Perforation of the gallbladder due to blunt abdominal trauma.

Gallbladder perforation due to blunt trauma is an uncommon finding. We report our experience with six patients. The factors predisposing to perforation include a distended gallbladder because of either fasting or alcohol ingestion in normal patients, and obstruction of the cystic in patients with cholelithiasis. The diagnosis of gallbladder perforation after blunt injury may be suspected in patients with signs of an acute abdomen and hypotension that is not explained by blood loss. Peritoneal lavage that contains bile suggests the tentative diagnosis of trauma to the biliary tract or gallbladder, as well as to the liver or upper bowel. A cholecystectomy is the preferred treatment when gallbladder perforation occurs in the traumatized patient.

Pancreatic polypeptide. A review.

Pancreatic polypeptide (PP), 36-amino acid peptide, may function as an important feedback inhibitor of pancreatic secretion after a meal. It arises from both islet and acinar cells of the pancreas. Release of PP by a meal, primarily protein, occurs in a biphasic manner. The first rapid release occurs as a result of vagal stimulation; the second, more prolonged rise (the so-called intestinal phase) occurs in response to hormonal stimulation, predominantly cholecystokinin. Plasma PP levels increase with age; PP levels are elevated above those of age-controlled normal subjects in diabetic patients and in some patients with pancreatic amine precursor uptake decarboxylase tumors. The value of plasma PP as a possible marker for pancreatic tumors is as yet unsettled but may be a valuable tool.

Prevention of upper gastrointestinal hemorrhage in 582 burned children.

In 582 burned children, neutralization of gastric acid and reduction of psychic stress were utilized to reduce upper gastrointestinal ulceration and hemorrhage. While receiving milk, diazepam, and psychologic support, two children required operation. Two of the children who died without clinically apparent gastrointestinal disease had ulcers discovered at autopsy. We conclude that a prophylactic regimen that reduced the amount of acid bathing the gastroduodenal mucosa, provides adequate calories, and minimizes psychic stress is useful in preventing gastrointestinal hemorrhage after burns.

Ectopic parathyroid adenomas.

Two cases of parathyroid tumours occurring in unusual situations are described. Such cases may cause difficulty in both the diagnosis and the surgical treatment of hyperparathyroidism. The cases described illustrate the importance of a definitive aetiological diagnosis in hypercalcaemia, if appropriate surgery is to be performed. The value of discriminant function analysis and hydrocortisone suppression tests are discussed.

Adult-onset Langerhans cell histiocytosis associated with severe abscesses.

We describe the case of an elderly lady who presented with a severe crusting skin eruption, mainly affecting the flexural areas and trunk. A diagnosis of Langerhans cell histiocytosis was confirmed by electron microscopy, and her condition was eventually controlled with systemic prednisolone and short courses of etoposide. An unusual feature of this case was the development of severe pyogenic abscesses, particularly involving the cervical region. No underlying immunological defect has been found to explain this.

Leiomyosarcoma of the colon.

Review of 36 cases of colonic leiomyosarcoma in the literature and our case demonstrate that most patients complain of an abdominal mass and a change in bowel habits of short duration. No physical finding has prognostic value. The mitotic activity of the tumor is the best index of survival time. Resection of the tumor mass appears to be the treatment of choice.

Correlation between gallbladder size and release of cholecystokinin after oral magnesium sulfate in man.

In order to determine the effect of oral magnesium sulfate on gallbladder contraction and release of cholecystokinin (CCK) in man, magnesium sulfate (25 g in 100 ml distilled water) was given by mouth to five fasting adult male volunteers. Plasma samples were collected for measurement of CCK by a specific radioimmunoassay. Gallbladder volumes were determined from sonograms obtained from a phased-array real-time ultrasound scanner. Basal concentrations of CCK (82.2 +/- 10.1 pg/ml) increased significantly at 20 minutes after oral magnesium sulfate (113.8 +/- 7.1 pg/ml), and reached a maximal value at 50 minutes (150.0 +/- 42.0 pg/ml). The mean basal volume of the gallbladder was 30.8 +/- 5.3 cm(3) and maximum reduction of gallbladder volume (to one third of original) was achieved at 50 minutes after ingestion of magnesium sulfate. Linear regression analysis showed a close correlation (r = -0.9337) between plasma concentrations of CCK and gallbladder size in response to magnesium sulfate. Oral magnesium sulfate also caused a significant increase in serum gastrin (from basal of 51.4 +/- 9.9 pg/ml to 69.8 +/- 15.5 pg/ml at 5 min); there was no significant correlation between gastrin release and gallbladder contraction. This study provides direct evidence that the mechanism of magnesium sulfate-stimulated gallbladder contraction occurs through the release of CCK, and shows a close correlation between CCK release and contraction of the gallbladder.

