ROLE OF HYPERCORTISOLEMIA IN PROGRESSION OF THE COMORBID COURSE OF CORONARY ARTERY DISEASE, DIABETES MELLITUS TYPE 2 AND ANEMIA
Abstract
INTRODUCTION: Hyperactivation of stress-limiting mechanisms of the organism is a unique physiological response of the human being to chronic hypoxia of different origins.
OBJECTIVES: Investigation of dynamics of cortisol synthesis changes in patients with coronary artery disease with comorbid diabetes mellitus type 2 and anemic syndrome in patients of older age groups.
METHODS: Blood cortisol level was measured in 40 old and senile coronary artery disease patients with comorbid diabetes mellitus type 2 and anemic syndrome of different degrees of severity. The control group consisted of 12 patients with coronary artery disease without comorbidities that were not significantly different through gender and age from the patients of the research groups. Possible effects of telmisartan on the degree of chronic hypoxia were also investigated.
RESULTS: In patients of old and senile age with coronary artery disease and comorbid anemic syndrome, same as in case of coronary artery disease and anemic syndrome on the background of diabetes mellitus type 2, activation of the cortisol synthesis is observed, likely in response to hypoxia as a stress factor in anemia. The degree of severity of the detected changes was different depending on the degree of anemia severity. There was no normalization of cortisol content in blood in any of the major experimental groups regardless the prescribed treatment with ACE inhibitors or telmisartan.
CONCLUSIONS: In patients with coronary artery disease, same as in the case of a comorbid course of coronary artery disease and diabetes mellitus type 2, an increase of cortisol secretion in response to anemic hypoxia was observed. As the degree of severity of the anemic syndrome progressed, gradual decreasing of cortisol blood level was detected. Reduction of the intensity of stress-limiting systems in the organism by telmisartan prescription may help to eliminate the adverse effects of hypercortisolemia on the progression of coronary artery disease, especially on the background of comorbid diabetes mellitus type 2 and anemia.
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