Background. Beta-cell antibody tests are used for the differential diagnosis of diabetes mellitus. They permit to discriminate between the type 1 diabetes (T1D) and non-autoimmune diabetes types. To choose an appropriate test for ruling in or ruling out the T1D a physician needs to know how conclusive test results are. The most powerful estimate of test conclusiveness is its likelihood ratio (LHR). The higher LHR of a positive result (LHR+), the more posttest probability of T1D; the lower LHR of a negative result (LHR−), the less posttest probability of T1D.

Aims. To compare conclusiveness of single and combined tests for antibodies to islet cells (ICA), glutamate decarboxylase (GADA), and tyrosine phosphatase IA-2 (IA-2A), and to evaluate posttest probabilities of T1D at various pretest probabilities.

Methods. All antibodies were tested in parallel in 169 children and adolescents with a new-onset T1D, and in 169 persons without this disease. ICA, GADA, and IA-2A were determined by indirect immunofluorescence, radioimmune assay, and ELISA, respectively. LHR+ and LHR− were calculated with the MedCalc Statistical Software. Posttest T1D probabilities were calculated from Bayes theorem-based equation.

Results. Among single tests, an ICA test had the greatest LHR+ and the smallest LHR−, and consequently was the most reliable either for ruling in or ruling out the T1D. Among test combinations, an ICA&GADA combination had the greatest LHR+ and was the most suitable for T1D confirmation. The triple combination ICA&GADA&IA-2A had the smallest LHR− and was the most suitable for T1D exclusion.

Conclusions. In the differential diagnosis of diabetes, the most appropriate test for ruling in the T1D is the double combination ICA&GADA. With both antibodies positive, this combination provides the highest posttest T1D probabilities at any pretest probability. The most appropriate test for ruling out the T1D is the triple combination ICA&GADA&IA-2A. With all three antibodies negative, this combination provides the lowest posttest T1D probabilities.

Background. Intensive glycaemic control in patients with type 1 diabetes may lead to hypoglycaemia and thus increase the risk of cardiovascular and cerebrovascular events. Platelet activation and/or decreased activity of physiological anticoagulants during hypoglycaemia may play a role in the development of cardiovascular or cerebrovascular complications.

Aims. To investigate induced platelet activity, the activity of physiological anticoagulants, and the von Wil-lebrand factor in patients with type 1 diabetes with the hyperinsulinaemic–hypoglycaemic clamp.

Materials and methods. We examined 11 patients with type 1 diabetes without macro- and micro-vascular complications (6 males, 5 females, mean age 23.7 ± 5.6 years, A1C 9.7 ± 2.3%). Induced platelet aggregation, physiological anticoagulants (Protein S, Protein C, AT III) and the von Willebrand factor were studied at hyperglycaemic, euglycaemic, and hypoglycaemic stages during use of a hyperinsulinaemic (1 mU/kg/min) hypoglycaemic clamp.

Results. Platelet aggregation to all agonists increased significantly during the hypoglycaemic stage, compared with the euglycaemic or hyperglycaemic stages. There was no difference in platelet aggregation between the euglycaemic and hyperglycaemic stages. Platelet aggregation to all agonists increased during the hypoglycaemic stage compared with the hyperglycaemic period: thrombin–23.9%, ADP–30.6%, arachidonic acid–30.9%, collagen–69.4% and ristocetin–70.8%. During hypoglycaemia aggregation to ADP, arachidonic acid and collagen remained within normal limits (upper quartile); aggregation to thrombin was significantly above normal limits and aggregation to ristocetin remained significantly below lower limits. Protein S activity was significantly increased during hypoglycaemia compared with euglycaemia (p = 0.046) and hyperglycaemia (p = 0.046). Antithrombin-III activity decreased significantly at the euglycaemic and hypoglycaemic stages, compared with the hyperglycaemic period, but still remained significantly elevated above the upper threshold. Protein C and vWf activity did not change significantly.

Conclusions. In patients with type 1 diabetes platelet aggregation and protein S activity increases significantly at the hypoglycaemic stage of the hyperinsulinaemic–hypoglycaemic clamp. Platelet activation is directly caused by hypoglycaemia and not by decreasing glucose levels. Increased protein S activity is a compensatory response to platelet activation.

Background. Gestational diabetes (GDM) due to GCK gene mutations is the most frequent form of monogenic diabetes mellitus (DM) presenting during pregnancy. It has been suggested that the use of insulin in pregnancies with fetuses carrying GCK mutations may lead to intrauterine growth retardation. In the present study we evaluated the effect of insulin therapy during pregnancy on birth weight and length in the offsprings of mothers with GDM due to GCK mutations.

