Relevance of duodenitis to non-ulcer dyspepsia and peptic ulceration.
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Biomedical subjects
Publications and source records attributed to S N Joffe.
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Three methods of in vitro culture of human oesophageal epithelium were assessed which included the Bijou bottle, cell suspension and organ culture. The epithelium did not survive in the Bijou bottle and the cell suspension caused a growth of oesophageal fibroblasts. Organ culture proved to be the best method with survival up to ten days. Organ culture of human oesophageal epithelium provides an easy in vitro method of studying various cytotoxic factors which may play a role in reflux oesophagitis.
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The gastric secretagogues, pentagastrin and carbachol, produced a 100% incidence of duodenal ulcers. Truncal vagotomy (TV) and parietal cell vagotomy (PCV) prevented these experimental ulcers in the early post-operative period. At 3 weeks TV rats showed a decrease in weight gain, gross gastric distension and the infusion of gastric secretagogues now caused hypersecretory-induced gastric ulcers. TV and gastroenterostomy rats developed stomal ulceration and PCV failed to prevent formation of duodenal ulcers at 3 weeks. These results indicate that vagotomy, irrespective if truncal or highly selective, only has a temporary effect. This may be due to ischaemia or an altered sensitivity of the parietal cell mass with a post-operative recovery.
A case of cholangiocarcinoma at the liver hilum presenting with jaundice is described. Pre-operative transhepatic cholangiography, hepatic arteriography and splenoportography led to liver split, with successful resection of tumour and triple hepatico-jejunostomy. Despite tumour recurrence eight months of palliation were achieved. Current methods of treating the condition are discussed.
This study tests the hypothesis that vagotomy and antrectomy are better operations than proximal gastric vagotomy in patients with duodenal ulcer who have a hypersecretion of acid. On the basis of gastric secretion tests preoperatively and the peak acid output, patients with duodenal ulcer were prospectively randomized into an ignore acid or tailor to acid group. Those in the ignore acid group had a proximal gastric vagotomy, while those in the tailored group had a proximal gastric vagotomy if the peak acid output was less than 40 milliequivalents per hour and a vagotomy and antrectomy if the peak acid output was greater than 40 milliequivalents per hour. At follow-up study, a mean of 2.1 years, the recurrence rate in the ignore acid group was 13.6 per cent compared with 9.5 per cent in the tailored group. However, in the ignore acid group, the recurrence rate was 30 per cent if the peak acid output was greater than 40 milliequivalents per hour and zero per cent if less than 40 milliequivalents per hour. In the tailored group, the vagotomy plus antrectomy recurrence rate was 12.5 per cent and the proximal gastric vagotomy rate, 7.7 per cent. Proximal gastric vagotomy has an unacceptably high recurrence rate in patients with a hypersecretion of acid, and selective duodenal ulcer operations based upon acid studies preoperatively may be of value.
This study was undertaken for the purpose of a serial investigation of the development and progression of the light-microscopic changes of acute pancreatitis and histologic criteria for evaluating pancreatitis. Acute pancreatitis, similar to that found in man, was induced in rats with the use of a closed duodenal loop technique (n = 36). Control rats underwent a laparotomy with mobilization of the duodenum (n = 12). Animals were killed every 2 hours for 24 hours, and a detailed and independent histologic evaluation was made of each. Focal acinar necrosis proceeding to a vasculitis appeared within 2--4 hours before the infiltration of inflammatory cells. Thereafter, the extent of acinar necrosis closely reflected the vasculitis with the later development of the acute inflammation. By the sixteenth hour, these changes were graded as moderate pancreatitis, and by 24 hours the process represented severe hemorrhagic pancreatitis. Vascular changes and acinar necrosis preceded the inflammatory cell infiltrate. The pancreatitis has been quantitated into minimal, moderate, or severe by assessing the severity of edema, acute inflammatory infiltrate, and changes in the vessels, ducts, and acini.
The effect of intravenous secretin on plasma immunoreactive gastrin is presumed to improve diagnostic accuracy in patients with a gastrinoma. To investigate this further, the secretin provocation test was performed in control patients (n = 10), patients with a primary duodenal ulcer (n = 10), patients who had previously had surgery for a duodenal ulcer (n = 20), patients with symptomatic recurrent peptic ulceration (n = 50) and 2 patients with a histologically proved gastrinoma. It was found that the secretin test gave a false positive result in 3 out of 10 symptomatic duodenal ulcer patients, 2 out of 20 patients who had had previous duodenal ulcer surgery and were now asymptomatic and 15 out of 50 patients with recurrent peptic ulceration. Both gastrinoma patients had positive secretin tests but there were no obvious criteria that separated the gastrin response of a gastrinoma patient from those with primary or recurrent peptic ulceration. It is concluded that the secretin test is probably of little value in both the screening and the diagnosis of a gastrinoma.
