Percutaneous trephine lung biopsy: evolving role

In 9 normal and 42 duodenal ulcer patients, acid and gastrin studies were performed. Basal, Oxo and Histalog stimulated acid secretion was conducted on each patient. In 24 patients post vagotomy pyloroplasty or vagotomy antrectomy, these studies were repeated within three months after surgery. Two groups of duodenal ulcer patients were identified; those who did respond and those who did not respond to Oxo stimulation. In the "responders," Oxo stimulated acid output and gastrin secretion increased significantly over basal values. Both vagotomy pyloroplasty and vagotomy antrectomy caused a similar significant decrease in Oxo and Histalog stimulated acid output. In two patients with incomplete vagotomy, antrectomy, but not pyloroplasty abolished the Oxo stimulated acid response. These data suggest that OXO stimulation test can select patients with a significant antral component in whom vagotomy and antrectomy would be the appropriate procedure. Our results also indicate that antrectomy will protect against recurrent ulceration in patients with incomplete vagotomy and may explain the lower incidence of stomal ulceration in patients with vagotomy antrectomy, compared to vagotomy pyloroplasty.     

Superselective vagotomy. Preliminary results

Twelve patients suffering from an intractable duodenal ulcer are included in this review. Eleven were treated by superselective vagotomy without drainage, one had a selective vagotomy with pyloroplasty. A peroperative control of the gastric acidity after pentagastrin stimulation was used in all cases and permitted section of forgotten nerve fibers. Short-term results are satisfactory: after 2-6 months the clinical state of the patients is excellent (Visick I and II), basal acidity is decreased by 58 to 66% of preoperative value, the Hollander tests are negative except two. After more than 6 months, the few available results are satisfactory except one case of recurrent ulcer. The one case with a 1 year follow-up is excellent, clinically and as to acid secretion.     

Gastritis duodenitis, and circulating levels of gastrin in duodenal ulcer before and after vagotomy

Biopsy specimens have been taken from five standard sites in the stomach and from the duodenal bulb in order to investigate the association of gastritis and duodenitis with duodenal ulcer. Twenty patients with chronic duodenal ulcer were investigated in this manner and in addition had gastric secretion tests and a radio-immune assay of serum gastrin under differing conditions. The patients were then treated either by a truncal vagotomy and pyloroplasty (TVP) or by a highly selective vagotomy without a drainage procedure (HSV). All the investigations were repeated three months postoperatively. Duodenal ulcer was usually associated with gastriitis, although this varied in extent and severity from patient to patient. In nearly all the patients, gastritis was present at the pyloric end of the stomach and along the lesser curve. In more than half of the patients, gastritis was also present in the body of the stomach but the fundus was usually spared. Chronic duodenitis was found in the duodenal bulb in all these patients. After vagotomy there was a marked increase in both the extent and severity of the proximal gastritis in both treatment groups but the distal gastritis remain almost unchanged. There was little change in the incidence of duodenitis after vagotomy but its severity was lessened. No correlation was found between the peak acid output (PAO) in response to Histalog and the severity of the gastritis or the duodenitis either before or after operation, with one exception. The postoperative PAO was significantly less in those patients who developed a severe proximal gastritis after vagotomy. No relationship was found between the severity of the distal gastritis and the levels of serum gastrin. No correlation was found between either the basal or peak acid output and the corresponding serum gastrin levels before or after vagotomy.     

The effects of highly selective vagotomy on secretion and emptying of the stomach

The results of a prospective study of 60 patients with nonobstructive duodenal ulcer treated by highly selective vagotomy show that the gastric acid secretion postoperatively is effectively reduced. Judgment of completeness of highly selective vagotomy is only possible by means of an intragastric pH-metry during operation. The Hollander test answers it insufficiently. In a number of patients, highly selective vagotomy caused a fast initial phase of gastric emptying of porradge. The impression is that the contractional activity of the antrum has the same pattern before and after highly selective vagotomy.     

