This review examined the current problem of low adherence to treatment in patients with chronic diseases, particularly type 2 diabetes mellitus. According to the definition of the World Health Organization, ‘adherence to treatment’ is the degree to which a patient’s behaviour corresponds to the doctor’s recommendations with respect to medications and implementation of dietary advice and/or lifestyle changes. The current medical literature includes a large number of scientific publications devoted to the study of various factors that lead to low adherence to treatment. The term ‘barriers’ is most often used to designate these factors. The first part of this work contains an analysis of the main factors that impede compliance to the doctor’s recommendations, such as socioeconomic and psychological (personal) barriers related to the disease itself, the peculiarities of its treatment and the organisation of medical care (the health care system).

The second part of this review examines the different theoretical models of patient behaviour and strategies that improve adherence to treatment. Most researchers believe that there is an unsatisfactory (low) adherence to treatment and that none of the existing intervention strategies can improve adherence to treatment among all patients. The cornerstone of the entire diabetes management system is the training of patients within the framework of developed structured programmes. Conversely,, success depends on the individual approach, the course of the disease and the mandatory consideration of the individual psychological characteristics of each person. Establishment of a partnership built on trust between a doctor and a patient contributes to greater patient satisfaction with treatment and improved adherence, and this relationship ultimately affects the treatment efficacy and clinical outcomes.

Many studies have demonstrated the high effectiveness of bariatric surgery in patients with grade 2–3 obesity and type 2 diabetes mellitus. Currently, surgery is one of the most effective ways to decrease body mass, to maintain long-term weight loss and to manage type 2 diabetes mellitus. Particular interest has been generated by the strong influence of bariatric surgical interventions on the disruption of carbohydrate metabolism in patients who undergo surgery. This change leads to an improvement in the course of type 2 diabetes mellitus as well as its full remission. This review presents information on the mechanisms that are needed to improve glycaemic control in patients with obesity even after bariatric surgery. This review also contains a comparative analysis of how various surgical interventions influence the course of diabetes, the reasons for postbariatric glycaemia and predictors of the effectiveness of bariatric surgeries in terms of metabolic control in patients with type 2 diabetes mellitus.

Until recently, the primary focus of the studies by bariatric surgeons was on patients with grade 2–3 obesity and type 2 diabetes mellitus. However, in this review, special attention is given to the patients with a body mass index that ranges from 30 to 35 kg/m. Gained experience of the bariatric surgeons leads to high effectiveness with respect to the influence on the course of diabetes in patients with grade 1 obesity, which allows us to significantly expand the range of patients who should be recommended for this surgery. In addition, some information concerning surgical and metabolic complications of bariatric surgical intervention is provided, which allows us to seriously consider this treatment.

Background. Osteoporosis and type 2 diabetes are common comorbidities in postmenopausal women. An important role in the bone remodeling over the menopausal transition can be played by cytokines and matrix metalloproteinases (MMPs). It was shown that allelic variants in polymorphic positions of the genes of cytokines and MMPs affect the expression of these molecules under normal and pathological conditions.

Aims. To examine associations between polymorphisms in the gene promoters of cytokines (TNFA, IL1B, IL4, IL6, IL10, VEGFA) and MMPs (MMP2, MMP3, MMP9) with bone mineral density (BMD) in postmenopausal women with type 2 diabetes.

Materials and methods. We studied 197 Caucasian diabetic women, from 50 to70 years of age. An examination of BMD in the spine, proximal femur and forearm was performed by DEXA. Thirteen polymorphisms in the promoters of TNFA: -238 A/G (rs361525), -308 A/G(rs1800629) and -863 C/A (rs1800630), IL1B: -31 C/T (rs1143627), IL4: -590 C/T (rs2243250), IL6: -174 C/G (rs1800795), IL10: -592 C/A (rs1800872) and -1082 A/G (rs1800896), VEGFA: -2578 C/A (rs699947) and +936 C/T (rs3025039), MMP2: -1306 C/T (rs243865), MMP3: -1171 5A/6A (rs3025058) and MMP9: -1562 C/T (rs3918242), were investigated.

Results. Seventy-three women had normal BMD, in 90 ones we revealed osteopenia, and 34 women had osteoporosis. Age, BMI and smoking were strongest predictors of BMD in multivariate regression analysis (p<0.0001, p=0.003 and p=0.01, respectively). In the additive model, C allele and CC genotype in MMP9 -1562 position were associated with low BMD (OR 2.16, p=0.0007 and OR 2.02, p=0.0008, respectively). Association of the polymorphism with BMD remained significant after adjustment for clinical risk factors (p<0.001). Twelve combinations of genotypes, associated positively with low BMD, were revealed by bioinformatic analysis (all p<0.005). The СС genotype in position -1562 of MMP9, CC genotype in position -863 of TNFA, GG genotype in position -308 of TNFA, and AA genotype in position -1082 of IL10 were the most prevalent variants in these combinations.

Conclusions. Variability in the gene promoters of cytokines and MMPs may confer individual susceptibility to osteoporosis in postmenopausal type 2 diabetic women.

Background. Subclinical hypothyroidism during pregnancy and gestational diabetes mellitus (GDM) is known to be associated with maternal and child morbidity. The concept of subclinical dysfunction of the thyroid gland in pregnant women depends on the population-specific and trimester-specific reference values so fixed universal cutoff concentrations for thyroid-stimulating hormone (TSH) that were recommended earlier now are put under the question. Population-specific and trimester-specific reference values have not been defined for pregnant women residing in Saint Petersburg. The data concerning the association of maternal thyroid status with GDM development are controversial.

