syndrome had a significantly higher Psoriasis Area Severity Index (PASI) values (p < 0.001). The strongest correlation was established for HOMA-IR and the PASI index (p < 0.001), even after adjustment for body mass index (BMI) in regression analysis model. In patients without MetS and severe forms of disease, the HOMA-IR and HOMA-β values were significantly higher compared to mild forms of disease (p < 0.001 for all) while in subjects with MetS no difference was established for HOMA-IR or HOMA-β based on disease severity. Conclusions: Psoriasis severity is an independent risk factor of HOMA-IR, the strongest association being present in the non-MetS group, who still had preserved beta cell function suggesting direct promotion of atherosclerosis via insulin resistance depending on the disease severity, but irrespective of the presence of metabolic syndrome.

Background: The discovery that genetic alterations in oncogenes and tumour suppressor genes accompany tumour formation in many human tumours has encouraged the search for genes that promote or suppress tumour spread and metastasis; nm23 is a promising candidate for a metastasis suppressing gene. Aims: To evaluate whether expression of nm23-H1 protein or loss of heterozygosity (LOH) of the nm23-H1 gene is associated with colon cancer progression. Materials/Methods: Paraffin wax embedded tissue sections were analysed immunohistochemically. DNA isolated from normal and tumour tissue was used for LOH analysis using a variable nucleotide tandem repeat (VNTR) marker located in the untranslated 59 region of the nm23-H1 gene. RNA isolated from tumour and normal tissue was used for ''real time'' RT-PCR. Results: Of 102 adenocarcinomas examined, 58.8% stained weakly for nm23-H1 protein. There was a negative correlation between nm23-H1 positivity and tumour histological grade. In VNTR analysis, 70.2% of patients were informative and 27.4% of tumours had nm23-H1 LOH. There was a positive correlation between nm23-H1 LOH and both tumour histological grade and Dukes's stage. Expression of nm23-H1 mRNA was increased in 22 of 30 colon tumours compared with normal tissue. No significant correlation was found between nm23-H1 mRNA expression and histological grade or Dukes's stage of tumours. Conclusions: These findings suggest that nm23-H1 protein expression in early stages may have a role in suppressing metastasis in sporadic colon cancer, whereas at a later stage both reduced nm23-H1 protein expression and LOH of the nm23-H1 gene may play role in colon cancer progression and metastasis.

Along with the increase in obesity and type 2 diabetes, the non-alcoholic fatty liver disease (NAFLD) incidence is escalating, thus becoming a leading cause of liver cirrhosis and a significant burden of liver-related outcomes. Since there is no pharmacotherapy available to address the NAFLD, the most effective solutions seem to be lifestyle changes centered on physical activity. Exercise could mediate its beneficial effects directly on the liver and indirectly via extrahepatic pathways, forming a dose-response relationship with NAFLD in terms of prevalence and disease severity. Health-enhancing physical activity (HEPA) levels are mainly needed to exert beneficial effects in obese subjects, while even a small amount of exercise can be beneficial for lean individuals to prevent NAFLD. This mini-review addresses three major points regarding physical activity and NAFLD: prevention, treatment, and extrahepatic benefits, offering recommendations on type and intensity of exercise in liver disease.

Colorectal cancer (CRC) is among the most prevalent cancers worldwide, and its prevention and reduction of incidence is imperative. The presence of diabetes has been associated with a 30% increased risk of CRC, likely through the mechanism of hyperinsulinemia, which promotes tumorigenesis via the insulin receptor in the epithelium or by insulin-like growth factor pathways, inflammation, or adipokines, inducing cancer cell proliferation and cancer spread. Metformin, the first-line agent in treating type 2 diabetes, has a chemopreventive role in CRC development. Additionally, preclinical studies suggest synergistic effects of metformin with oxaliplatin in inhibiting in vitro models of colon cancer. Although preclinical studies on the post diagnostic use of metformin were promising and suggested its synergistic effects with chemotherapy, the data on the possible effects of metformin after surgery and other CRC treatment in the clinical setting are less conclusive, and randomized controlled trials are still lacking.

Non-alcoholic fatty liver disease (NAFLD) is closely related to insulin resistance, type 2 diabetes mellitus, and obesity. It is nowadays considered a multisystem disease with a strong association with cardiovascular disease and arterial hypertension, which interfere with changes in the coagulation system. Coagulation disorders are common in patients with hepatic impairment and are dependent on the degree of liver damage. Patients with NAFLD may have preserved overall hemostatic profile, but many studies suggest a trend toward a procoagulant state. Hypercoagulable state in NAFLD patients may even induce progression of hepatic injury. Endothelial dysfunction is present in the systemic and portal vein circulation in NAFLD patients, and platelets are being recognized as modulators of liver diseases through various mechanisms. Through a literature review, we discuss possible disorders in the coagulation cascade and fibrinolysis, endothelial dysfunction, and platelet abnormalities in patients with NAFLD. Considering the processes and mechanisms involved in the hemostatic abnormalities associated with NAFLD, directly related to liver disease or indirectly related through inflammatory processes and metabolic disorders, several potential therapeutic targets have been identified and reviewed here.

No abstract