Effect of calcium infusions of serum calcium and gastric acid secretion

37 patients were studied with calcium infusions. Of these, 20 had previously undergone truncal vagotomy and pyloroplasty for duodenal ulcer disease, and 17 were unoperated patients with duodenal ulcer disease. Calcium was given intravenously either at a dose of 5 mg/kg/h for 3 h, or 4 mg/kg/h for 4 h. Gastric juice was collected by continuous suction. Results showed the 3-hour infusion raised calcium more than the 4-hour infusion. Top serum calcium achieved, however, did not correlate with calcium-stimulated gastric acid output, either with or without vagotomy. Stimulated gastric acid secretion was markedly less with vagotomy than without. It is suggested that the level of gastric acid stimulated by infusions might discriminate complete, from incomplete, vagotomies better than insulin, and that the 4-hour infusion is safer.     

Gallbladder sensitivity to CCK in duodenal ulcer disease, highly selective and truncal vagotomy

BACKGROUND/AIMS: Following truncal vagotomy, a heightened contractile response of the gallbladder to cholecystokinin (CCK) has been reported in patients. We investigated whether the gallbladder responsiveness to the CCK analog cerulein is also affected in patients with a highly selective vagotomy (HSV) and in duodenal ulcer patients, since most patients had truncal vagotomy for recurrent peptic ulcer disease. MATERIALS and METHODS: Gallbladder emptying (cholescintigraphy) and plasma cholecystokinin like immunoreactivity (CCK-LI) levels were studied during infusion of graded doses of the CCK analog cerulein. RESULTS: In duodenal ulcer patients (n = 9), patients with HSV (n = 9), patients with truncal vagotomy (n = 9) and control subjects (n = 9), infusion of stepwise increasing doses of cerulein (1-16 ng.kg-1.h-1) induced dose related changes in plasma CCK-LI. In patients with truncal vagotomy, the gallbladder contraction in response to 1, 2 and 4 ng.kg-1.h-1 of cerulein was significantly increased over controls; whereas the gallbladder contraction to cerulein in duodenal ulcer patients and patients with HSV was not significantly different from controls. CONCLUSIONS: Thus, in patients with truncal vagotomy, gallbladder contractile response to CCK is significantly enhanced, possibly due to denervation of hepatic vagal branches since gallbladder contraction after CCK infusion shows no difference between post HSV or duodenal ulcer patients and the controls.     

Inhibition of basal and pentagastrin-stimulated gastric acid secretion after treatment with benzilonium bromide and after selective proximal vagotomy

50 consecutive patients with radiographically verified duodenal ulcer and a history of peptic ulcer disease for more than 3 years and with elevated gastric acid secretion in the basal state and after stimulation with pentagastrin were randomly allocated to two groups. The first group of 25 patients was treated with benzilonium bromide (Ulcoban Prolongatum, Parke, Davis & Co.) and the second group was subjected to selective proximal vagotomy (SPV). The patient's gastric acid secretion was determined before the start of treatment and after 1, 6, and 12 months. After one year the basal acid output had decreased by 58.2% in the group treated with benzilonium bromide and by 82.9% in the patients who had undergone SPV. The peak acid output fell by 49.4% in the benzilonium group and by 66.1% in the SPV group.     

Gastric emptying in control subjects and patients with duodenal ulcer before and after vagotomy

The emptying of a solid meal labelled with Indium 113mDTPA from the stomach was studied with a gamma camera in 26 normal subjects, 27 patients with duodenal ulcer, on 41 occasions after truncal vagotomy and pyloroplasty and 38 times after highly selective vagotomy. Applying the method of principal component analysis to the results, differences were detected between control and duodenal ulcer subjects and two probable subgroups of duodenal ulcer were observed. Half emptying times did not reveal these patterns. After vagotomy, delayed emptying was general at one week. At one month, patients after highly selective vagotomy had a more normal result than those with truncal vagotomy and pyloroplasty (TV), but by six months no significant difference in overall emptying rate was found, although changes in the pattern of gastric emptying persisted in some patients after TV.     

