Changes in gallbladder bile composition and crystal detection time in morbidly obese subjects after bariatric surgery

Abstract

The aim of the present study was to elucidate the mechanisms of development of cholesterol crystals and gallstones during weight reduction in obese subjects. Twenty-five morbidly obese, gallstone-free subjects underwent vertical-banded gastroplasty. Gallbladder bile was collected at the time of the operation via needle aspiration and 1.1-7.3 months after the operation via ultrasound-guided transhepatic puncture of the gallbladder. The mean weight loss was 17 kg. Two patients developed gallstones and 10 patients displayed cholesterol crystals in their bile. In patients with a follow-up time of less than 2 months (n ‫؍‬ 13), cholesterol saturation increased from 90% to 114% but tended to decrease in the patients with a follow-up time of more than 2 months. The extraction of the concanavalin-A-binding fraction from gallbladder bile obtained after weight reduction in 7 patients prolonged crystallization detection time from 6 to 10 days. The hexosamine concentration, a marker for mucin, was increased by about 100% in bile obtained in 6 of 7 patients after weight reduction. In conclusion, the results indicate that crystallization-promoting compounds (mucin) are of great importance in the development of cholesterol crystals and gallstones in obese subjects during weight reduction, probably because of defective gallbladder emptying.

Risk of biliary complications in bariatric surgery

“…Postbariatric modifications include cholesterol hypersaturation of bile (through cholesterol mobilization from fatty tissues enhancing cholesterol crystallization [13]), decreased secretion of biliary acids (caloric restriction), increased mucin production (enhancing crystallization) and last, gallbladder hypomotility [3,[14][15][16] (secondary to decreased cholecystokinin secretion related to the hypocaloric diet, or obesity-related resistance to cholecystokinin, to gastroduodenal exclusion, or due to intraoperative injury to the hepatic branches of the vagus nerves [17]). …”

Cholecystectomy Concomitant with Laparoscopic Gastric Bypass: A Trend Analysis of the Nationwide Inpatient Sample from 2001 to 2008

“…However, the formation of gallstones in these patients remains a subject of concern [8,9]. Despite the benefits of bariatric surgery, obesity and rapid weight loss increase the risk of gallstone formation [8][9][10] with a 1-year cumulative incidence after bariatric surgery ranging from 30% to 53% [11,12]. Although routine prophylactic cholecystectomy [13][14][15] can be performed to remove gallstones or to prevent gallstone formation, several alternative approaches have been suggested regarding the management of the gallbladder during bariatric surgery.…”

“…Bariatric surgery not only decreases morbidity and mortality in obese patients [4,6], but also has been estimated to reduce health care costs up to 45% by 5 years postoperatively [6,7]. However, the formation of gallstones in these patients remains a subject of concern [8,9]. Despite the benefits of bariatric surgery, obesity and rapid weight loss increase the risk of gallstone formation [8][9][10] with a 1-year cumulative incidence after bariatric surgery ranging from 30% to 53% [11,12].…”

Prévention de la lithiase biliaire et de ses complications après chirurgie bariatrique

“…Ces modifications associent une augmentation de la saturation de la bile en cholestérol (par la mobilisation de graisse à partir du tissu adipeux, favorisant la cristallisation du cholestérol [13]), une diminution de la sécrétion d'acide biliaires (restriction calorique), une augmentation de la sécrétion de mucine (favorisant la cristallisation) et enfin une hypomotilité vésiculaire [3,[14][15][16] (secondaire à la diminution de la sécrétion de cholécystokinine due au régime hypocalorique, à la résistance à cette dernière induite par l'obésité, au court-circuit gastroduodénal, voire au traumatisme peropératoire des branches hépatiques du nerf vague [17]). Ces modifications associent une augmentation de la saturation de la bile en cholestérol (par la mobilisation de graisse à partir du tissu adipeux, favorisant la cristallisation du cholestérol [13]), une diminution de la sécrétion d'acide biliaires (restriction calorique), une augmentation de la sécrétion de mucine (favorisant la cristallisation) et enfin une hypomotilité vésiculaire [3,[14][15][16] (secondaire à la diminution de la sécrétion de cholécystokinine due au régime hypocalorique, à la résistance à cette dernière induite par l'obésité, au court-circuit gastroduodénal, voire au traumatisme peropératoire des branches hépatiques du nerf vague [17]).…”