The effects on gastrin and gastric secretion of five current operations for duodenal ulcer.

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.

The effect of glucagon on pancreatic secretion and plasma secretin in dogs.

The inhibitory effect of glucagon on pancreatic exocrine secretion induced by endogenously released secretin was studied in 4 dogs with chronic pancreatic fistulas and open gastric fistulas. After a constant level of pancreatic secretion was established by intraduodenal hydrochloric acid perfusion (9 mEq/hr), glucagon (30 microng/kg-hr) was administered intravenously for 1 hr. Compared to a separate control study in which dogs received intraduodenal HC1 alone, glucagon caused a significant decrease in both pancreatic volume flow and bicarbonate output. Glucagon had no effect on pancreatic protein secretion, and circulating levels of endogenously released secretin remained unchanged. It is concluded that the inhibitory effect of glucagon on pancreatic secretion is not mediated through inhibition of secretin release. The chemical homology between glucagon and secretin suggests that glucagon may mediate its inhibitory action by competing with secretin at the level of the pancreatic receptor site.

Emergency diagnosis of upper gastrointestinal bleeding by fiberoptic endoscopy.

Emergency esophagogastroduodenoscopy has been performed in 192 consecutive patients admitted with massive gastrointestinal bleeding. Accurate endoscopic diagnosis was made in 184 or 96%; 58 patients underwent emergency operations to control bleeding with an overall operative mortality of 26%. Excluding 16 patients who underwent emergency portacaval shunting, the operative mortality was 7%. In 6 patients, the bleeding was controlled by endoscopic electrocoagulation. There were no complications. Emergency endoscopy should be done routinely as the primary diagnostic approach in the diagnosis of upper gastrointestinal bleeding.

Reduction of postprandial release of pancreatic polypeptide after development of pancreatic fibrosis.

We have measured the plasma pancreatic polypeptide response to a meal before and after the development of pancreatic fibrosis in dogs. Peripheral blood samples were collected in five dogs before and after a standard meal for measurement of pancreatic polypeptide by a specific radioimmunoassay. The next day, all of the pancreatic ducts were ligated in each dog, and one month after pancreatic ductal ligation, the food study was repeated. The dogs were sacrificed on the following day, and the pancreas of each dog was studied morphologically. Before pancreatic ductal ligation, plasma pancreatic polypeptide concentrations showed a biphasic response to a meal; a primary, rapid increase lasted 30 to 45 minutes, and a secondary, prolonged increase lasted for more than 180 minutes. One month after pancreatic ductal ligation, plasma concentrations of pancreatic polypeptide, at each time period during the initial 60 minutes after food, were significantly less than the corresponding sample before pancreatic ductal ligation. The total amount of pancreatic polypeptide released after a meal during the initial 60 minutes was diminished significantly by pancreatic ductal ligation. Neither plasma concentrations of pancreatic polypeptide nor the total amount of pancreatic polypeptide release after a meal showed a significant change during the last 180 minutes after food. Results of histologic observations showed destruction and fibrotic replacement of the acini of the pancreas after ligation of the pancreatic ducts. The islets were well preserved. Since the cells of origin of pancreatic polypeptide are distributed in both the acini and islets of the pancreas in dogs, we suggest that the primary, rapid phase of pancreatic polypeptide after a meal may be derived chiefly from cells in the acini, whereas the secondary phase of response may be derived chiefly from cells in the islets.

Release of cholecystokinin in man: correlation of blood levels with gallbladder contraction.