Helicobacter pylori infection after gastrectomy and vagotomy in duodenal ulcer patients

The eradication of Helicobacter pylori (Hp) is known to reduce the recurrence rate of duodenal ulcer (DU) to similar extent as gastrectomy but it is not clear what is the prevalence of Hp in DU patients after surgical interventions such as gastrectomy or vagotomy. The purpose of this study was to evaluate the influence of gastrectomy or truncal vagotomy with pyloroplasty on the prevalence of Hp in 51 DU patients just before and 6-8 months after these procedures. Using C14-urea breath test (UTB), rapid CLO-test and histology of the biopsy samples of gastric mucosa obtained during gastroscopy, the Hp was detected in all DU subjects submitted to operation. Following distal gastric resection (antrectomy) with Billroth II anastomosis (N = 32) due to an ulcer resistance to conservative therapy, peptic ulceration was not observed during 6-8 months in any of the examined subjects and the Hp was only rarely observed (only in 3 out of 32 operated patients). Histologically, in antral biopsies taken prior to surgery, all DU patients presented chronic active gastritis. After the surgery, the absence of Hp was confirmed also by histology. Histological evaluation of gastrectomy stump biopsies revealed typical chronic gastritis with concomitant foveolar hyperplasia and focal gland dilation. Following selective vagotomy and pyloroplasty (N = 19), the scarring of duodenal bulb (without active ulcer) was seen in 4 out of 19 operated patients but the Hp was detected in all (100%) cases. Gastric biopsies prior and after vagotomy revealed chronic active gastritis associated with Hp infection. Basal plasma gastrin was reduced after gastrectomy by about 30% and basal and maximal pentagastrin-induced acid secretion was decreased by about 60% and 70%, respectively. Vagotomy did not reduce activity of the mucosal inflammation and the incidence of Hp. Basal plasma gastrin level was increased by about 60%, while basal and pentagastrin induced acid secretion was decreased by 25% and 40%, respectively. Because of the high ulcer recurrence rate after vagotomy as opposed to low recurrence after gastrectomy, it is reasonable to conclude that (1) the disappearance of Hp and reduction in plasma gastrin and gastric acid secretion were probably the major factors responsible for the high efficacy of gastrectomy in prevention of ulcer recurrence, (2) in non-complicated DU, gastric surgery should be avoided and replaced by conservative anti-Hp therapy involving both antisecretory or bismuth agents and antimicrobial drugs which should provide similar therapeutic effects as surgery and (3) vagotomy should be eliminated as the method of treatment of DU because of the high recurrence of peptic ulceration and the failure of this procedure to affect the Hp status.     

The vagus

The surgical physiology of the vagus is reviewed with respect to vagotomy in the treatment of duodenal ulcer. All types of vagotomy (truncal, selective gastric, or proximal gastric) produce similar reduction in acid secretion and comparable elevation in serum gastrin. The evidence is mounting that the vagus may have opposing influences on gastrin release: stimulation and inhibition. Division of only the extragastric vagal branches leads to withdrawal of an inhibitory mechanism rendering the denervated stomach more sensitive to the action of gastrin. The loss of this vagally controlled inhibitory mechanism, rather than more meticulous dissection, may explain the higher incidence of more complete vagotomies in selective than in truncal vagotomy. Proximal gastric vagotomy may be the ideal elective operation yet devised for duodenal ulcer. It does, however, cause elevation in serum gastrin and more than 90 per cent of patients after this operation will have positive insulin test in two to four years. This is higher than the positivity seen with truncal vagotomy. Results of controlled trials are needed before this operation becomes fully established.     

The place of gastrin determination in ulcer surgery

This paper is concerned with the place of gastrin determination in ulcer surgery. Only the acid-stimulating properties of gastrin are considered. The role of the vagus in the gastrin response to a test meal was investigated in patients with duodenal ulcer. 50 patients were studied before and 3, 6, and 12 months after highly selective vagotomy without (25 patients) and with Wnagensteen-pyloroplasty (25 patients). Basal and stimulated gastrin concentration in serum, as determined by radioimmunoassay, were higher 3 months after the operation and 3h after the test meal gastrin levels were still 50% higher than the basal levels. No difference was found between the patients treated with highly selective vagotomy and the patients treates with HSV and additional pyloroplasty. 6 and 12 months after the operation a moderate decrease of gastrin secretion was observed, but basal as well as stimulated levels were still elevated after 12 months compared to the values before operation. Our results indicate that the pattern of gastrin secretion changes as time passes after highly selective vagotomy with or without additional pyloroplasty.     

