Gallbladder sludge and stone formation in relation to contractile function after gastrectomy. A prospective study.

In a prospective trial to determine whether gastric surgery induces gallbladder sludge and stone formation, 48 patients with gastric cancer were ultrasonographically examined with simultaneous observation on changes in gallbladder contractile function before and serially for 5 years after gastrectomy. Gallbladder sludge formation was induced with a high frequency of 42% 1 month after gastrectomy, with corresponding significant lowering of gallbladder contractile function. Most of gallbladder sludges, however, disappeared within 12 months in relation to the gradual recovery of gallbladder contractile function. Conversely, gallstone developed in nine patients (18.8%), mostly more than 6 months after gastrectomy. Interestingly, gallstone formation was induced in seven patients who were sludge negative. An evolvement of gallbladder sludge into stone was observed in only two patients, who were, however, treated with intravenous hyperalimentation. This study first provides evidence for the relationship between gastrectomy and a considerably high frequency of incidence of gallbladder sludge and stone in relation to changes in gallbladder kinetics after gastrectomy.

[The effect of gastrectomy on cholecystokinin (CCK) release and gallbladder contraction in patients with early gastric cancer--preliminary report].

Gastrectomy has been implicated in cholelithiasis. Impaired gallbladder motor function after the operation has been thought to be one of the major mechanisms. This study was undertaken to determine the effect of gastrectomy on release of cholecystokinin and contractile motility of gallbladder in five patients with early gastric cancer. After 14 hours fast, the gallbladder area was estimated by ultrasonography every 10 minutes for 120 minutes both before and after oral administration of 200 ml of Clinimeal. Blood samples were collected simultaneously via a peripheral vessel for measurement of plasma CCK levels by radioimmunoassay. Gallbladder contraction correlated well with the elevation of plasma CCK levels indicating that CCK might be one of the major factors governing gallbladder contraction both in pre- and post-gastrectomized conditions. Compared with preoperative cases, the postgastrectomized patients showed a significantly exaggerated postprandial response of CCK release in the initial 60 minutes, however, their gallbladder, responding to rapid reduction of plasma CCK levels, refilled significantly earlier. Postprandial rapid gastric emptying was thought to be related to the exaggerated postprandial CCK release, and the early refilling of the gallbladder might be attributed to the indefinite vagal or sympathetic denervation that might occurs during the necessarily wide lymph node dissections for gastric cancer operations.

[Postoperative changes in cholecystosonogram and gallbladder motor function following gastrectomy--a prospective serial ultrasonographic study].

In 48 gastrectomized patients, presence of gallstones (GS) and debris echoes (DBS) in the gallbladder were examined serially before and 1, 2 weeks, 1, 3, 6 and 12 months after operation. Fasting gallbladder area (FGBA) and maximal gallbladder contraction rate (MGCR) after caerulein injection (0.2 micrograms/kg i.m.) were measured ultrasonographically. GS developed in 7 (14.6%) of 48 patients. Within 1 month, DBS were visualized in 19 (45.2%) of 42 patients. However, in only 2 of these 19 patients, transition from DBS to GS was confirmed thereafter. No DBS were detected in 4 of 7 patients who developed GS. FGBA, measured postoperatively, increased significantly compared with preoperative value. MGCR decreased significantly compared with preoperative value in 1 month, but gradually recovered thereafter. Although 19 patients with DBS showed significant increase of FGBA and decrease of MGCR within 1 month compared with 23 patents without DBS, no discrepancies were observed between 7 patients with GS and 41 patients without GS, as to these postoperative changes of FGBA and MGCR. These findings suggest that enlargement and contractile dysfunction of gallbladder in early postgastrectomy periods, which are closely related to the formation of DBS, are not necessarily essential factors in the pathogenesis of postgastrectomy gallstones.

Plasma cholecystokinin and pancreatic polypeptide response after radical pancreatoduodenectomy with Billroth I and Billroth II type of reconstruction.