Although it is generally assumed that release of cholecystokinin (CCK) is the chief mechanism by which a fatty meal causes contraction of the gallbladder, measured release of CCK and gallbladder contraction have never been correlated. We have achieved this correlation in eight adult male volunteers, by means of a specific radioimmunoassay for CCK and by ultrasonographic imaging of the gallbladder. This study validates our CCK radioimmunoassay and correlates measured concentrations of CCK with changes in gallbladder size measured by ultrasonographic examination. Basal concentrations of CCK (82.6 +/- 10.4 pg/ml) rose significantly to a maximum of 411.1 +/- 79.9 pg/ml at 16 minutes after intraduodenal instillation of medium-chain triglyceride (Lipomul). Mean basal volume of the gallbladder was 34.6 cm3; maximum reduction of gallbladder volume (to one-third of original) was achieved at 18 minutes. Elevated CCK concentrations began to fall toward basal, and the gallbladder began to refill at 25 minutes. Results obtained after oral ingestion of Lipomul provide similar results. Linear regression analysis demonstrated excellent correlation between concentrations of CCK and gallbladder size during both contraction and relaxation phases. Future study of this correlation may be useful in patients with manifest dysfunction of the gallbladder, as well as in individuals known to be at risk of gallbladder disease.

Removal of circulating gastrin and cholecystokinin into the lumen of the small intestine.

This study was undertaken to investigate the mechanism by which the small intestine removes circulating gastrin and cholecystokinin (CCK). A 100-cm (acute study, 10 dogs) or a 50-cm (chronic study, 5 dogs) segment of midjejunum was excluded in all 15 dogs. The excluded loop was perfused with 0.1 M phosphate buffer (pH 7.4), which was constantly recirculated by a peristaltic pump. It the acute control study (5 dogs), gastrin concentrations in the intestinal perfusate were increased gradually to a level of 320 +/- 49 pg/ml at 90 min (i.e., 7.6 +/- 0.9 times higher than serum gastrin levels). In the antrectomy group (5 dogs), perfusate gastrin concentrations were greatly decreased after antrectomy, in consonance with the decrease in serum gastrin concentrations. In the chronic study (5 dogs), perfusate gastrin concentrations were significantly increased after food stimulation, in consonance with the increase in serum gastrin concentrations. CCK was also released into the bowel lumen in considerable amounts basally and after endogenous release. Although one cannot exclude the possibility that a considerable amount of gastrin or CCK in the lumen may originate from the bowel segment, this study shows that the small bowel removes gastrin and CCK from the circulation by their secretion into the bowel lumen. Loss of this mechanism might partially explain the rise in gastrin levels that is observed in some patients after extensive small bowel resections.

Effect of colectomy on cholecystokinin and gastrin release.

Studies were conducted to determine the effect of resection of the colon on the release of cholecystokinin (CCK) and gastrin. A standard food stimulation test was performed in five dogs. Peripheral blood samples were collected for future measurement of CCK and gastrin by specific radioimmunoassay. Each dog underwent subtotal colectomy with side-to-end ileoproctostomy. The food stimulation test was repeated at approximately weekly intervals for eight weeks after colectomy. Basal plasma CCK levels of 139 +/- 21 pg/ml before colectomy did not change after colectomy. Total amount CCK released after food was increased significantly at both four (5.94 +/- 0.78 ng min/ml) and eight (13.00 +/- 2.72 ng min/ml) weeks after colectomy in comparison with that observed prior to colectomy (2.94 +/- 0.54 ng min/ml). Basal serum gastrin levels of 28 +/- 9 pg/ml did not change significantly after colectomy. Total amount of gastrin released after food was increased significantly at both two (8651 +/- 2294 pg min/ml) and three (6940 +/- 1426 pg min/ml) weeks after operation, but at none of the later weeks. The precolectomy output, used for comparison, was 5608 +/- 1346 pg min/ml. It was concluded that resection of the colon leads to an increase in release of CCK and gastrin after food stimulation. This finding provides further evidence that the colon contains a factor that inhibits the release of CCK and gastrin, and that the colon functions as an endocrine organ.