Clinicopathological Evaluation of Cholesterolosis in Cholecystitis: Histopathological Patterns and Metabolic Correlates

<b>Background/Objectives</b>: Cholesterolosis is a relatively common, yet often incidental, histopathological finding in cholecystectomy specimens, frequently associated with chronic cholecystitis. Although its clinical significance remains unclear, possible associations with glycemic regulation have been proposed. This study aimed to examine the relationship between cholesterolosis, glycemic parameters, and inflammatory markers in patients with chronic cholecystitis. <b>Methods</b>: We retrospectively analyzed gallbladder specimens from patients who underwent cholecystectomy for chronic cholecystitis between 2014 and 2023. Histopathology assessed cholesterolosis presence, distribution, and inflammatory features. Patients were grouped according to diabetes status (diabetic vs. non-diabetic) as well as the presence or absence of cholesterolosis. Demographic data, gallstone status, one-year mean fasting glucose, HbA1c levels, and hematological/inflammatory indices were compared between groups. <b>Results</b>: Among diabetic patients, those with cholesterolosis had significantly lower fasting glucose than those without cholesterolosis (129.04 ± 28.02 vs. 158.41 ± 54.23 mg/dL, <i>p</i> < 0.05). The presence of cholesterolosis was not significantly associated with diabetes status (<i>p</i> > 0.05). Inflammatory indices, including neutrophil count, did not differ significantly between groups (<i>p</i> > 0.05), although fasting glucose correlated positively with neutrophil count (<i>r</i> = 0.167, <i>p</i> < 0.05). Gallstones were less frequent in cholesterolosis cases compared with non-cholesterolosis cases (59.4% vs. 75%, <i>p</i> < 0.05), suggesting a distinct pathophysiology. <b>Conclusions:</b> This is the first study to assess one-year glycemic profiles in diabetic and non-diabetic patients with and without cholesterolosis. The findings suggest that cholesterolosis may occur independently of poor glycemic control and systemic inflammation, supporting the concept of a distinct underlying mechanism.