BIOCHEMICAL BASIS OF THE ORIGIN AND TREATMENT OF ACUTE PANCREATITIS

Acute pancreatitis is a severe inflammatory condition caused by the autodigestion of pancreatic tissue due to the premature activation of digestive enzymes. This article provides a comprehensive analysis of the etiology, biochemical pathogenesis, and therapeutic foundations of acute pancreatitis. Particular attention is given to the early activation of enzymes such as trypsin, lipase, and amylase; the effects on cell membranes and mitochondrial function; the role of oxidative stress; and alterations in the balance of inflammatory mediators such as IL-1, IL-6, and TNF-α. The study also highlights the importance of antioxidant defense mechanisms, lipid peroxidation processes, and microcirculatory disturbances as key biochemical factors in disease progression. Modern biochemical treatment strategies — including enzyme therapy, antioxidant administration, amino acid balance restoration, and microcirculation improvement — are described with scientific justification. Research demonstrates that early identification of biochemical markers (amylase, lipase, CRP, LDH, and AST/ALT ratios) facilitates timely diagnosis and significantly improves patient survival rates. The scientific significance of this work lies in its detailed biochemical analysis of the pathogenesis of acute pancreatitis and its evaluation of the effectiveness of modern therapeutic approaches, providing a methodological foundation for future clinical research.

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