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    • Furthermore Kobayashi et al reported that the incidence of

    2018-10-29

    Furthermore, Kobayashi et al reported that the incidence of gallstones was significantly higher after total gastrectomy than after partial gastrectomy; our study presented similar findings (40% vs. 17.8%; odds ratio, 3.8). Furthermore, an increased incidence of acute cholecystitis was observed in patients who had undergone total gastrectomy compared with those who had undergone distal subtotal gastrectomy [35.7% (5 of 14 patients) vs. 6.2% (2 of 32 patients); p = 0.02]. However, the difference between total gastrectomy and distal gastrectomy was nonsignificant in the study of Fukagawa et al. Gastrectomy as a risk factor might be affected by the extent of cholesterol absorption inhibitor node dissection. The reconstruction method applied affects the risk of gallstone formation. Segawa et al and Ikeda et al reported no difference between Billroth II and Billroth I reconstruction in terms of the risk of gallstones. Similarly, Inokuchi et al found no difference between Roux-en-Y and Billroth I reconstruction after laparoscopic distal gastrectomy. However, Kobayashi et al identified duodenal exclusion as a crucial risk factor for gallstone formation. Our results showed that Billroth II was associated with an increased incidence of gallstones compared with Billroth I (31.4% vs. 10.7%). The differences in the effects of Roux-en-Y, uncut Roux-en-Y, and Billroth I reconstruction were nonsignificant. We observed gallstone formation in half of the analyzed patients within 2 years of gastrectomy; this incidence gradually decreased in the following years (Figure 2). Fukagawa et al reported that 64.7% of the detected gallstones appeared within 1 year of radical gastrectomy. A prospective observational study conducted by Inoue et al showed that 42% of 46 patients had gallbladder sludge formation and significantly decreased gallbladder contractility 1 month after radical gastrectomy. However, most sludge disappeared within 12 months, in tandem with the gradual recovery of gallbladder contractility. Nevertheless, further follow-up revealed that 18.8% of the patients developed gallstones, mostly at > 6 months after gastrectomy. Gallbladder stones evolved in only two patients who had received intravenous hyperalimentation. Gallbladder enlargement and suddenly decreased contractile dysfunction in the early postgastrectomy period is closely associated with the formation of debris echogenicity in the gallbladder, but it is not presumed to be the essential factor in the pathogenesis of gallstone formation. In our study, a subgroup analysis of 35 patients diagnosed with gallstones at > 6 months after gastrectomy showed that almost all radiographic findings demonstrated small stones with or without sludge. These stones typically persisted throughout the follow-up period, and gallstones could not be visualized later in only one patient. Gallbladder stones development is considered a multifactorial process. The motility of the gallbladder is controlled by both neural and hormonal interactions, such as vagal signaling and cholecystokinin (CCK); both factors induce gallbladder contraction, and the disruption of either pathway can potentially cause gallbladder dysfunction. Yi et al conducted an anatomical study of the human gallbladder and showed three pathways of nerve innervation of the gallbladder: through the anterior hepatic plexus, posterior hepatic plexus, and phrenic nerve. In particular, the preservation of the neural pathway from the anterior hepatic plexus through the cystic artery and duct is crucial for maintaining gallbladder innervation. Because patients with total gastrectomy typically undergo the division of both vagal trunks, vagal signaling would be blocked at the proximal site. CCK, a peptide secreted in the duodenum, stimulates the release of digestive enzymes from the pancreas and bile from the gallbladder. Masclee et al reported significantly delayed gallbladder emptying after the ingestion of a fatty meal in patients who had undergone partial gastrectomy compared with normal patients. Both groups exhibited the same basal CCK levels, but gastrectomy patients had a lower CCK peak after oral intake. However, an analysis of CCK levels an hour after meal ingestion showed that both groups had comparable CCK levels and gallbladder emptying. The correlation between CCK levels and gallstone formation has not yet been reported, possibly because of its minor role or other compensatory mechanisms.