Background and Objective — Subclinical gestational hypothyroidism (SGH) and gestational diabetes mellitus (GDM) constitute two most common endocrine pathologies encountered during pregnancy. SGH and GDM have common pathophysiological mechanisms, being interrelated pathological conditions that are capable of complicating the course of pregnancy, labor and the postpartum period both on the part of the mother and on the part of the fetus. We aimed to analyze the relationship between these pathologies and to assess the risk of developing GDM against the background of hypothyroidism. Materials and Methods — the study included 200 pregnant women observed at the Perinatal Center of the Maternity Hospital the Bauman State Clinical Hospital No. 29 during 2018-2020. The main group consisted of 133 women who visited the perinatal center for hypothyroidism (both SGH and primary hypothyroidism, detected prior to pregnancy); the control group comprised 67 women without endocrine pathology. Both groups were comparable in terms of age, height, weight, and the number of pregnancies in the anamneses. The main group received levothyroxine sodium therapy with the achievement of the target trimester-specific level of thyroid-stimulating hormone (TSH). The criteria for the diagnosis of SGH were the TSH level above 2.5 μIU/mL in combination with an enlarged titer of antithyroid antibodies and/or a burdened medical history of thyroid pathology, or the TSH level above 4.0 μIU/mL in the absence of antithyroid antibodies [1]. The diagnosis of GDM was established on the basis of fasting hyperglycemia (≥5.1 mmol/L), or based on the results of an oral glucose tolerance test (OGTT) with 75 g of glucose: fasting glucose level of ≥5.1 mmol/L; the concentration 1 hour after glucose intake ≥10.0 mmol/L; the content 2 hours after glucose intake ≥8.5 mmol/l) [2]. In both groups, the frequency of developing GDM, the timing of diagnosis, and the need for insulin therapy were evaluated. Statistical data processing was carried out using the StatTech v. 2.1.0 software. Quantitative indicators were assessed for compliance with the normal distribution via Shapiro-Wilk criterion or Kolmogorov-Smirnov criterion. Intergroup comparison was performed using Mann-Whitney U test or Pearson’s chi-squared test. Results — We discovered that among women with a burdened family history of thyroid pathology and diabetes mellitus, as well as with thyroid pathology prior to pregnancy, the prevalence of hypothyroidism was higher. The presence of thyroid pathology in the anamnesis of pregnant women was associated with an earlier diagnosis of hypothyroidism. We revealed a significant difference in the prevalence of GDM between two groups of subjects. The chances of detecting GDM in the hypothyroidism group were 8.6 times higher than in the euthyroidism group. The threshold level of TSH for the first trimester, predicting the development of GDM, was identified. The sensitivity and specificity of the model were 71.4% and 63.1%, respectively. Conclusion — Hypofunction of the thyroid and GDM are interrelated endocrine pathologies. In the presence of hypothyroidism (both primary and SGH), GDM develops significantly more often. The level of TSH in the first trimester ≥2.7 μIU/mL amplifies the chance of developing GDM by over 8 times; hence, it could be considered a signal for timely prevention and detection of this pathology.
The study included 74patients (22 men and 52 women) aged 48-75yr with type 2 diabetes mellitus (DM2). 62 (88,6%) of them had grade II hypertensive disease (grade II-III by the WHO/ISH-2010 classification), 46 (67%) presented with II- III class functional stable angina of effort, 7 patients survived myocardial infarction, two ones underwent coronary artery stenting. Patients of the main group (n=50) received oral hypoglycemic agents in combination with 1-exenatide (mimetic of glucagon-like peptide) in the form of two daily subcutaneous injections of 5 mcg for 1 month and 10 mcg during the next 5 months. Control patients (n=20) were given standard hypoglycemic therapy. Analysis of highly sensitive CRP demonstrated its increase to 3 mg/l and more in 72.8% of the patients that was responsible for the high risk of cardiovascular disorders. 22,8% of the patients had a CRP level 1,0-2,9 mg/l (moderate risk) and only in 4,2% it was lower than 1 mg/l (low risk). Six months of exenatide therapy resulted in normalization of glycemia, glycated hemoglobin and significant decrease of CRP level which suggested the improvement of the functional state of vascular endothelium due to reduction of chronic inflammation objectively reflected in the highly sensitive CRP level.
The prevalence of type 2 diabetes (T2D) is very high and grows dangerously, being the most common cause of death. Severe vascular and neurological complications, which result in early disability and high mortality, and reduction in life expectancy and the quality of life, account for the medical and social relevance of T2D. T2D is characterized by progressive dysfunction of pancreatic β-cells in the development of insulin resistance. This paper addresses the mechanisms of action of glucose-lowering medications, i.e., pioglitazone belonging to a group of peroxisome proliferator-activated receptor (PPARγ) agonists, and alogliptin belonging to a group of dipeptidyl peptidase 4 (DPP-4) inhibitors. Pioglitazone increases insulin sensitivity via enhancing the expression of numerous genes encoding proteins that modulate glucose and lipid metabolism. Alogliptin improves the glucose-dependent activity of β-cells and inhibits the increased secretion of glucagon. Alogliptin is characterized by low risks of hypoglycemia and cardiovascular safety. Pioglitazone-alogliptin fixed-dose combination is helpful to control T2D effectively and safely since this combination affects 10 out of 11 pathophysiological defects resulting in T2D. KEYWORDS: type 2 diabetes, insulin resistance, β-cells, dipeptidyl peptidase 4 inhibitor, thiazolidinediones, gliptin. FOR CITATION: Mkrtumyan A.M., Sviridova M.I. New powerful treatment approach to type 2 diabetes. Russian Medical Inquiry. 2021;5(9):592–597 (in Russ.). DOI: 10.32364/2587-6821-2021-5-9-592-597.
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