The role of endogenously released cholecystokinin (CCK) in mediating gallblader (GB) contraction was evaluated in 12 normal volunteers and 24 patients with gallstones (11 additional gallstone patients were excluded because of failure of adequate ultrasonographic visualization). CCK concentrations before and after oral administration of fat (Lipomul((R))) were measured by a specific radioimmunoassay. CCK release was correlated with changes in GB volume determined simultaneously by ultrasonography. On the basis of gallbladder contraction and operative findings, gallstone patients were divided into "contractors" (14), "noncontractors" (6), and "hydrops" (4). Lipomul caused prompt release of CCK in normal volunteers and all groups of gallstone patients. The changes (basal to peak) in plasma CCK (pg/ml) for the different groups were as follows: normal volunteers (108 +/- 9 to 200 +/- 16), contractors (77 +/- 10 to 128 +/- 13), noncontractors (59 +/- 7 to 159 +/- 38), and hydrops (43 +/- 5 to 113 +/- 47). The total integrated output of CCK (0-60 min) was greater in normal volunteers (3975 +/- 762 pg-min/ml) than in contractors (1530 +/- 567 pg-min/ml). Lipomul caused similar GB contraction in normal volunteers and contractors (from basal volumes to maximal contraction); these changes were from 19.5 +/- 2.3 ml to 5.6 +/- 1.0 ml in normal volunteers, and from 19.6 +/- 3.2 to 5.2 +/- 1.0 in contractors. Plasma concentrations of CCK and GB volume were highly correlated in the 12 normal volunteers (r = -0.89, p < 0.01) and in the 14 contractors (r= -0.99, p < 0.01)), but the GB was significantly (p < 0.01) more sensitive to changes in plasma CCK in the gallstone contractors than in the normal volunteers. The authors suggest that there may be two groups of gallstone patients, noncontractors and contractors. Stasis may be important in the pathogenesis of gallstones in the noncontractors, whereas in contractors, the authors speculate that an abnormality in the CCK-gallbladder relationship (characterized by diminished CCK release and increased GB sensitivity to CCK) may be involved in the evolution of the disease.
One of the syndromes commonly encountered in the outpatient clinic is flatulent dyspepsia. By this we mean epigastric discomfort after meals, a feeling of fullness so that tight clothing is loosened, eructation with temporary relief, and regurgitation of sour fluid to the mouth with heartburn. The At the interview the patient was asked how she had been since the operation and was led to speak of her indigestion. Then specific questions were put concerning the common symptoms of dyspepsia. Seventy-two patients with dyspepsia were asked to attend for review, but only 66 were seen. Four had left the district, one could not be traced, and one refused to attend-in the latter case we accepted her own doctor's opinion that the dyspepsia persisted unchanged. We do not feel that these absences invalidate our findings shown in the It will be seen that after cholecystectomy more than half the patients were completely free from dyspepsia and less than a quarter were unchanged. A history of attacks of biliary colic did not affect these proportions. The few males included in the survey did not have results that differed obviously from the females. The type of gall stone did not affect the result, nor did the impaction of a stone.Ten cases had a hiatus hernia as well as gall stones ; the results in these cases did not differ significantly from the rest. It was noted, however, that in the cases that were cured gastro-oesophageal reflux was not a prominent feature before operation; when it was a prominent feature in the preoperative symptoms it seldom improved. In contrast, several patients without a hiatus hernia had severe preoperative symptoms of gastro-oesophageal reflux and most of these were completely relieved of their symptoms after operation.The mere passage of time does not cure flatulent dyspepsia, as is shown by our review of the patients with radiologically negative dyspepsia ; only two of these patients were cured, and both ascribed their cure to the reassurance that there was nothing seriously wrong. After cholecystectomy the patients who were not improved usually complained in the early postoperative period; the others did not show a tendency to relapse after the psychotherapeutic effect of an operation might be expected to diminish. SummaryCholecystectomy for gall stones cures flatulent dyspepsia in more than half the cases, and less than a quarter are not improved. The presence of a hiatus hernia does not lessen the probability of cure unless the dominant symptoms indicate gastro-oesophageal reflux.
We have measured serum gastrin and gastric acid secretion in 66 duodenal ulcer patients before and after vagotomy and pyloroplasty (V + P--15 patients), selective proximal vagotomy without drainage (SPV - D--11 patients), and with drainage (SPV + D--19 patients), and vagotomy, antrectomy, and either gastroduodenostomy (V + BI--15 patients) or gastrojejunostomy (V + BII--6 patients). Basal and peak postprandial gastrin levels were increased in postoperative V + P, SPV - D, and SPV + D patients. Basal and peak postprandial levels of gastrin were unchanged after V + BII, indicative of duodenal release of gastrin. Gastrin response to food was abolished in V + BII patients. Acid output was reliably reduced after all five operations; reduction was greatest in patients after antrectomy and least in patients after SPV. No beneficial results were found with drainage in SPV patients. Acid secretion increased with time in SPV patients, especially those with drainage.
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