Some thoughts on tolerance

In 4 duodenal ulcer patients the morphology of parietal cells has been studied before and one year after proximal gastric vagotomy (PGV). The average basal gastric acid secretion of the 4 patients was reduced from 9.2 m.mol/h before to 0.9 m.mol/h one year after PGV (90% reduction). The reduction in acid secretion was not accompanied by changes in the morphology of the parietal cells. Light microscopical studies indicated that the average cell size was about the same before and one year after PGV. Electron micro scopical studies showed only negligible changes in the parietal cell ultrastructure.     

Helicobacter pylori infection and duodenal ulcer in children and adolescents

To investigate the relationship between H. pylori infection and duodenal ulcer in children and adolescents, the markers of H. pylori infection were studied in 22 children and adolescents who had duodenal ulcers and were followed prospectively (Group A). Another 36 patients with gastrointestinal symptoms, but without ulcer, were also studied for comparison (Group B). Antral and duodenal tissues were biopsied and analyzed for the presence of H. pylori using three standard methods: urease test, culture and histology. The specific IgG antibody against H. pylori positivity using the ELISA method were also analysed. By these three methods, H. pylori positivity in the antral tissues, chronic active antral gastritis, and seroprevalence rate were found to be much higher in Group A than Group B. However, a similar trend was not found in the duodenal tissues. H. pylori was found in four of five patients during postoperative follow-up for duodenal ulcer. Among the four patients, no duodenal ulcer but chronic active gastritis was detected endoscopically in three who received vagotomy. Only the one who received simple closure of the perforated duodenal ulcer had a recurrent duodenal ulcer. It was concluded that a close relationship among duodenal ulcer, chronic active gastritis and H. pylori is present in children and adolescents.     

Influence of various forms of vagotomy on the exocrine function of the pancres]

In surgical treatment of the duodenal ulcer a selective proximal vagotomy is the only method to vagotomize parietal cell area of the stomach alone and to let the motoric and endocrine function of the antrum, as well as the vagal innervation of the liver, the pancreas and the gut indisturbed. Our experimental investigations on dogs with total and selective proximal vagotomy show, that an intact vagal innervation of the pancreas is important for its normal function and that selective proximal vagotomy does not change the exocrine pancreatic secretion. Otherwise a total vagotomy diminishes significantly the pancreatic production of volume and enzymes after insulin stimulation. In respect of the vagal innervation and normal function of the pancreas, a selective proximal vagotomy therefore seems to be the best method in surgical treatment of the duodenal ulcer.     

Recurrence of peptic ulcer

In the paper, the causes, clinic and treatment in 15 patients with recurrent peptic ulcer after repeated operative procedures for duodenal ulcer are described. The main causes of the recurrence were as follows: the remaining of the mucous membrane of the antral gastric portion in Finsterer gastric resection for ulcer exclusion (5) and Zollinger-Ellison syndrome (10). The surgical therapy consisted in resection of the antral portion and repeated gastric resection (the first group) or in subtotal gastrectomy associated with trunk vagotomy (the second group).     

Zollinger-Ellison syndrome and antral G-cell hyperfunction in patients with resistant duodenal ulcer disease

We measured basal and pentagastrin-stimulated acid secretion, as well as basal and meal-stimulated plasma gastrin concentration to determine, in 67 patients affected by resistant duodenal ulcer, whether their condition could be related to gastric acid secretion and/or gastrin-related syndromes. We then compared them to 46 duodenal ulcer control patients. The outpatients were investigated consecutively. The resistant duodenal ulcer patients differed from the controls only in their higher complication rates (bleeding or perforation, P < 0.05). We identified five patients in the resistant duodenal ulcer group with Zollinger-Ellison syndrome and 12 with antral G cell hyperfunction, whereas in the control group only one patient was affected by antral G cell hyperfunction. IgG anti-Helicobacter pylori antibodies were positive for the presence of infection in 7 of the hypergastrinaemic patients. When Zollinger-Ellison syndrome or antral G cell hyperfunction were excluded, no differences could be found in gastric acid secretion, or basal and meal-stimulated plasma gastrin levels, between the resistant and control duodenal ulcer patients, except for basal acid hypersecretion (resistant duodenal ulcer 16% vs duodenal ulcer 2% P = 0.0144). In the presence of duodenal ulcer disease resistant to H2-blockers, it is mandatory to measure basal plasma gastrin concentration since it was possible to diagnose the gastrin-related syndromes, Zollinger-Ellison syndrome and antral G cell hyperfunction, in 26% of this group of patients.     

