Double pylorus (DP) or duplication of the pylorus is an uncommon condition that is either congenital or acquired. Acquired double pylorus (DP) results from a peptic ulcer eroding through and creating a fistula between the duodenal bulb and the distal stomach. We report a case of an acquired double pylorus in an adult gentleman that resulted from the erosion of a duodenal and prepyloric ulcer.
A review of 82 (68 male) Kelantanese patients with non-alcoholic cirrhosis who underwent gastroduodenal endoscopy revealed duodenal and gastric ulcers in 4.9% and 7.3% of patients respectively. Comparing with prevalence rates of peptic ulcer disease reported in the literature, there was no evidence to suggest that duodenal ulcers occur more frequently in patients with non-alcoholic cirrhosis. There is a suggestion, albeit a tenuous one, that non-alcoholic cirrhosis may be associated with gastric ulceration.
A 60 year old woman with chronic duodenal ulcer not responding to Cimetidine, was changed to Ranitidine. She had symptomatic improvement, but had bilateral breast engorgement and tenderness for which treatment was discontinued. A therapeutic trial on a second occasion had the same side effect which came on more rapidly and quickly. This complication in such severe form and recurrence on rechallenge requiring withdrawal of drug was observed for the first time with any H2 receptor antagonist.
A double-blind randomized study in 230 Malaysian patients with duodenal ulcer was conducted to compare the proton-pump inhibitor, omeprazole 20 mg, given once daily in the morning, with ranitidine 300 mg, administered once daily at night. After 2 and 4 weeks of treatment, 222 and 220 patients, respectively, were evaluable according to the study protocol. Omeprazole produced significantly higher healing rates than ranitidine at both 2 weeks (75% versus 46%, respectively, P less than 0.0001) and 4 weeks (97% versus 83%, respectively, P = 0.001). Ulcer symptoms were relieved more rapidly by omeprazole than ranitidine. After 2 weeks, daytime epigastric pain was reported by 30% of ranitidine-treated patients but only by 15% of omeprazole-treated patients, which is a statistically significant difference (P = 0.004). No major clinical or biochemical side effects were recorded for either omeprazole or ranitidine. In conclusion, omeprazole 20 mg was found to be superior to ranitidine 300 mg administered once daily for the treatment of duodenal ulcer as measured by ulcer healing and pain relief.
Fulminant necrotising amoebic colitis is a complication of untreated amoebiasis. This is seen in mainly low-income countries. It has a high mortality rate and is difficult to diagnose. We present an extremely rare case of fulminant necrotising amoebic colitis that caused diagnostic confusion in mimicking an acute abdomen, presumably caused by a perforated duodenal ulcer.
The influence of the age of onset of symptoms on various clinical features of peptic ulcer was studied in a personal series of 492 patients (duodenal ulcer 363, gastric ulcer 98, combined gastric and duodenal ulcer 31). Duodenal ulcer patients whose age of onset of symptoms was within the first three decades (n = 166) were more likely to be men (77%) and to have a positive family history of dyspepsia (45%) and a history of haemorrhage (46%) when compared with late onset patients (n = 197, men 57%, positive family history 23%, history of haemorrhage 36%). Early onset duodenal ulcer patients also secreted more gastric acid than late onset patients. In contrast, while early onset gastric ulcer patients were more likely to be men, when compared to late onset patients, the two groups were similar in their family history of dyspepsia, their history of haemorrhage, and their gastric acid output. The age of onset of Malay duodenal ulcer patients (mean (SD) 43.6 (16.0] was higher than those for Chinese patients (33.7 (16.1].
A total of 1,688 non-repeat upper gastrointestinal endoscopies performed over a 33-month period from April 1985 to December 1987 at a University Medical Unit in Kuala Lumpur was analysed for a profile of peptic ulcer disease amongst Malaysians. There was a total of 360 peptic ulcer patients with a gastric ulcer to duodenal ulcer ratio of 1:1. The male: female ratio was 2.8: 1 for duodenal ulcer and 1.8:1 for gastric ulcer, and 2.3:1 for peptic ulcer overall. In both sexes, gastric ulcers were seen at an older age group compared to duodenal ulcers.
