Percutaneous pancreatic cystogastrostomy guided by ultrasound scanning and gastroscopy.
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Biomedical subjects
Publications and source records attributed to F W Henriksen.
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The isoamylase pattern in serum and the amylase thermolability have been suggested as screening tests for the development of pancreatic pseudocysts. To study whether serum reflects the contents of pseudocysts, we have investigated the isoamylases and their thermolability in cyst fluid and in serum from 13 patients with pancreatic pseudocysts. No significant correlation was found between the contents in serum and cyst fluid with regard to total amylase and isoamylase P2 and P3 or with regard to the thermolability of total amylase and isoamylase P2 and P3. Thus, serum does not reflect the cyst contents of isoamylases or their thermolability. Therefore these serum amylase determinations can hardly be expected to be useful in distinguishing patients developing pseudocysts among patients with pancreatitis.
In a two-year period from June 1981, two cases of acute upper gastrointestinal bleeding caused by pancreatitis were observed. In both cases the bleeding was caused by erosion of the gastric mucosa contiguous to, respectively, a pseudocyst and an abscess of the pancreas. Both patients were successfully treated with cystogastrostomy. Erosive bleeding from gastrointestinal mucosa adjoining pancreatic lesions may be a more common source of upper gastrointestinal bleeding than has hitherto been assumed.
In a prospective, controlled clinical trial, vagotomies for duodenal, pyloric, and prepyloric ulcers were performed on 259 patients. Eighty-three patients were randomly selected for truncal vagotomy and drainage (TV + D), 93 patients were randomly selected for selective gastric vagotomy and drainage (SV + D) and 83 patients were randomly selected for parietal cell vagotomy without drainage (PCV). This interim report deals with the primary results, reduction in acid secretion, sequelae, and recurrence rates two to five years after the operation. One patient died after the operation. Postoperative complications were evenly distributed between the three operations. No differences in spontaneous acid secretion (BAO), peak acid output after pentagastrin stimulation (PAOP), or peak acid output after insulin stimulation (PAOI) were found. Patients with recurrent ulcers ahd smaller reductions in BAO than patients without ulcer recurrences, although not significantly. Patients with ulcer recurrences after TV + D had, in contrast to ulcer recurrences after SV + D and PCV, a significantly smaller reduction in PAOP than patients without recurrences. The overall recurrence rate was 13%: 10% after TV + D, 14% after SV + D and 16% after PCV. The risk of ulcer recurrence within the first three years, calculated by an actuarial method, was found to be significantly higher after PCV (0.52% per month) than after TV + D (0.32% per month), but not different from SV + D (0.42% per month). In contrast to TV + D and SV + D, no recurrences after PCV occurred after three years--25% of the patients were followed for five years. It is concluded that the trial, at present, does not point to any evident superiority of PCV.
In eight volunteers the effect of pentagastrin (0.15, 1.0 and 6.0 microgram/kg body weight/h), secretin (0.5 and 1.0 clinical units/kg b.w./h), and cholecystokinin (CCK) (0.5 and 1.0 Ivy dog units/kg b.w./h) on the gastric secretion of pepsin was investigated to ascertain whether interaction occurred. A high intraindividual variation was found, and also a significant washout of pepsin in the initial period after stimulation. Pepsin secretion was stimulated after pentagastrin (50% above basal level) and even more after secretin (75%-200% above basal level), whereas no stimulation but a tendency for depression was seen after CCK. With the doses of gastrointestinal hormones used in this investigation, no interaction between secretin and CCK on gastric secretion of pepsin in man was demonstrated.
Two dogs were equipped with gastric and duodenal cannulas permitting quantitative collection of pure pancreatic juice. Two series of experiments were performed: 1) collection through a short catheter, length 35 cm, volume 0.3 ml, and internal diameter 1.0 mm, and 2) collection through a long catheter used for duodenoscopic cannulation in man, length 110 cm, volume 1.7 ml, and internal diameter 1.0 mm at the tip and 1.4 mm in the other part of the catheter. After a basal period of 30 min the secretion was stimulated with secretin in the doses 0.1, 0.5, and 2.0 clinical units/kg/h, each dose being infused over a period of 30 min. With the long catheter the dose-response curve for fluid and bicarbonate was shifted to the right. The basal secretion of fluid was depressed 40%; with increasing secretory rates the depression was less pronounced. No significant depression of the bicarbonate concentration was seen. The protein secretion was insignificantly reduced.
The survival rate in 709 patients with chronic inflammatory bowel disease (CIBD) was calculated by the log rank test. There were 297 patients with Crohn's disease (CD) and 412 patients with ulcerative colitis (UC). In both diseases there was a survival rate of about 94% in the first year of observation against an expected rate of 99.5% in a general population matched for sex and age. This was because a large number of patients were severely ill at their first admission and required immediate or early surgery. During the subsequent 11 years the death rate in CIBD was higher (two to three times) than in the general population. After 12 years the survival rate was about 77% in both CD and UC. The difference was statistically insignificant. There was no significant difference in the sex ratio. The cancer rate was low. No gastrointestinal cancer occurred among patients with CD. Colorectal cancer was found in four patients with UC, three of whom presented with cancer on their first admission. It is concluded that recurrence and reoperation for recurrence in Crohn's disease have not impaired the prognosis compared to ulcerative colitis in this series.
