Aim.
To consider association of type 1 diabetes mellitus (DM1) with polymorphous alleles of HLA-DRB1 HLA-DQB1, and DQA1 genes in two Russian populations of Moscow (MP) and Vologda (VP) regions.
Materials and methods.
Identification of alleles of HLA-DRB1 HLA-DQB1, and DQA1 genes in 138 patients with type 1 diabetes and a random sample of 242 subjects from the local population (residents in at least three successive generations) of the Vologda region, 204 patients and a random sample of 300 subjects from the city of Moscow and Moscow region.
Results.
MP and VP exhibited identical predisposing alleles. The occurrence of DRB1*4 (RR=5.96 and 3.93 in MP and VP respectively), DRB1*17 (RR=4.33 and 4.23), DQA1*0301 (RR=5.70 and 3.66), DQB1*0201, (RR=2.06 and 1.77), DQB1* 0302 (RR=7.10 and 3.95), DQB1* 0304 (RR=8.94 and 19.98) alleles was significantly higher in DM1 patients. The following protective alleles were identified in MP and VP respectively: DRB1*7 (RR=0.37 and 0.18), DRB1*11 (RR=0.12 and 0.21), DRB1*13 (RR=0.09 and 0.26), DRB1*15 (RR=0.23 and 0.04), DQA1*0102 (RR=0.29 and 0.23), DQA1*0103 (RR=0.13 and 0.23), DQA1*0201 (RR=0.37 and 0.17), DQb1*0301 (RR=0.16 and 0.24), and DQB1*0602/8 (RR=0.10 and 0.13).
Conclusion.
?New? associations unknown in other populations (e.g. DQB1*0304) were revealed, besides the majority of classical predisposing and protective alleles characteristic of European populations. DQB1*0304 proved the strongest predisposing allele in MP and especially in VP. These data suggest different contribution of predisposing alleles to the development of DM1 in individual populations.
To measure gastrointestinal hormones in plasma, evaluate morphofunctional state of G- and beta-cells in patients with gastric pathology and concomitanttype 2 diabetes mellitus (DM2).
Materials and methods.
A total of 84 patients with gastric ulcer (GU) and chronic gastritis (CG) were available for observation including 46 with DM2.Semi-quantitative evaluation of stomach infection by H.pylori. was performed by a histological method. Stained G- and beta-cells were counted under 400xmagnification in 10 fields of vision for each medicinal preparation used in the study. Chromogranin A, somatostatin, and gastrin were detected by immunohistochemicalmethods, gastrin-17 and somatostatin-14 by the respective immunoassays. Control group comprised 10 practically healthy volunteers.
Results.
Patients with combined GU (or CG) and DM2 pathology had smaller density of G- and beta-cells, lower plasma gastrin and somatostatin levelsthan those without DM2 (p<0.05). Biopsies from DM2 patients infected with H.pylori showed higher density of beta-cells (p<0.05) and lower density ofbeta-cells (p<0.05) than those from non-infected ones. The number of gastrin-positive cells in patients with DM2, gastric pathology, and grade 2 infectionwas significantly greater than in case of grade 3 infection. Endocrine cells in gastric mucosa of DM2 patients were less abundant than in controls(23 and 56% respectively, p<0.05). The density of gastric epitheliocytes significantly decreased in patients with the duration of DM2 above 10 years.
Conclusion.
Metabolic disorders, local trophic disturbances, accelerated extrusion of erythrocytes, H.pylori colonization, and impaired regenerationin patients with DM2 cause atrophic changes in gastric mucosa, alter the number and ratio of G- and beta-cells.
Screening for erectile dysfunction (ED) in patients with type 1 and 2 diabetes mellitus.
Materials and methods.
The study included 611 patients with type 1 (n=276) and 2 (n=335) diabetes mellitus. The control group comprised 70 patients.The methods used were a questionnaire survey, HbA1c measurement, evaluation of renal and cardiovascular function, examination of ocularfundus, lower extremities and genital organs. Differences were considered significant at p<0.05 probability level.
Results.
Prevalence of ED among DM 1 and DM2 patients was estimated at 38.7 and 66.2% respectively compared with 15.7% in controls. It increasedwith patients age and duration of DM. Patients having ED showed poorly compensated metabolic disorders and significantly higher frequency of other diabeticcomplications compared with those without ED. The predominant etiological factor of ED was neuropathy (91.7% in DM1 and 76.3% in DM2). Thecontribution of vasculopathy (19.6% and 47.3% respectively) became apparent with aging of the patients. The vascolugenic form of ED in DM patients precededclinical signs of macroangiopathy in the lower extremities at least in 53% cases and myocardial infarction in 25.7%. Neurogenic ED developed priorto clinical manifestations of diabetic neuropathy at least in 46.1% of the patients. General practitioners diagnosed ED not more than in 22.7% patients.
Conclusion.
