Bohachuk M. Muramylpeptide immunomodulation in the complex treatment of purulent-inflammatory soft tissue diseases in patients with diabetes mellitus.

For the first time, the concept of overcoming the metabolic immunodepression in patients with purulent-inflammatory soft tissue diseases against type 2 diabetes mellitus has been pathogenetically substantiated. It was proven that the chronicity of inflammation and prolonged stagnation of repair are based on a combination of energy-dependent deficiency of phagocytic activity and structural disorganization of the lymphocyte pool. For the first time, morphometric analysis verified the phenomenon of subpopulation lymphocyte imbalance, manifesting as a decrease in the proportion of small lymphocytes (up to 7 μm), reflecting a deficiency of the T-helper link (CD4+) against a compensatory increase in large cell forms (over 12 μm). It was established that such compensatory hyperactivation of the B-lymphocyte sector is functionally insufficient and does not ensure complete cleansing of the purulent focus. For the first time, the mechanism of suppression of non-specific resistance was verified, consisting in a profound exhaustion of the reserve of non-enzymatic cationic lysosomal proteins with a deficiency of 17.7% compared to the physiological norm. It was proven that a decrease in the content of non-enzymatic cationic proteins to 70.9±2.1% acts as a key marker of functional exhaustion of the effector link of immune defense under decompensated hyperglycemia. For the first time, it was established that the primary link in the decline of neutrophil bactericidal activity is profound disorders of intracellular glycolysis, providing up to 95% of the immunocyte's energy requirements. Cytochemically, this deficit manifests as complete inertia of the myeloperoxidase (MPO) response and NBT-test parameters, presenting as a stable energy-dependent blockade of degranulation and oxygen-dependent intracellular killing of pathogens. For the first time, based on the induced modulation method, the preservation of the internal resource potential of azurophilic granules was proven even during profound metabolic immunodepression. The possibility of a compensatory increase in MPO activity up to 72.0±6.1% under external stimulation was justified, providing a scientific basis for targeted immunocorrection with muramyl peptide series drugs. For the first time, the understanding of chronic oxidative stress as a trigger for secondary autoimmune aggression in perifocal wound tissues was expanded. A dynamic increase in the lymphocyte-granulocyte index against metabolic disorders allows for the differentiation of the endogenous intoxication level and the prediction of risks for further progression of surgical complications. For the first time, the concept of overcoming the regenerative plateau phase in patients with PISTD against type 2 DM has been pathogenetically substantiated through priority systemic and local immunocorrection with muramyl peptide series drugs combined with targeted correction of regional microcirculation with prostaglandin series drugs. It was proven that the developed algorithm ensures rapid morphological transformation of the inflammatory infiltrate and full restoration of the bactericidal potential of phagocytes, with an increase in MPO-positive cells exceeding 72.0±6.1%, achieved due to the elimination of capillary sludge syndrome under concomitant vasoactive therapy as early as the 2nd–3rd day of treatment. For the first time, based on comprehensive cytological and histological monitoring, clear temporal parameters of the transition from inflammation to regeneration have been verified, allowing for an objective evaluation of wound readiness for early reconstructive interventions. The simultaneous overcoming of immunometabolic imbalance and tissue hypoxia leads to a rapid acceleration of neoangiogenesis and orderly maturation of granulation tissue, which clinically manifests as a significant reduction in the wound defect area and a substantial shortening of the duration of patients' inpatient treatment.