Solid-cystic (papillary-cystic) tumours (SCT) of the pancreas are distinctive neoplasms with a predilection for young female patients. This is the first detailed report describing the occurrence of SCT in two young male patients. Except for the extrapancreatic occurrence of one of the tumours (in the retroperitoneal region behind the head of the pancreas), all other clinicopathological features were identical to those characterizing the SCT in women. Immunostaining was (at least focally) positive for Lu 5 (broad spectrum keratin marker), vimentin and alpha-1-antitrypsin. The tumours were negative for neuroendocrine markers (except for neuron-specific enolase), pancreatic hormones and enzymes, pancreatic stone protein, carcinoembryonic antigen, CA 19-9 and nuclear oestrogen and progesterone receptors. This report does not support the suggested female sex hormone dependence of SCT.

One hundred patients with duodenal or pyloric/prepyloric ulcer disease were operated with parietal cell vagotomy (PCV) and followed for a minimum of 10 years. At 6 weeks, 1,5 and 10 years postoperatively gastric secretory tests, haematological work-up and clinical examination or telephone interview were performed. There was no operative mortality and the frequency of postoperative sequelae was minimal. The cumulative ulcer recurrence rate was 18 per cent and another 14 per cent had slight to moderate symptoms of epigastric pain without any signs of ulcer. Upper gastrointestinal endoscopy was used to reveal recurrences but was performed only if the patient had symptoms of recurrence. A rise in basal acid secretion and in pentagastrin-stimulated secretion was observed the first year postoperatively, whereas insulin-stimulated peak acid output increased during the first 5 years. We conclude that PCV has a low rate of per- and postoperative complications and an acceptable recurrence rate. Therefore, it seems that PCV is the method of choice in chronic duodenal ulcer disease.

Abstract One hundred patients with duodenal or pyloric/prepyloric ulcer disease were operated with parietal cell vagotomy (PCV) and followed for a minimum of 10 years. At 6 weeks, 1,5 and 10 years postoperatively gastric secretory tests, haematological work-up and clinical examination or telephone interview were performed. There was no operative mortality and the frequency of postoperative sequelae was minimal. The cumulative ulcer recurrence rate was 18 per cent and another 14 per cent had slight to moderate symptoms of epigastric pain without any signs of ulcer. Upper gastrointestinal endoscopy was used to reveal recurrences but was performed only if the patient had symptoms of recurrence. A rise in basal acid secretion and in pentagastrin-stimulated secretion was observed the first year postoperatively, whereas insulin-stimulated peak acid output increased during the first 5 years. We conclude that PCV has a low rate of per- and postoperative complications and an acceptable recurrence rate. Therefore, it seems that PCV is the method of choice in chronic duodenal ulcer disease.

Congenital duodenal diaphragm presenting with symptoms in adult life is a rare entity. Two cases are reported. They were treated with Finney pyloroplasty and excision of the duodenal diaphragm. The literature is reviewed.

The aim of the present study was to evaluate the role of gastric acid secretory tests in predicting ulcer recurrence in a consecutive series of patients before and up to 5 years after parietal cell vagotomy (PCV). Included in the study are 405 patients with prepyloric or duodenal ulcer disease (57 recurrences). There were no differences in acid secretion in the group of patients with pyloric or prepyloric ulcer disease, with or without recurrences. Thus pre- and post-operative acid secretory tests are of no value in predicting the outcome of PCV in this group of patients. In the duodenal ulcer group both postoperative basal acid output and peak acid output after pentagastrin and after insulin were higher in patients with recurrences. The two best discriminatory values were the ratio between the preoperative and the 6-week value of basal acid output and the 6-week value of peak acid output after insulin. The results of the study suggests that the ratio of the basal output before surgery and 6 weeks after surgery is enough for judging the acid reduction after PCV and that only in the case of a recurrence should an acid stimulation test be used.