Six duodenal ulcer patients were investigated before and after truncal vagotomy and pyloroplasty. Four doses of gastrin-17 were injected intravenously (15.625, 31.25, 62.5, and 125 micrograms/kg body weight); the gastric secretory response and the disappearance rate of gastrin were measured. After vagotomy the basal level of gastrin increased from 64 pg/ml to 106 pg/ml. When corrected for the basal levels of gastrin, the peak levels and disappearance rate of gastrin-17 were observed to be the same after vagotomy as before (half-life before vagotomy, 5.6 min; after, 5.8 min). This indicates that vagus does not influence the metabolism of exogenous gastrin-17. The gastric secretion of acid was reduced to 30% after vagotomy, which shows that there is a synergism between vagus and gastrin-17.
The diagnosis of carcinoid syndrome has been confirmed by selective abdominal angiography in a consecutive series of 18 patients. In eight patients the primary carcinoid tumour was removed before angiography. The primary lesion was demonstrated in eight of ten cases. Metastases from the carcinoid tumours was present in all 18 patients. All cases of mesenteric metastases and 12 of 14 cases with liver metastases were visualized by angiography. All but one of the liver metastases were highly vascularized and therefore easy to recognize, making angiography a good monitor in the control of medical therapy or in planning of surgical intervention.
Eighteen patients with metastatic carcinoid tumours were admitted to surgical gastroenterological department of Rigshospitalet during the period 1974--1978. Thirteen had primary carcinoid tumours in the terminal ileum, two in the lungs, one in the pancreas, one in the testis, and one possibly in the retroperitoneum. All patients had distant metastases, 13 in the liver. Carcinoid syndrome with flusing and diarrhoea was present in 15 patients (83%). The time elapsing from onset of symptoms until diagnosis was on an average 2 1/2 years. The most valuable screening test for carcinoid syndrome was determination of the excretion of 5-hydroxy-indol- acetic-acid. The most sensitive investigation for determination of primary tumour and/or metastases was abdominal angiography, which was positive in all cases. Other radiological investigations were less sensitive.
Twenty-one consecutive patients with endoscopically proven recurrent ulcer were treated continuously with cimetidine, 1 g daily for 8 weeks. After 4 weeks' treatment 18 (86%) of the patients were free of symptoms, and the ulcers had healed in 17 (81%). At the 8th-week examination symptoms had disappeared, and ulcers were healed in 19 patients (91%). Within 6 weeks after withdrawal of cimetidine six patients (28%) presented recurrence of ulcers and symptoms. This study demonstrates that recurrent ulcer patients respond to cimetidine with regard to healing of ulcers and disappearance of symptoms, as do unoperated duodenal ulcer patients. Because operation for recurrent ulcer carries an increased mortality, we suggest that cimetidine should be attempted in the treatment.
Resection with the object of cure was undertaken in 20 patients with Crohn's disease in the terminal ileum. These patients were followed up more than five years after operation. Recurrence took place in eight patients, in half of them more than five years after the primary operation. Six patients were submitted to reoperation and two died. Seven out of the eight recurrences were localized to the anastomosis. These results may support the results of a bigger Swedish material which favours more radical primary resections in Crohn's disease.
Three cases of Gardner's syndrome are reported. Two patients had one and two carcinomas in the colon respectively. Postoperatively the two patients developed desmoid tumours in the abdominal wall, and one of them also an intraabdominal desmoid. The literature is briefly reviewed with respect to diagnosis and treatment of the components of the syndrome. A special section is devoted to the differentialdiagnostic problems. The reports from the last years concerning this problem are surveyed, and the rationale for maintenance of Gardner's syndrome and familial polyposis of the colon as two different genetic entities is questioned.
The inhibitory effect of combined secretin (0.5 and 1.0 clin. unit/kg b.w./hour) and cholecystokinin (0.5 and 1.0 IDU/kg b.w./hour on the pentagastrin-stimulated (0.15--1.0 and 6.0 ug/kg b.w./hour) gastric secretion was investigated in twelve volunteers and in twelve duodenal ulcer patients. Regardless of the dose level no difference was found between normals and duodenal ulcer patients, indicating that a decreased sensitivity to secretin and cholecystokinin is not a pathogenetic factor for the development of duodenal ulcer.
The inhibition of the pentagastrin-stimulated (1 ug/kg b.w./hour) gastric secretion by glucagon (20 ug/kg b.w./hour), cholecystokinin (0.5 IDU/kg b.w./hour), and a combination of these were investigated in 7 volunteers. Glucagon as well as CCK given isolated inhibited the gastric secretion, but no augmentation of inhibition was demonstrated when the hormones were in combination.
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