The effect of various forms of milk on gastric-acid secretion. Studies in patients with duodenal ulcer and normal subjects

Milk is commonly recommended as therapy for patients with peptic ulcer. The purpose of this study was to examine the effect of various forms of milk and 0.15 M NaCl (control) on gastric-acid secretion in five patients with duodenal ulcer during a period of remission and in five normal subjects. A significant (P less than 0.05) increase in acid secretion in both groups was produced by 240 ml of whole, low-fat, and nonfat milk. The acid secretory responses to milk were equivalent to approximately 20% to 35% of maximal betazole - or pentagastrin-stimulated acid output. Gastric-acid secretion produced a significant (P less than 0.05) increase in acid secretion in the patients with duodenal ulcer but not in the normal subjects. Because milk contains both protein and calcium, and each are stimulants of gastric-acid secretion, there is reason to question its frequent ingestion by patients with peptic ulcer.     

Definitive emergency treatment of perforated duodenal ulcer

A retrospective survey was made of all patients with a proved diagnosis of perforated duodenal ulcer admitted to a regional hospital during a recent six year period. The over-all mortality from this condition in the 192 patients was 11.4 per cent and mortality after operation, 6.3 per cent. One hundred and seventy-six patients were treated surgically. Seventy-seven patients underwent simple suture only with a mortality of 13 per cent and are compared with 99 patients treated by emergency vagotomy and pyloroplasty procedures with a 1 per cent mortality. Emergency definitive operations were performed without increased morbidity, mortality or hospital stay by junior surgeons with greatly improved long term results compared with simple suture. At the present time, emergency vagotomy and pyloroplasty procedures are the treatment of choice for a perforated duodenal ulcer.     

Duodenal ulcer in South Indian children

Twenty-nine children with duodenal ulcer received treatment during an 18 year period. Twenty-five were followed over a period that ranged from 3 to 18 years; 53.8 percent of the patients who received medical treatment either had recurrence or persistence of ulcer symptoms during adolescence or adulthood. Two patients with acute bleeding ulcers have remained well after vagotomy and drainage procedures. Pyloric stenosis was the most common indication for surgical intervention and in all such cases the patients underwent truncal vagotomy and drainage procedures and continue to live without any symptoms, except one in whom anastomotic ulcer due to incomplete vagotomy has developed.     

Platelet-derived growth factor BB mediated regulation of 12-lipoxygenase in porcine aortic smooth muscle cells

BACKGROUND & AIMS: Recently, we postulated a new concept of duodenal ulcer pathogenesis suggesting that antral Helicobacter pylori infection blocks inhibitory pathways to the gastrin and parietal cells, resulting in an increased and prolonged postprandial acid secretion. the aim of this study was to examine duodenal acid load and duodenal bulb pH after a meal before and after eradication of H. pylori. METHODS: Using a marker-dilution method and a pH electrode in the duodenal bulb, gastric emptying, acid secretion, gastrin release, duodenal acid load, and duodenal bulb pH were studied during 2 hours after peptone meals of pH 7.0 and 2.0 in 8 H. pylori-negative controls and 8 H. pylori-infected subjects before and 6 months after eradication. RESULTS: The H. pylori-infected subjects had an increased gastric emptying, gastrin release, and acid secretion, higher duodenal acid load, and lower duodenal bulb pH after the meals. These responses were normalized after eradication. CONCLUSIONS: H. pylori-infected subjects have an increased and prolonged postprandial acid secretion, partly caused by an impaired low pH inhibition of acid secretion, gastrin release, and gastric emptying, resulting in an increased duodenal acid load and a prolongation of low pH in the duodenal bulb, as a general prerequisite for the development of duodenal ulcer disease.