Gastrin is a trophic stimulant of the acid producing gastric mucosa. Experiments have been carried out in rats, in which chronic states of either low or high serum gastrin levels were induced by surgical manipulation or drug treatment. A relationship between circulating gastrin and a trophic effect could be demonstrated in the oxyntic mucosa, but not in the pancreas and small intestine. Endocrine cells in the oxyntic mucosa (the ECL cells and A-like cells) are among the target cells for the trophic action of gastrin. The functional significance of these two cell populations is unknown. There is much experimental evidence indicating that they are under functional as well as tropic control of gastrin. The vagus nerve also exerts trophic control on the oxyntic mucosa, including the endocrine cells within it. This could be demonstrated by one-sided truncal vagotomy which caused atrophy of the mucosa and hypoplasia of endocrine cells (notably the ECL cells) on the denervated side of the stomach. Conversely, portacaval shunt greatly increased the number of ECL cells. There was no hypergastrinaemia after portacaval shunt, and no trophic effect on other cell types in the oxyntic mucosa. The factors responsible for the ECL cell proliferation after portacaval shunting remain unknown. Tumours may arise spontaneously from the ECL cells. Such neoplasias have been described in Mastomys (Praomys natalensis) and in man. ECL cell hyperplasia and neoplasia in man, but not in Mastomys, are usually associated with hypergastrinaemia either as a result of a gastrin producing tumour or as a result of achylia (sometimes associated with pernicious anaemia). It is unlikely that gastrin alone is responsible for the neoplasia, though it is quite likely that long-standing hypergastrinaemia triggers or facilitates a sequence of events that ultimately leads to tumour formation, via diffuse ECL cell hyperplasia.

Ranitidine, 300 mg daily, was given to 92 patients with duodenal ulcer (DU), 38 with prepyloric ulcer (PPU), and 21 with gastric corporeal ulcer (GCU). The healing rates at 4 weeks differed for the different types of ulcers (P less than 0.01), being 91% for DU, 68% for PPU, and 81% for GCU. After established ulcer healing, maintenance treatment with either ranitidine, 100 mg twice daily or 150 mg at night, or placebo was given for 1 year or until ulcer relapse in a total of 108 patients--71 with DU, 24 with PPU, and 13 with GCU. There were no significant differences in relapse rates between the two groups treated with active drug or between the three ulcer groups. However, the overall relapse rate in the active drug groups was 16%, against 72% in the placebo group (P less than 0.001).

In portacaval-shunted rats, basal but not pentagastrin-stimulated acid secretion was higher than in sham-operated controls. The basal serum gastrin concentration was unchanged and the postprandial serum gastrin concentration lowered following portacaval shunt. Thus, gastrin is not responsible for the elevated basal acid secretion. The present study provides evidence that there is no trophic effect on the oxyntic mucosa as a whole and that there is no change in parietal cell-associated gastrin receptors after portacaval shunting. Interestingly, however, endocrine cells in the oxyntic mucosa (the histamine-containing ECL cells) proliferated greatly and the pentagastrin- and cholecystokinin octapeptide-induced activation of the histamine-forming enzyme, histidine decarboxylase, in these cells was much greater than in control rats. Analysis of the dose-response curves for the enzyme-activating effect of pentagastrin and cholecystokinin-octapeptide indicated that the D50 values for these two stimulants were not altered by shunting but that the maximal enzyme activation was greatly elevated. The enhanced enzyme activation can be partly, but not fully, explained by the fact that the ECL cells were increased in number. The enhanced response following portacaval shunt probably reflects also an increased number of gastrin receptors per ECL cell. The effect of portacaval shunting on gastric ECL cells can perhaps be explained by impaired degradation in the liver of intestinal substance(s) exerting a highly specific trophic effect on the ECL cells or, alternatively, causing an enrichment of gastrin receptors on these cells, thereby making them more sensitive to the trophic effect of gastrin. The ECL cell hyperplasia is manifest about 4 weeks after the shunting. A modified procedure for portacaval shunting which left the gastroduodenal vein (otherwise ligated) drained to the liver produced the same trophic effect as conventional portacaval shunt, suggesting an intestinal rather than gastroduodenal origin of the agent(s) responsible for the trophic action.

Selective upper abdominal sympathectomy increased basal acid output in rats but was without effect on stimulated acid output, serum gastrin concentration, and gastric mucosal histidine decarboxylase activity. The sympathectomy was verified by fluorescence histochemistry and determination of tissue catecholamines. A drastic reduction in tissue noradrenaline, adrenaline, and dopamine levels occurred after sympathectomy, and fluorescence microscopy showed a complete loss of adrenergic nerve fibers. Vagotomy reduced catecholamine levels in the stomach wall by 50% but did not affect the catecholamine content in the pancreas and small bowel. Surprisingly, combined vagotomy and upper abdominal sympathectomy resulted in lower catecholamine levels than sympathectomy alone in extragastric but not in gastric tissues.

It is a well established fact that women with recurrent colorectal carcinoma have a high frequency of ovarian metastases. This study was undertaken to see if microscopic metastases could be found in serial sections of ovaries removed at the time of primary operation. Of 58 patients, 4 had microscopic metastases and an additional 2 patients had macroscopic metastases. This finding, plus the risk of the development of a primary ovarian carcinoma, favors prophylactic oophorectomy in women with colorectal carcinoma.