ED is a common complication of DM depending on the quality of its compensation, duration of the disease, and patients age. Active casedetection of ED is necessary since it may be a clinical marker of neuropathy and macroangiopathy. Adequate correction of metabolic disturbancesmay reduce the number of patients with ED. The risk of ED may be used as a motivational factor for the patients.
To measure Na-K-ATPase activity in erythrocytes from patients with diabetes mellitus (DM), elucidate its relationship with clinical manifestationsof the disease and biochemical blood characteristics.
Materials and methods.
A total of 76 DM patients were enrolled in this study (39 with DM1 and 35 with DM2). Control group consisted of 11 subjectswithout DM. They were examined for HbA1c, nitrite and nitrate levels in blood and membranes, sialidase activity in erythrocytes and Na-KATPaseactivity measured from variations of inorganic phosphorus content in the presence of ATP.
Results.
Na-K-ATPase activity in MD patients was significantly lower than in controls (p<0.05). It was unrelated to the patients age and sex butdropped insignificantly with MD duration. Na-K-ATPase activity depended on blood HbA1c and membrane phosphorus levels, enhanced sialidaseactivity in erythrocytes, nitrite and nitrate concentrations in plasma.
Conclusion.
Na-K-ATPase activity reflects the degree of metabolic disturbances and endothelial dysfunction in patients with DM.
To evaluate efficiency of trimetazide MR combined with basic therapy of type 2 diabetes mellitus (DM2) in patients with myocardial infarction (MI).
Materials and methods.
The study included 106 patients with DM2 who underwent MI. Polycomponent basic therapy supplemented by trimetazideMR at a daily dose of 70 mg was given to 51 patients. The patients condition 6 and 12 months after treatment was evaluated from the results of echo-CG, 24 hr ECG monitoring, and 6 min walking test. Quality of life was estimated using modified Minnesota questionnaire scores.
Results.
Trimetazide MR combined with polycomponent basic therapy reduced consumption of nitroglycerine by DM2 patients after myocardial infarction,frequency of ventricular and supraventricular extrasystole in 25.3 and 25.3% of the cases respectively. Episodes of painless myocardial ischemiaoccurred only in 35.6% of the patients. Long-term treatment with trimetazide MR as a component of combined therapy increased injectionfraction in patients with abnormal myocardial contractility (p<0.05) and decreased the frequency of painless myocardial ischemia (p<0.05).
Conclusion.
Inclusion of trimetazide MR in a year-long polycomponent basic therapy of DM2 in patients with IM effectively prevented dysadaptiveremodelling of the heart and improved quality of life.
To assess expedience of metformin combination with long-acting insulin, determine optimal doses of metformin for patients with type 2 diabetesmellitus (DM2), and accomplish pharmacoeconomic analysis of clinical efficiency of various therapeutic modalities.
Materials and methods.
Patients with decompensated DM2 (n=126) were under observation for 1 year during which they received rational hypoglycemictherapy with metformin and long-acting insulin (LAI) at bedtime, with the dose being titrated until the desired level of glycemic control wasachieved. The patients were randomly allocated to the following 3 groups: group 1 (sulponylurea derivatives (SUD), LAI, and metformin at a doseof 1000 mg b.i.d.), group 2 (SUD, LAI, and metformin at 500 mg b.i.d.), group 3 (SUD and LAI). In case of postprandial glycemia >9 mmol/l at amaximum dose of SUD, it was replaced by short-acting insulin. Cost-effectiveness analysis of different therapeutic regimes was performed.
Results.
The cost of examination and treatment of patients given SUD and LAI in combination with metformin at a daily dose of 2000 mg to achievethe desired quality of glycemic control was lower compared with two other groups. Moreover, this therapy was most efficacious and ensured the desiredlevel of glycemic control in a greater number of patients. Cost-effectiveness analysis confirmed advantages of this treatment.
Conclusion.
Combined hypoglycemic therapy with SUD, LAI, and metformin (200 mg daily) has the advantage of lowest cost and maximum efficiencycompared with other modalities.
AIMS: To elucidate the prevalence of delayed gastroduodenal transit in patients with type 1 diabetes mellitus (DM1) compared with controls havingunaffected carbohydrate metabolism.
MATERIALS AND METHODS: The study included 159 DM1 patients and 128 ones with symptoms of dyspepsia and normal carbohydrate metabolism. The presenceof food remains in the stomach after the 12-hour fast (detected by oesophagogastroduodenoscopy) was regarded as a delay of gastroduodenal transit.
RESULTS: In a group of DM1 patients, 13.70% of the cases had endoscopically confirmed delay of food evacuation from the stomach. No signs of gastroparesiswere documented in the control group.
CONCLUSIONS: Certain patients with DM1 suffer a marked impairment of gastroduodenal transit (13.7% of the cases in the present study). This disorderaffects the time of onset of carbohydrate absorption. Therefore, such patients need their mealtimes to be chosen on an individual basis.
ISSN 2072-0378 (Online)
