CHEMICAL BURN INDUCED OXIDATIVE STRESS AND MORPHOFUNCTIONAL CHANGES IN THE THYROID GLAND

This article presents an analytical review of systemic pathophysiological mechanisms that arise after chemical burns, particularly corrosive injury of the upper digestive tract, and evaluates their possible influence on the morphofunctional state of the thyroid gland. Chemical burn injury is interpreted not only as a local lesion of the mucosa, but also as a complex systemic process involving exotoxic shock, microcirculatory impairment, metabolic acidosis, hemolysis, inflammatory mediator activation, oxidative stress and secondary organ dysfunction. The thyroid gland is highly sensitive to systemic stress because thyroid hormones regulate energy metabolism, oxygen consumption, thermogenesis, protein synthesis, immune response and reparative processes. In severe burn disease, changes in thyroid hormone economy may reflect non-thyroidal illness syndrome rather than primary thyroid pathology. Therefore, the assessment of the thyroid gland after chemical burns requires an integrated analysis of hormonal, biochemical and morphological indicators. Particular attention is paid to follicular diameter, thyrocyte height, colloid condition, stromal edema, vascular congestion and signs of cellular dystrophy as morphologic criteria that may characterize post-burn endocrine adaptation. The article substantiates the relevance of studying oxidative stress as a key pathogenetic link connecting chemical injury, systemic intoxication and thyroid tissue remodeling. The proposed analytical model can serve as a theoretical basis for experimental morphological research within doctoral dissertation studies devoted to post-burn thyroid changes and their possible correction.