BACKGROUND: The occurrence of gallstones following Roux-en-Y gastric bypass (RYGB) has been extensively reported. As RYGB promotes improvement in insulin resistance (IR), which is one of the factors enrolled in the pathophysiology of gallstones, this study aims to determine the influence of IR and its post-RYGB course on the development of gallstones. METHODS: This is a prospective cohort study that enrolled 108 morbidly obese subjects free of gallstones which underwent RYGB and were followed up for 24 months, through clinical, laboratory, and ultrasound examinations. IR was assessed through the surrogate marker homeostasis model assessment (HOMA). RESULTS: Of the individuals evaluated, 29 (26.8%) developed gallstones following RYGB. In the univariate analysis, postsurgical gallstones were associated with preoperative HOMA (p < 0.0001), preoperative fasting glucose (p = 0.0019), preoperative fasting insulin (p = 0.0001), and preoperative triglycerides (p = 0.0001). Multivariate analysis revealed that preoperative HOMA was the only factor independently associated with gallstones (p < 0.0001). The incidence of gallstones among individuals with IR was 46.8%; in the non-IR subjects, the incidence was 7.4% (p < 0.0001). Preoperative IR led to a relative risk of 6.02 (95% CI = 2.1-17.3; p = 0.0009) of gallstones. CONCLUSIONS: As gallstones often occur following RYGB, there is controversy regarding their management. Some authors propose systematic cholecystectomy along with RYGB, while others suggest that the aggregate risk of the concomitant approach is significantly higher. As IR was a significant risk factor in this study, an individualized approach for this population may be proposed. Further research is needed to confirm these findings.
BACKGROUND: The occurrence of gallstones following Roux-en-Y gastric bypass (RYGB) has been extensively reported. As RYGB promotes improvement in insulin resistance (IR), which is one of the factors enrolled in the pathophysiology of gallstones, this study aims to determine the influence of IR and its post-RYGB course on the development of gallstones. METHODS: This is a prospective cohort study that enrolled 108 morbidly obese subjects free of gallstones which underwent RYGB and were followed up for 24 months, through clinical, laboratory, and ultrasound examinations. IR was assessed through the surrogate marker homeostasis model assessment (HOMA). RESULTS: Of the individuals evaluated, 29 (26.8%) developed gallstones following RYGB. In the univariate analysis, postsurgical gallstones were associated with preoperative HOMA (p < 0.0001), preoperative fasting glucose (p = 0.0019), preoperative fasting insulin (p = 0.0001), and preoperative triglycerides (p = 0.0001). Multivariate analysis revealed that preoperative HOMA was the only factor independently associated with gallstones (p < 0.0001). The incidence of gallstones among individuals with IR was 46.8%; in the non-IR subjects, the incidence was 7.4% (p < 0.0001). Preoperative IR led to a relative risk of 6.02 (95% CI = 2.1-17.3; p = 0.0009) of gallstones. CONCLUSIONS: As gallstones often occur following RYGB, there is controversy regarding their management. Some authors propose systematic cholecystectomy along with RYGB, while others suggest that the aggregate risk of the concomitant approach is significantly higher. As IR was a significant risk factor in this study, an individualized approach for this population may be proposed. Further research is needed to confirm these findings.
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