Of the three main Malaysian ethnic groups of Malays, Chinese and Indians, Chinese of both sexes had the highest frequency of gastric ulcers. Chinese females had the highest frequency of duodenal ulcers.
This prospective randomized study investigated the possibility that duodenal ulcer relapse associated with Helicobacter Pylori infection is mediated by oxygen-derived free radicals. To this end, the radical scavengers allopurinol (50 mg 4 times daily) and dimethyl sulphoxide (DMSO, 500 mg 4 times daily) were administered orally. One hundred and forty-six consecutive patients with previous symptomatic endoscopy proven duodenal ulceration, which had been shown endoscopically to have healed in the presence of gastric mucosal infection with Helicobacter Pylori, were randomized to receive for the period of one year either placebo, or cimetidine 400 mg at bedtime, or allopurinol, or DMSO. In one hundred and twenty-six patients evaluable for efficacy, the cumulative relapse at one year was: placebo 47%, cimetidine 24%, allopurinol 6% and DMSO 6%. Cimetidine was significantly effective in preventing the relapse (p < 0.01), however allopurinol and DMSO were superior to cimetidine in this respect (p < 0.05). In the patients who relapsed, ulcer recurrence tended to occur early in those on placebo and cimetidine and to be evenly distributed over the year in those on free radical scavenging therapy. In all groups, ulcer recurrence throughout the maintenance year was more frequently symptomatic than silent. The incidence of infection with Helicobacter Pylori was not influenced by any of the regimens employed and the bacterium was detected with every relapse noted in this study and during the follow-up endoscopy which was carried out at 6 months and at 12 months during the maintenance year. The results suggest that oxygen-derived free radicals are involved in the relapse of duodenal ulceration in patients infected with Helicobacter Pylori.
Basal and pentagastrin stimulated acid output was measured in 80 normal and 179 duodenal ulcer subjects of Chinese, Indian and Malay origin. Basal and maximally stimulated acid output was significantly higher in duodenal ulcer patients compared with normal subjects. There was however considerable overlap and less than one in four duodenal ulcer patients were hypersecretors. The acid output (and hence the parietal cell mass) was lower than in Caucasian subjects and this was possibly related to weight differences. The acid output did not differ significantly in the Chinese, Indian and Malay subjects, suggesting that parietal cell mass in the three racial groups is closely similar. The difference in frequency of duodenal ulcer disease in the three racial groups is thus not related to gastric secretory capacity.
The Helicobacter pylori infection rate was determined in 124 consecutive patients with duodenal ulcers (DU), gastric ulcers (GU), duodenal erosions or gastric erosions diagnosed by endoscopy at a single institution in north-eastern peninsular Malaysia in 1996-97. Biopsies of the gastric antrum and body were subjected to the urease test, Gram staining of impression smears, culture and histopathological examination. Serology was undertaken on all patients using a locally validated commercial kit. Infection was defined as a positive result in at least one test. The infection rates were 20% (10/50), 21.2% (7/33), 16.7% (1/6) and 17.1% (6/35) in DU, GU, duodenal erosion and gastric erosion patients, respectively. The infection rate among Malays [7.0%, (6/86)] was lower than in non-Malays [47.4% (18/38)] (P < 0.001). There was a higher infection rate among males, who constituted 62.1% (77/124) of the sample. Seventy-eight patients (62.9%) were receiving non-steroidal anti-inflammatory drugs (NSAIDs) and 33 patients (26.6%) were neither receiving NSAIDs nor were infected with H. pylori. The H. pylori infection rate among peptic ulcer patients in this predominantly Malay rural population appears to be the lowest reported in the world thus far. Empirical H. pylori eradication therapy in peptic ulcer patients is clearly not indicated in this community. The possible reasons for the low prevalence of H. pylori infection are discussed.
