Abstract

Introduction Gallbladder disease (GBD) encompasses several medical conditions, including gallbladder stone formation, biliary colic, and cholecystitis. These conditions may arise following bariatric surgery, including bypass or laparoscopic sleeve gastrectomy (LSG). The development of GBD after surgery may be attributed to various factors, including the formation of stones shortly after the procedure, the exacerbation of existing stones due to the surgery, or inflammation of the gallbladder. Rapid weight loss after surgery has also been proposed as a contributing factor. Methodology This observational study consisted of a review of retrospective hospital patient medical records of 350 adult participants who underwent LSG, with 177 participants included in the study after excluding those with cholecystectomy or GBD prior to surgery. The participants were followed for a median of two years, during which we recorded any hospitalizations, emergency department visits, clinic visits, and incidents of cholecystectomy or abdominal pain due to GBD. The participants were grouped into two: those with GBD and those without GBD after bariatric surgery, and quantitative data were summarized using mean and standard deviations. The data were analyzed using IBM SPSS Statistics for Windows, Version 20.0. (IBM Corp. Released 2020. IBM SPSS Statistics for Windows, Version 27.0. Armonk, NY: IBM Corp), with a statistical significance of P<0.05. Results In our retrospective study of 177 patients who underwent LSG, the incidence of GBD after bariatric surgery was 4.5%. Most patients with GBD after bariatric surgery were White, but this difference was not statistically significant. Patients with type 2 diabetes had a higher incidence of GBD after bariatric surgery than those without diabetes (8.3% vs. 3.6%, P=0.355). Patients with HTN had a lower incidence of GBD after bariatric surgery than those without HTN (1.1% vs. 8.2%, P=0.032). Anti-hyperglycemia medication use did not significantly increase the risk of GBD after bariatric surgery (7.5% vs. 3.8%, P=0.389). None of the patients on weight loss medication developed GBD after bariatric surgery, compared to 5% of patients who did not take weight loss medication. Our sub-data analysis showed that patients who developed GBD after bariatric surgery had a high BMI (above 40 kg/m2) before surgery, which decreased to 35 kg/m2 and below 30 kg/m2 at six months and 12 months post-surgery, respectively. Conclusions Our findings demonstrate that the prevalence of GBD after LSG is low and comparable to the general population without LSG. Thus, LSG does not increase the risk of GBD. We found that rapid weight loss after LSG is a significant risk factor for GBD. These findings suggest that patients who undergo LSG should be informed of the risks of GBD and undergo careful screening before surgery to detect any pre-existing gallbladder issues. Overall, our study highlights the importance of continued research into the factors associated with GBD after bariatric surgery and the need for standardized prophylactic measures to prevent this potentially serious complication.

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