This study was conducted to elucidate plasma cholecystokinin (CCK) and pancreatic polypeptide (PP) response after pancreatoduodenectomy and to compare response of CCK and PP in patients who had pancreatoduodenectomy with Billroth I and Billroth II type of reconstruction. Basal levels of plasma CCK were significantly lower in patients who had pancreatoduodenectomy (9.6 +/- 0.8 pmol/L) than in the control (preoperative patients: 14.6 +/- 2.0 pmol/L) probably because of the removal of the entire duodenum due to pancreatoduodenectomy, since vagotomy, which is concomitantly brought about by pancreatoduodenectomy, does not appear to interfere with release of CCK. Significant amounts of CCK (integrated CCK: 497 +/- 111 pmol-120 min/L), although less amounts than in the preoperative patients (integrated CCK: 901 +/- 167 pmol-120 min/L), were still released in response to oral fatty meal after pancreatoduodenectomy. Plasma CCK response to oral fatty meal was significantly greater in patients who had pancreatoduodenectomy with Billroth I type of reconstruction (integrated CCK: 705 +/- 153 pmol-120 min/L) than in patients who had pancreatoduodenectomy with Billroth II type of reconstruction (248 +/- 63 pmol-120 min/L). Simultaneous measurement of plasma levels of PP revealed complete abolishment of PP response by pancreatoduodenectomy. Since PP secretion can be produced by vagal stimulation, it is most likely that the decreased PP secretion is due to vagotomy rather than removal of the duodenum and pancreas. Significant amounts of CCK released after pancreatoduodenectomy, in which the main sources of release of CCK are removed, may suggest the compensatory mechanism of the remnant upper small intestine. This study also suggests the necessity of re-evaluating Billroth I type of anastomosis as a physiologic reconstruction procedure for the remnant alimentary tract after pancreatoduodenectomy.

Release of cholecystokinin and gallbladder contraction before and after gastrectomy.

The contraction of the gallbladder by ultrasonography and release of cholecystokinin (CCK) by specific radioimmunoassay in response to the ingestion of oral fatty meal before and 1 month after gastrectomy in five patients with early gastric cancer was studied. Before gastrectomy, basal concentrations of CCK (13.4 +/- 2.3 pmol/L) rose significantly to a maximum of 23.3 +/- 3.6 pmol/L at 20 minutes after ingestion of oral fatty meal, and remained significantly elevated during the study. Gallbladder contraction began as CCK concentrations rose, demonstrating significant correlation with plasma CCK. One month after gastrectomy, CCK showed a rapid and greater response to the ingestion of fatty meal, attaining a maximum of 53.7 +/- 7.3 pmol/L at 10 minutes, then gradually falling to basal level. The maximal contraction of the gallbladder after gastrectomy was almost the same as before gastrectomy (62.7 +/- 4.0% of original area), showing a significant correlation with plasma CCK, but refilling of the gallbladder was induced earlier with corresponding reduction of plasma CCK. Simultaneous measurement of plasma concentrations of pancreatic polypeptide revealed a fairly similar response to plasma CCK before and after gastrectomy. The release of CCK is the chief mechanism by which the ingestion of a fatty meal causes contraction of the gallbladder even after gastrectomy as well as before gastrectomy.

[Mass survey for gastric cancer].

Mass survey of the stomach would appear to be at an important stage with the implementation of the Health of the Aged Law. In accordance with this situation, nationwide totalization, indirect X-ray examination, and the proportion of the population receiving mass survey and accurate management vary somewhat at present. The recent state of these items are discussed in the present study.

Skeletal maturity of Japanese children in Amami-Oshima Island.

This report describes the TW-2 skeletal maturity status of 723 Japanese children aged 7-16 years old in Naze, Amami-Oshima Island (southern island in Japan). Naze children showed retarded skeletal maturity scores under the age of 12 years for boys and eight years for girls, and thereafter they were advanced in relation to the British standard. In the comparison with Western Kyushu children Naze boys showed almost similar RUS maturity score throughout the age range studied; Naze girls had a similar RUS maturity pattern during the pre-adolescent period, but thereafter they showed advanced pattern. Marked advanced carpal maturation was observed in girls compared with that of Western Kyushu children. No socio-economic factor accounted for the advanced skeletal maturity status of Amami children in comparison with that of Western Kyushu children.