Aims. The aim was to study birth weight and length in offsprings of mothers with gestational diabetes mellitus due to mutations in GCK, depending on the therapy during pregnancy.

Materials and methods. The study included 38 patients with GDM caused by GCK gene mutations (18.7%) and the 45 offsprings. To define molecular basis of GDM in pregnant women we used a targeted NGS. ‘Diabetes panel’ genes were sequenced using a custom Ion Ampliseq gene panel and PGM semiconductor sequencer (Ion Torrent). To found the same mutations in their offsprings was used Sanger sequencing. All children were divided into 3 groups depending of their genotype and therapy received by the mothers during pregnancy.

Results. We found statistically significant differences in birth length (p=0.04) and weight (p=0,031) depending on the genotype of the child and therapy in the mother. The risk of macrosomia was shown in non-mutation-carrying offsprings only. The birth weight in children with GCK gene mutations whose mothers received insulin during pregnancy was significantly lower. However, the birth weight remained in the normal range.

Conclusions. Since prenatal diagnostics in the mothers with GCK gene mutations is not always justified, we recommend insulin therapy in order to prevent fetal macrosomia, which, however, should be less aggressive than in GDM due to other causes.

Background. The inactive stage of the diabetic Charcot arthropathy foot (CA) is characterised by fixed foot deformities and an absence of inflammation. However, it remains unclear if the shape of the foot and its biomechanics change during long-term follow-up.

Aim. To evaluate changes in loading distribution of the affected foot, in patients with inactive CA, during long-term follow-up.

Materials and methods. Twenty seven patients with unilateral inactive CA (19 females, 8 males) were studied. Computer pedography (emed AT, novel gmbh) was performed and baseline and the last studies were analysed. Maximal peak pressures (PP) were obtained for the first and the last studies and the percentage of the PP change was calculated for the total follow-up period and for periods: <24 months, 24–48 months, >48 months.

Results. PP increased: under the hallux 50%; 1st metatarsal–30.7%; 2nd toe–20%; 2nd toe–6%; midfoot–9%. PP decreased under 3–5 toes up to 67%. Significant changes at the first period were found under 3–5 toes only (−62%). The increase in loading under the other parts of the foot appeared at 24 months; however, these changes became significant between 24 and 48 months and peaked after 48 months of follow-up. The maximal increase of PP was noticed under the hallux, the 2nd toe, metatarsals 1–3 and the midfoot.

Conclusions. We revealed the gradual redistribution of PP, under the different parts of the foot, in patients with inactive CA. This redistribution reflects changes in the shape of the affected foot. The loading increased under the hallux, the 2nd toe and the corresponding metatarsals, 3rd metatarsal and midfoot, and decreased under the 3–5 toes. These changes increased during the follow-up, becoming more pronounced after 4 or more years. Our data may be useful for constructing custom-made footwear for patients with CA.

Background. Problems surrounding comorbidities of type 2 diabetes mellitus and coronary heart disease are some of the most important in medical science and practice, given their mutually negative impact on patients’ prognoses and quality of life.

Aims. To study the impact of type 2 diabetes on the long-term prognoses of patients of different age categories, status-post acute myocardial infarction. (Data obtained from the ‘Register of Acute Myocardial Infarction’.)

Materials and methods. The main data source was the ‘Register of Acute Myocardial Infarction’, maintained in Tomsk for more than 30 years. The study included 862 patients with acute myocardial infarction. The patients were monitored for 5 years. The primary endpoint was death from any cause during the observation period.

Results. We separated the study cohort into 2 groups depending on patients’ ages: Group 1 (n = 358) included patients older than working age, Group 2 (n = 504) consisted of younger, employable patients. The combination of ischaemic heart disease and type 2 diabetes mellitus were diagnosed in 208 patients. The combination of ischaemic heart disease and type 2 diabetes was the cause of adverse prognosis among elderly patients and led to increased mortality rate during the 5-year post-infarction period (p = 0.0003). However, among younger, working patients who suffered myocardial infarction, the presence of type 2 diabetes did not have an independent negative effect on long-term disease prognosis. While in employable patients, a long history of diabetes mellitus significantly aggravated the course of the post-infarction period (p = 0.004).

Conclusions. These data suggest an ambiguous prognostic effect of type 2 diabetes mellitus among working age and elderly patients status post myocardial infarction, in agreement with experimental studies conducted on laboratory animals. Further comprehensive analyses of the clinical and experimental data are needed to optimise therapies for patients who suffer from type 2 diabetes and comorbid ischaemic heart disease.