A continuous subcutaneous infusion for 24 hr of the gastric secretagogues, pentagastrin (4 micrograms/kg/min) together with carbachol (0.8 micrograms/kg/min) produced a 100% incidence of duodenal ulcers (DU) in male albino Wistar rats. The mean acid output producing these duodenal ulcers was 2.3 mmol/24 hr, with a gastric secretory volume of 25 (+/- 1) ml/24 hr at an acid concentration of 91 (+/- 2) mmol/liter. The pepsin activity in the gastric juice was 185 micrograms/ml. To simulate this acid-pepsin hypersecretion, acid and/or pepsin was infused intragastrically for 24 hr. The intragastric infusion of hydrochloric acid (0.1 M, 0.2 M, 0.5 M) alone and hog purified pepsin (2.5, 5, 10 mg/24 hr) at a constant rate of 1 ml/hr for 24 hr failed to produce duodenal ulcers in rats although gastric lesions in the body of the stomach were produced. The infusion of 0.2 M HCl with 5 mg pepsin over 24 hr produced DU in two of 10 rats. However, pooled secretagogue-stimulated gastric juice, infused intragastrically, produced DUs in 11 of 12 rats. Acid alone does not produce DU experimentally in rats at the rate of infusion used in these experiments. Acid and exogenous procine pepsin (similar to human pepsin 3 on agar gel electrophoresis) rarely produced duodenal ulcers. However, acid and endogenous rat pepsin are needed together for the duodenal ulcerogenesis. This pepsin may be an obligatory ulcerogenic factor in the rat.
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There is no accepted specific treatment for acute pancreatitis in man in spite of extensive investigations. Evidence is presented based on histology, vascular and blood flow studies to support the hypothesis that acute pancreatitis is unlike most inflammatory conditions since a rapid and severe ischaemia develops in the pancreas. In dogs for example there is an instant and maintained reduction in pancreatic blood flow reducing by 72% at 3 hours. Various treatments have been advocated in acute pancreatitis. Based upon the effect of dextran 40 in improving pancreatic blood flow and percentage cardiac output, it would appear to be a treatment of choice in acute pancreatitis.
Using a methylene blue staining techique, the innervation in the rat stomach has been studied. Several distinctive patterns of beaded and unbeaded nerves were seen. Axons in the muscle coat gave branches which ramified in connective tissue and were occasionally related to blood vessels. Further nerve fibres passed directly between the muscularis mucosae and muscle coat whilst others ran between the epithelium and muscularis mucosae. A few fine terminal axons were observed close to cells throughout the epithelial layer. This method of identifying nerves will be useful in studying the consequences of vagal denervation and reinnervation following vagotomy in man and animals.
Fine-needle aspiration biopsy was performed in 30 consecutive women with clinically non-malignant breast lumps. All aspirates were shown to be benign on cytology and the lumps were excised under local anaesthetic at the outpatient department. Frozen section and paraffin section histology of the excised lump confirmed the diagnosis. Follow-up at the outpatient department and a postal questionnaire revealed the following wound complications: redness (70%), bruising (55%), and discharge (35%). Outpatient excision of solid breast lumps is a safe, rapid, and economical method of treating non-malignant breast lumps, if it is preceded by an accurate cytological interpretation of a technically satisfactory aspirate.
A proximal gastric vagotomy (PGV) prevented experimental duodenal ulcers in rats for only 5 days and thereafter all rats developed duodenal ulceration. In sham-operated rats the mean stimulated gastric acid output was 186 mumol/60 min. Immediately following a PGV there was a significant decrease in gastric juice volume and acidity (P less than 0.001) with a fall in the mean stimulated acid output to 12 mumol/60 min. On the seventh day after vagotomy the stimulated acid output (volume and concentration) significantly increased to 88 mumol/60 min (P less than 0.001). When the dose of gastric secretagogues was reduced by 50 per cent, a PGV on day 0 prevented any changes occurring in the duodenal mucosa, but when repeated at 4 weeks after a PGV the severity of duodenal ulcers in vagotomized rats was greater than in those having had a sham operation (P less than 0.05). This transient effect of a PGV on duodenal ulcerogenesis and gastric secretion may be due to recovery of the parietal cell mass.
The mean amylase level in 42 human bile samples was 154 IU/l and there was no significant difference in the amylase activity of 32 paired serum and bile samples. Estimation of the amylase thermolability of bile showed it to be similar to that of serum. This suggests that the amylase activity in bile may have filtered through the liver from the hepatic circulation rather than refluxed from the pancreatic duct. The presence of amylase in human bile provides further evidence that the liver might have a role in the regulation of serum amylase.
The incidence of hyperamylasaemia in serial serum amylase levels from patients with pancreatic pseudocysts is not well documented in the literature. Accordingly serial amylase levels were estimated in 5 patients with proven pancreatic pseudocysts. The majority of the values were normal or only minimally elevated. In contrast the amylase thermolability was persistently elevated and appeared to be a more sensitive measurement than serum amylase activity for indicating the presence of pancreatic pseudocysts.