Omeprazole has been shown to have a suppressive effect on Helicobacter pylori. The aim of this study was to determine if prolonged treatment with omeprazole would result in a higher eradication rate than short course treatment. Twenty patients with endoscopy proven duodenal ulcers and unequivocal evidence of Helicobacter pylori (HP) infection based on culture, histology, urease test and Gram's stain of a fresh tissue smear were treated with omeprazole 40 mg om for 2-4 weeks. Following ulcer healing, patients received either maintenance omeprazole 20 mg om or placebo for up to one year. All 20 patients had healed ulcers following a 2-4 week course of omeprazole 40 mg om.. All were negative for HP at the end of treatment. Thirteen patients received short course therapy with omeprazole only, followed by placebo. On follow-up endoscopy at 3 months, only one of 13 (7.7%) had eradicated the bacteria. Seven patients received maintenance treatment with omeprazole 20mg om for one year. Following completion of treatment, patients were followed up at 1, 3 and 6 months. Only one of 7 (14.3%) patients had eradicated the infection on long term follow-up. The eradication rates of HP with both short and long course omeprazole monotherapy were low.
The treatment of perforated duodenal ulcer is controversial. Since the advent of H2 antagonists, the number of ulcer operations has declined tremendously. We wanted to find out if the addition of a H2 antagonist after simple closure of a perforated duodenal ulcer would change the outcome and therefore reviewed 46 patients treated in this fashion. Our results show that this is a safe and effective way of treating patients with perforated duodenal ulcer.
Intramural duodenal haematoma is a rare injury of the duodenum. Most reported cases are secondary to blunt trauma to the abdomen. Such injury following endoscopic intervention is even rarer, and there are no definite guidelines for its management. We report a case where endoscopic haemostasis of a bleeding duodenal ulcer resulted in a massive dissecting intramural duodenal haematoma with gastric outlet obstruction and obstructive jaundice.
We report the first double-blind, placebo-controlled study that assesses the efficacy and safety of omeprazole 20 mg daily in the maintenance treatment of duodenal ulcer. For the healing phase, 128 patients with endoscopically proven active duodenal ulcer and a history of three or more relapses during the 2 years prior to the study were treated until healing with omeprazole 40 mg daily for 2 and up to 8 weeks. One hundred and twenty-three patients whose ulcers were healed were randomized to receive omeprazole 20 mg daily (n = 60) or placebo (n = 63) for 12 months as maintenance treatment. Patients were interviewed at 3, 6, 9 and 12 months, and endoscopy was performed at 3, 6 and 12 months and whenever symptoms recurred. The healing rates of the 124 patients completing the healing phase were 84, 98 and 100% at 2, 4 and 8 weeks, respectively. During the maintenance phase, eight and four patients discontinued treatment from the omeprazole and placebo groups, respectively. The proportion of patients in remission in the omeprazole group and placebo group after 12 months were 94 and 9% respectively (life table estimates, P < 0.0001). No significant clinical or laboratory changes were observed in patients on therapy with omeprazole. Patients with a history of frequent relapses thus continued to have a very high relapse rate without prophylactic treatment. Omeprazole 20 mg daily was effective and safe in maintaining such patients in remission.
Twenty-seven patients with peptic ulcer (19 with duodenal ulcer (DU) and eight with gastric ulcer (GU] refractory to H2-antagonists were treated with 40 mg of omeprazole once daily for 4-8 weeks, depending on the rate of ulcer healing. Clinical assessment, endoscopy and laboratory tests were performed at entry, after 2 and after 4 weeks, and if unhealed, also after 8 weeks' treatment. Ten healed patients were given a maintenance therapy of omeprazole 20 mg daily for up to 12 months during which the patients returned for endoscopy, gastric biopsy and laboratory tests at 3-monthly intervals. The initial treatment healed 15 of 19 (79%) DU patients in 2 weeks and all DU patients by 4 weeks. Seven of eight (87%) GU patients healed in 4 weeks and only one required 8 weeks' treatment. Symptom relief was rapid, with most patients being symptom-free within the first day of treatment. Six patients received 12 months' continuous maintenance therapy, one patient 9 months and three patients 6 months' treatment. All patients remained in remission whilst on omeprazole therapy. No adverse events were reported throughout the study. There were no clinically significant changes in haematology or blood chemistry after healing or during the long-term treatment. Biopsy samples revealed no histological changes in the gastric mucosa at any stage. Omeprazole 40 mg therefore was found to produce rapid healing and symptom relief in Asian patients with H2-antagonist-resistant peptic ulcers. Maintenance therapy with omeprazole 20 mg daily was shown to be safe and effective in preventing recurrence of peptic ulceration.