Aims. The aim of the study was to determine the reference values of TSH and free thyroxin (fT4) in the first trimester of pregnancy in women living in St. Petersburg, and to assess the relationship between thyroid status and the risk of subsequent development of GDM.

Materials and methods. The levels of TSH, fT4 and thyroid peroxidase antibodies (TPO-Ab) were analyzed in 503 pregnant women before the 14th week of gestation. The women underwent oral glucose tolerance test (OGTT) at 24–28 weeks to find out those with GDM. The association between thyroid function, thyroid autoimmunity and the risk of GDM we estimated.

Results. The reference values for TSH were 0.07 – 4.40 mU /L, and for fT4 11.7 – 20.3 pmol/L. The prevalence of subclinical hypothyroidism in the 503 pregnant women was 16.9% according to the diagnostic criteria of TSH> 2.5 mIU / L and 3.8% using our calculated reference interval. Hypothyroxinemia was registered in 5,3% using reference values recommended by diagnostic tests manufacturer and in 2,8% according to our calculated reference interval for fT4. GDM was diagnosed in 23% of women. Logistic regression analysis showed associations of hypothyroxinemia and TPO-Ab-positivity with the increased risk of GDM that remained significant after adjustments on age and body mass index (BMI) [adjusted OR (95% CI) = 7.39 (1.27–42.93) for hypothyroxinemia, p=0.026; and adjusted OR (95% CI) = 2.02 (1.01–4.04) for TPO-Ab-positivity, p=0.047).

Conclusions. Reference intervals for first trimester TSH and fT4 have been established for pregnant women living in St. Petersburg. Hypothyroxinemia and TPO-Ab-positivity were associated with the increased risk of GDM.

Background. Autoimmune polyglandular syndrome type 1 (APS type 1) is a rare inherited autoimmune disease caused by mutations in AIRE gene (autoimmune regulator) and characterized by list of components. Diabetes mellitus (DM) can be one of components of this disease.

Aims. To show frequency of DM in patients with APS type 1 in Russia, to describe clinical and immunological aspects of DM in patients with APS type 1

Materials and methods. 113 patients have been enrolled in the study, 16 of them had DM (15/16) or impaired glucose tolerance (1/16). Antibodies against glutamate decarboxylase, tyrosine phosphatase, zinc transporter-8, insulin and β-cells of pancreas were investigated in 30 patients with APS type 1 without DM and in 11 patients with APS type 1 and DM. ELISA test was used for detection autoantibodies.

Results. Frequency of DM in patients with APS type 1 in Russia is 14.1% (16/113). Some patients had slow-progressive DM – 19%(3/16). Antibodies against insulin and β-cells were not specific and also were not sensitive markers for DM in APS type 1. Antibodies against tyrosine phosphatase and zinc transporter-8 test showed high specificity (100% и 97%), but low sensitivity (42% и 33,3%). Antibodies against glutamate decarboxylase were less specific (70%) and had very low sensitivity (58,3%).

Conclusions. Frequency of DM in patients with APS type 1 in Russia is high to compare to other countries. 20% of Russian patients had slow-progressive course of DM. Antibodies against tyrosine phosphatase and zinc transporter-8 were the most specific for DM in patients with APS type 1, but sensitivity of these antibodies was low.

Background: The efficacy of the treatment of type 1 diabetes can be markedly improved using artificial pancreas (AP), which is a technology to automatically control blood glucose levels.

Aim: In this paper, we propose the construction of a controller for controlling the automated delivery of insulin in AP based on a proportional–integral–derivative (PID) algorithm using intraperitoneal (IP) insulin delivery.

Methods: The project used rapid-acting insulin in the IP space when setting up a PID controller with feedback to ensure the safe and efficient delivery of insulin. The controller was configured to satisfy feedback insulin present in blood. Controller check was performed In Silico using the metabolic simulator UVA|Padova T1DMS on 10 virtual patients.

Results: The proposed controller design has time to reach 83% within the glycaemic range of 70–140 mg/dl (3.9–7.8 mmol/l), without time spent in hypoglycaemia.

Conclusions: In a future study we plan to test this controller in vivo to evaluate its performance in vivo.

Wolcott-Rallison syndrome is a rare autosomal recessive disease characterized by neonatal diabetes mellitus in combination with osteodysplasia and liver failure. This disease is the most common cause of neonatal diabetes mellitus in consanguineous families. Wolcott-Rallison syndrome is associated with mutations in the EIF2AK3, the gene encoding a transmembrane enzyme PERK (pancreatic endoplasmic reticulum kinase) which inhibits the synthesis of proteins in the event of misfolding in the endoplasmic reticulum. In addition to the core symptoms patients may develop multisystemic clinical manifestation including acute renal and liver failure, short stature, exocrine pancreatic insufficiency, neuro-motor deficit, hypothyroidism, anemia, neutropenia, recurrent hypoglycemia. The disease is characterized by high mortality, more than 50% of patients die from fulminant liver failure. The awareness of Wolcott-Rallison syndrome is extremely low due to the rarity of detection, however in view of the severity of the disease and the unfavorable prognosis patients with this syndrome require timely diagnosis and care of well-organized team of specialists.