[Diabetes mellitus and chronic liver diseases. Literature review (part 2): treatment features].

Diabetes mellitus (DM) and chronic liver disease (CLD) are pathological conditions associated with each other and reaching epidemic proportions. There is a strong pathogenetic relationship of carbohydrate metabolism disorders and a number of CLD. Common mechanisms that provoke metabolic and autoimmune disorders in the development of various CLD, leading to steatosis, insulin resistance (IR), impaired glucose tolerance and the development of DM are described. Effective glycemic control can have a beneficial effect on the treatment of these patients, and, conversely, there is evidence of a positive effect of CLD therapy on carbohydrate metabolism. This review discusses the correction of carbohydrate metabolism in patients with CLD, the main groups of modern hypoglycemic drugs, mechanisms of their action, the impact on the physiology of the liver, the possibility of using each of these pharmacological groups in patients with impaired liver function. The modern approaches and possibilities of drug effects on the process of fibrogenesis in CLD, the effect of these drugs on carbohydrate metabolism are listed.

[Diabetes mellitus and chronic liver diseases. Part 1: general mechanisms of etiology and pathogenesis].

In recent years there has been an active discussion about the relationship between diabetes mellitus (DM) and chronic liver diseases (CLD). On the one hand, patients with diabetes have an increased risk of developing CLD. On the other hand, patients with CLD very often identify abnormal glucose metabolism which ultimately leads to impaired glucose tolerance and the development of diabetes. This review outlines potential causal relationships between some CLD and DM. Common mechanisms that provoke metabolic and autoimmune disorders in the development of various nosologies of the CKD group, leading to steatosis, insulin resistance, impaired glucose tolerance and the development of diabetes are described. Certain features of the assessment of carbohydrate metabolism compensation in patients with hepatic dysfunction, anemia and protein metabolism disorders are described.

[Risk factors and glycation end products in patients with different forms of coronary heart disease and type 2 diabetes mellitus]. / Faktory rosta i konechnye produkty glikirovaniya u bol'nykh s razlichnymi formami ishemicheskoi bolezni serdtsa i sakharnym diabetom 2-go tipa.

AIM: To determine the levels of growth factors and glycation end products in patients with different forms of coronary heart disease (CHD) and type 2 diabetes mellitus (T2DM). MATERIAL AND METHODS: A total of 134 patients with CHD and T2DM, including 38 patients with non-ST-elevation acute coronary syndrome (ACS), were examined. The arterial and venous serum levels of basic fibroblast growth factor-ß (FGF-ß), transforming growth factor-ß (TGF-ß), placental growth factor (PlGF), advanced glycation end products (AGEs) and their receptors (RAGE) were estimated in all the patients. RESULTS: A direct correlation was found between the degree of arterial stenosis and the level of growth factors and AGEs in the patients with T2DM; there was also a direct correlation of the examined factors with lipid metabolic parameters. There was a significant two-fold increase in FGF-ß, PlGF, and RAGE levels in the patients with ACS. CONCLUSION: Hyperglycemia was found to negatively affect the progression of atherosclerotic changes in the vessel wall and on that of fibrotic processes.

[Analysis of the -238(G/A)TNF polymorphism in breast cancer patients].

TNF is an inflammatory cytokine that involved in pathogenesis of different malignancies. Promoter single nucleotide polymorphism -238(G/A)TNF (rs361525) is investigated for the detection of susceptibility to the infectious, autoimmune and oncological diseases. The goal of the study was to investigate the association of-238(G/A)TNF polymorphism (rs361525) with breast cancer (BC) prognosis. -238(G/A) TNF allelic variants were detected by PCR-RFLP. We failed to reveal the genotype distributions disparity among groups with different stages of the disease, ER, PR or Her2/neu positive versus negative status. The AG genotype frequency was about 10% and there were no BC patients with AA genotype in all separated groups. However the overall survival was significantly lower for AG then for GG carriers with II stage or ER-positive BC. Our data suggest that -238(G/A)TNF polymorphism perhaps is not involved in the initiation of malignancies but it is a substantial factor of BC prognosis.