Chemical burns of the digestive tract can lead to severe local tissue damage and provoke systemic responses that affect distant organs. This literature review summarizes current knowledge on morphometric changes in the thyroid gland following corrosive injury to the gastrointestinal (GI) tract and discusses potential mechanisms and interventions for correction. The introduction outlines the epidemiology and pathophysiology of caustic GI burns, emphasizing that injury severity ranges from mild mucosal damage to full-thickness necrosis with life-threatening complications [1].The analysis focuses on reported thyroid gland alterations in experimental models and clinical observations: inflammatory and stress-mediated pathways are implicated in thyroid microstructural changes (follicular architectural distortion, cellular infiltration) and functional suppression (euthyroid sick syndrome) after severe burns [5]. Key mechanisms include systemic release of inflammatory cytokines (e.g. IL-6, TNF-α) [1], acute stress hormone surges, and neuroendocrine disruption of the hypothalamic-pituitary-thyroid axis. Diagnostic approaches from the literature range from histopathological examinations of the thyroid (showing colloid depletion and thyroglobulin clumping in burn victims) to imaging and hormonal assays. Therapeutic strategies for correction have been explored in animal studies and clinical practice: anti-inflammatory treatments, antioxidant therapy, and hormonal replacement are considered for mitigating thyroid damage and dysfunction. However, data on targeted interventions remain limited. In conclusion, chemical GI burns can induce significant morphometric and functional changes in the thyroid gland via complex systemic mechanisms. Early recognition and management of thyroid involvement in burn patients may improve outcomes, but further research is needed to establish effective therapeutic protocols.

Chemical burn; Digestive tract; Thyroid gland; Morphometric changes; Correction

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