The modified sham feeding procedure has been advocated to replace the insulin test as the method of choice for the assessment of denervation after vagotomy. One of the reasons for this changing attitude is the assumption that insulin hypoglycaemia causes non-cholinergic stimulation of acid secretion, possibly mediated via the sympatho-adrenal system. This study has therefore compared the effects of these two different tests on acidity and release of catecholamines into the circulation in 7 duodenal ulcer patients 6 weeks after highly selective vagotomy. It was found that insulin, but not modified sham feeding, caused a marked increase in plasma adrenaline and noradrenaline concentrations whereas gastric acid secretion was of a similar magnitude in the two tests. The results suggest that the increased plasma catecholamine levels during insulin hypoglycaemia do not influence gastric acid secretion in duodenal ulcer patients.

The amount of sick-listing in 75 patients operated on with highly selective vagotomy (HSV) was studied during two periods, the first consisting of 12 months and ending 1 year before operation and the second period, also consisting of 12 months, starting 1 year after operation. Patients with suspected ulcer recurrences were excluded and only patients who, at the 1-year postoperative follow-up study, were without symptoms suggestive of ulcer recurrence are included. The median amount of sick days was 31.3 for the period preceding and 37.2 (NS) after the operation. Before operation 60% of all sick-leave diagnoses were ulcer or gastritis, compared with 20% after operation. A 50% increase in infectious diseases and lumbago occurred. Psychiatric disorders rose from 1 to 16 occasions. We therefore conclude that patients apparently cured of chronic ulcer disease change target and develop symptoms elsewhere. The study shows no potential economic benefits of HSV, at least not with regard to a diminishing amount of sick days after operation.

Chronic stimulation of the antral gastrin cells by elevated antral pH was achieved by fundectomy, antrum exclusion, fundectomy plus antrum exclusion, antrocolic transposition, and vagal denervation plus pyloroplasty. For comparison we studied also the effects of pyloroplasty alone and of portacaval shunting. All operations that elevated the antral pH resulted in high gastrin concentrations in serum. Particularly high concentrations were observed in fundectomized rats. Vagal denervation of fundectomized or antrum excluded rats reduced the serum gastrin concentration slightly compared with the corresponding innervated animals. Portacaval shunting reduced the gastrin concentration in serum. The antral gastrin concentration was raised or unchanged following fundectomy and vagal denervation, and reduced following antrum exclusion, antrum exclusion plus vagotomy, fundectomy plus antrum exclusion, fundectomy plus vagotomy, antrocolic transposition and portacaval shunt. The gastrin cell density in the antral mucosa was raised following fundectomy, vagotomy, and fundectomy plus vagotomy, unchanged following fundectomy plus antrum exclusion and antrocolic transposition, and reduced following antrum exclusion and portacaval shunting. Ultrastructurally the gastrin (G) cells in the excluded antrum and in the antrum of fundectomized rats showed signs of secretory activity in that the granule volume density or the number of granules per unit cytoplasm was lowered. In the fundectomized rats moreover, the endoplasmic reticulum of the G cells was increased, the Golgi area enlarged and the proportion and volume density of electron dense granules greatly increased. The granule profile diameter was not affected by either antrum exclusion or fundectomy. The results on the excluded antrum indicate that elevated antral pH per se is not sufficient to produce gastrin cell proliferation. In the fundectomized rats, where the hyperlasia of antral gastrin cells was considerable, there is the added stimulus of ingested food. In fundectomized plus antrum excluded rats this stimulus is eliminated and no proliferation ensues. The passage of intestinal material, as in the rats subjected to antrocolic transposition, did not elicit gastrin cell proliferation which seems to suggest that the character of the luminal material is important. We propose therefore that gastrin cell proliferation is due to the combined stimulation of high antral pH and passage of food. Vagal innervation is not required.

1. Following antrum exclusion the serum gastrin concentration was raised and independent of the prandial state. The antral gastrin concentration and number of gastrin cells were greatly lowered. 2. The histamine content and the number of histamine-storing endocrine ('entero-chromaffin-like') cells in the oxyntic mucosa was almost doubled and the mucosal histidine decarboxylase activity was greatly elevated following antrum exclusion. 3. At the ultrastructural level both types of histamine-storing endocrine cells (ECL and A-like) were found to be enlarged and to have a reduced number of granules per unit cytoplasm. These changes are compatible with an increased secretory activity. The G (gastrin) cells were not increased in size but their granule volume density was lowered. 4. We propose that antrum exclusion results in uninhibited gastrin release causing profound changes in the histamine-storing endocrine cells of the oxyntic mucosa. The cells respond to the hypergastrinemia by an increase in functional activity (activation of histidine decarboxylase and reduction of granule volume density) as well as by an increase in number and size.