Shalimova A. The role of genetic, cardiac hemodynamic and metabolic mechanisms in the development of comorbid pathology - essential hypertension and type 2 diabetes..

Українська версія

Thesis for the degree of Doctor of Science (DSc)

State registration number

0516U000266

Applicant for

Specialization

  • 14.01.02 - Внутрішні хвороби

25-03-2016

Specialized Academic Board

Д 64.600.04

Essay

The thesis work represents a new approach to the diagnosis and treatment of comorbid pathology - essential hypertension and type 2 diabetes - based on the study of genetic, cardiac hemodynamic and metabolic mechanisms in the development of comorbidity. The character of structural and functional changes of the heart and vessels, as well as the state of oxidative stress - antioxidant defense of patients with essential hypertension and concomitant type 2 diabetes - have been determined. The influence of various pathogenetic links of insulin resistance (adiponectin, leptin, interleukin-6, tumor necrosis factor-?) on the development of the comorbidity has been ascertained. The modulating effect of polymorphism of genetic markers of arterial hypertension (angiotensin II receptor type 1 gene) and type 2 diabetes (peroxisome proliferator-activated receptors-?2, insulin receptor substrate-1 gene, transcription factor 7-like 2 gene) on hemodynamics and metabolism in patients with essential hypertension and type 2 diabetes has been determined. The basic determinants of comorbidity of essential hypertension and type 2 diabetes have been distinguished. The effectiveness of the use of the angiotensin-converting enzyme inhibitor ramipril and the angiotensin II receptor antagonist telmisartan depending on the genetic polymorphism of the angiotensin II receptor type 1 gene in patients with comorbidity has been evaluated. The dynamics of remodeling of the heart and vessels, factors of immune inflammation, lipid and carbohydrate profiles have been estimated in patients with essential hypertension and concomitant type 2 diabetes after the treatment with drugs which affect various pathogenetic links of these diseases considering the genetic polymorphism.

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