Keywords
Abstract
This review presents data from various regions of the world indicating that diabetes is a risk factor for the development of tuberculosis. In addition, the literature data on the immunological and biochemical mechanisms of susceptibility to tuberculosis in diabetes mellitus are given. Analysis of the results of some studies suggest that the presence of diabetes mellitus is associated with a delayed immune response when infected with M. tuberculosis. Hyperglycemia causes a disturbance in the function of macrophages, lymphocytes and neutrophils. In particular, the chemotactic and phagocytic function of macrophages decreases, the expression of signals from infected macrophages is blocked, the rate of migration of lymphocytes and neutrophils decreases, as well as the level of cytokines associated with congenital and acquired immunity. The combination of all these processes during the first two weeks after infection creates conditions for rapid multiplication of the M. tuberculosis and thereby increases the risk of tuberculosis.