Differential expression of preoperative cholestatic biochemical profiles, inflammatory factors, and electrolytes: Risk stratification based on complicated GS

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Background: Gallstones (GS) are a highly prevalent digestive disorder worldwide and can readily progress to complicated GS. Most previous studies on GS have focused on isolated indicators. At the same time, the interplay among multisystem biochemical markers has received far less attention; the mechanisms underlying this interplay in disease progression remain poorly understood. The present study was designed to systematically compare preoperative multidimensional biochemical indices between patients with simple GS and those with complicated GS, and to provide laboratory evidence for clarifying the mechanisms underlying disease progression. Methods: A total of 107 preoperative patients with GS confirmed by imaging between January 1, 2024 and December 31, 2025, were included, including 49 patients in the simple GS group and 58 in the complicated GS group. The test panel covered five modules: the core cholestatic biochemical profile (10 items), bile duct-specific injury and metabolic regulatory markers (GST-α, C4, and FGF19), inflammationand tissue remodelling-related markers (10 items), electrolyte and acid-base homeostasis indices (10 items), and 15 bile acid subspecies. Results: The core cholestatic indices were significantly elevated in the complicated group, with TBIL and GGT increasing by 1.87-fold and 4.82-fold, respectively (both P<0.05). GST-α, a bile duct-specific injury marker, was markedly upregulated, whereas the bile acid metabolic regulators FGF19 and C4 were both downregulated (both P<0.05). Among the inflammatory markers, CRP Presepsin, and several related indices were several-fold higher in the complicated group. These patients also showed statistically significant electrolyte alterations, including lower serum potassium and sodium levels, with a subset developing clinically significant hypokalaemia and hyponatraemia, along with compensated metabolic acidosis (BE=-3.36±1.81 mmol/L). All 15 serum bile acid subspecies were significantly increased. The rise in conjugated bile acids (8to 10-fold) was far greater than that in unconjugated bile acids (2to 5-fold) (all P<0.05). Conclusion: Simple and complicated GS differed significantly across multiple biochemical dimensions. The findings suggest that cholestasis, inflammatory activation, disturbance of internal homeostasis, and abnormal bile acid metabolism act in concert and form a vicious cycle during the transition from simple to complicated GS.

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