Aim. To evaluate the short-term effects of the empowerment program on glycemic and lipid profiles in an inpatient setting for DM type 2 patients.

Materials and methods. This was a quasi-experimental study conducted between October 2013 and June 2015. We enrolled diabetes patients admitted to the hospital, age over 35 years, and HbA1c > 7%. During the admission, the intervention group received the empowerment course three times prior to discharge, the control group received standard diabetes and nursing care. All patients’ body weight, HbA1c, HDL-c, and LDL levels were evaluated at three and six months after discharge. All outcomes were compared between the control and intervention group.

Results. A total of 57 diabetes patients participated in the study, with 27 in the intervention group and 30 in the control group. The intervention group had significantly higher HbA1c levels than the control group (10.3% vs 8.0%; p value < 0.001). After discharge, the mean HbA1c and LDL-c levels of the intervention group were significantly lower than those of the control group at three and six months, while the mean HDL-c level of the intervention group was significantly higher than that of the control group at six months (1.54 vs 1.29 mmol/L; p value <0.001). The average body mass index of the intervention group was also significantly lower than that of the control group at six months (22.74 vs 25.54 kg/m2; p value = 0.016).

Conclusion. The individual empowerment program improved short-term glycemic and lipid outcomes in admitted diabetes mellitus patients.

Background. In modern medicine, several diseases exist that require an interdisciplinary approach, and type 2 diabetes mellitus (DT2), which can be considered as an initially comorbid pathology, is certainly one of these. Reportedly, a high level of comorbidity not only changes the presentation of the disease and makes diagnosis challenging, but in patients with comorbid diseases, the progression of the disease also increases, the prognosis worsens, and approaches to diagnosis and therapy change. For patients with DT2, a significant hallmark in the progression of the disease is the formation of insulin dependence. Determination of the mechanism behind comorbidity affecting the course and progression of diabetes, including the development of insulin dependence, necessitates research. In addition, the mutual influence of the quality of disease management of diabetes and the level of comorbidity also require investigation.

Aims. We aimed to assess the influence of the quality of metabolic control and severity of comorbidity on the risk of insulin dependence in patients with DТ2.

Materials and methods. A total of 166 patients with DT2 were divided into groups on the basis of the variant of hypoglycemic therapy, which was with either oral hypoglycemic agents or insulin therapy. The diagnostic complex included regular monitoring of glycaemia and the evaluation of the level of comorbidity.

Results. The relationship between the quality of disease management and the level of comorbidity was established. With comorbidity measured using the Cumulative Illness Rating Scale (CIRS), a score above 14 points reduced the effectiveness of the therapy and triggered the initiation of more intensive glycemic control. Data on the influence of the quality of glycemic control and the parameters of comorbidity on the risk of insulin dependence in patients with DT2 were obtained.

Conclusions. High CIRS scores in patients with DТ2 reduce the likelihood of achieving glycemic control targets. These patients require more intensive self-monitoring (at least four times during the day), and the risk of formation of insulin dependence is increased by 1.5 times.

Secondary hyperparathyroidism is an early complication of chronic kidney disease, with increasing severity as the glomerular filtration rate decreases and characterized by a progressive increase in parathyroid hormone and growth of the parathyroid glands. It is generally accepted that a deficiency in active form of vitamin D or calcitriol levels seems to play a relevant role in its development and progression of secondary hyperparathyroidism. A reduction in plasma calcitriol levels occurs early in renal disease. Major renal guidelines recommend use of vitamin D for secondary hyperparathyroidism in chronic kidney disease. In the treatment vitamin D receptor activation inhibit glandular hyperplasia; reduce parathyroid hormone levels impact on bone turnover and mineral density. Treatment with calcitriol can occasionally result in hypercalcemia and hyperphosphatemia in renal patients due promotes intestinal calcium and phosphorus absorption. This limits its suitability for the treatment. But next generation vitamin-D analogs such as paricalcitol have lower intestinal absorption of calcium, phosphorous and significantly lowers renin levels, albuminuria and blood pressure.

In this article, we present the case of a Caucasian male with type 2 diabetes and secondary hyperparathyroidism in stages 3–4 chronic kidney disease. Our case study shows that in treating for secondary hyperparathyroidisms selective vitamin D receptor activation with paricalcitol reduction of levels parathyroid hormone, albuminuria, offering low chance hypercalcemia, hyperphosphatemia and other side effects.