Drug therapy of patients treated in hospitals for duodenal ulcers

Drug therapy in hospitalized patients treated for duodenal ulcer disease was reviewed retrospectively. The information was obtained by the means of a medical audit of patient records indexed by the discharge diagnosis of duodenal ulcers. A total of 485 cases were abstracted. Antacids were found to be the cornerstone of duodenal ulcer drug therapy. Anticholinergic drugs occupied a central role throughout the medical treatment of duodenal ulcers. The investigators identified a need for the dissemination of information concerning the use of anticholinergics in duodenal ulcer patients experiencing the complications of hemorrhage and obstruction.     

Duodenal tuberculosis: a difficult diagnosis

BACKGROUND: The polymorphous clinical presentation of tuberculosis located in the duodenum may mislead diagnosis. CASE REPORT: A 69-year-old man had duodenal stenosis associated with calculous common bile duct obstruction. Crohn's disease was initially diagnosed and the patient was treated with corticosteroids. Two months later, the diagnosis was rectified when pulmonary tuberculosis developed. DISCUSSION: This case emphasizes the lack of specific clinical, radiological, endoscopic and histological signs of duodenal tuberculosis.     

Endoscopic diagnosis of chronic obstruction of the duodenum in association with peptic ulcer

The results of gut endoscopic examination in 460 patients with duodenal ulcer disease concurrent with its chronic obstruction (CI) are adduced. Direct and indirect endoscopic signs of duodenal CI are revealed in 399 (86.73%) of patients. Endoscopic criteria of the CI stage determination are described: duodenal stenosis, pyloric sphincter deformity and insufficiency, reflux-gastritis and the gastrostasis signs while satisfactory pyloric passability.     

Duodenal phytobezoar: a case report and review of the literature

Phytobezoars are an unusual cause of small bowel obstruction. We report a case of small bowel obstruction due to phytobezoar in a 63 year-old female patient who had undergone gastric surgery (truncal vagotomy with pyloroplasty) for duodenal ulcer disease complicated by gastric outlet obstruction 10 years ago. We diagnosed this bezoar case by radiologic methods and these methods keep their importance for the diagnosis of small bowel obstruction with phytobezoars.     

Duodenal tuberculosis presenting as acute ulcer perforation

Gastrointestinal tuberculosis (TB) is rare, but its incidence is increasing in industrialized countries because of the growing numbers of individuals at risk for TB. Herein, we report the exceptional case of a young, HIV-negative, African refugee who presented with acute perforation of an isolated duodenal tuberculous ulcer. Clinical patterns of duodenal TB are discussed. The difficulty of obtaining a diagnosis on the basis of clinical features, endoscopy, and imaging is emphasized, as well as the importance of obtaining a biopsy specimen and its limitations.     

Helicobacter pylori infection in patients with chronic pancreatitis and duodenal ulcer

BACKGROUND: The prevalence of duodenal ulcer is high in patients with chronic pancreatitis. Patients with simple duodenal ulcer without chronic pancreatitis are mostly Helicobacter pylori-infected, and the prevalence of IgG seropositivity is > 95%. The prevalence of H. pylori infection in patients with chronic pancreatitis is not known. METHODS: IgG antibodies against H. pylori were measured in a cross-sectional survey of consecutive patients who had their exocrine pancreas function examined with a Lundh meal test in the period 1988-95 and in a control group of patients with simple duodenal ulcer. RESULTS: Twenty-seven per cent of the patients with chronic pancreatitis had duodenal ulcer during the observation period. The prevalence of IgG antibodies against H. pylori was 22% in patients with chronic pancreatitis without duodenal ulcer as compared with 27% with non-organic abdominal pain. The prevalence of IgG antibodies against H. pylori was 60% in patients with chronic pancreatitis complicated by duodenal ulcer as compared with 86% in controls with simple duodenal ulcer. CONCLUSIONS: H. pylori infection contributes but may not be the only cause of duodenal ulcer in patients with chronic pancreatitis.     

A study of various complications in arterial infusion chemotherapy

Complications of arterial infusion chemotherapy were analyzed in 261 cases from December 1983 to December 1993 in our department. Their complications involved nausea and vomiting (40.6%), bone marrow suppression (33.3%), liver dysfunction (20.3%), gastric and duodenal ulcer (9.6%) and so on. Complications involving an implantable device were hepatic arterial obstruction (29.1%), reservoir obstruction (5.7%), dislocation of catheter (4.6%), infection of catheter (3.8%), and obstruction of catheter (1.9%). In another cases with hepatic arterial obstruction, we performed arterial infusion in another artery as a bypass or stopped the infusion. In cases with obstruction of catheter not able to be reopened, we reinserted the catheter. An obstructed and/or infected reservoir was removed or replaced. Nausea and vomiting were found in 46.3% of FAM arterial infusion method (FAM) cases, in 53.3% of 5-FU persistent arterial method (5-FU) + FAM cases, and in 40.5% of intermittently persistent arterial method (IP) cases. Gastric and duodenal ulcer were noted in 9.8% of FAM, 13.3% of 5-FU + FAM, and 8.1% of IP cases. There were no significantly statistical differences between the methods. Hepatic arterial obstruction predominantly occurred in 32.4% of IP and 26.7% of 5-FU + FAM and bone marrow suppression was predominant in cases in which ADM was used. The duration of obstruction after administration was 154.0 +/- 117.4 days on average (21-455 days). Complications of hepatic arterial infusion chemotherapy are based on various causes which can be managed for prevention. We intend to enhance safety and assure the greater effectiveness of hepatic arterial chemotherapy.     

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.     

Evaluation of a new chromogenic substrate assay for the measurement of the prothrombin time

Since the ingestion studies by Marshall and Morris, Helicobacter pylori has been known to cause both acute and chronic infection in the human stomach activating both the cellular and the humoral immune system. It is of little or no value to evaluate the causative relationship of an infectious agent using Koch's criteria. The more recent criteria for causative relationships used in the science of epidemiology are more useful. These criteria include: (i) the characteristic of the association which is fulfilled for most cases of both duodenal and gastric ulcer; (ii) the temporal relationship which is fulfilled for duodenal ulcer and has not been investigated for gastric ulcer; (iii) the biological gradient which has been fulfilled for duodenal ulcer in a few studies but not investigated for gastric ulcer; (iv) the biological plausibility which is easily fulfilled for both duodenal and gastric ulcer; (v) the effect of an intervention which has been fulfilled for duodenal ulcer and in a few studies for gastric ulcer; and (vi) the coherence of these data with what is known about the disease which is fulfilled for both duodenal and gastric ulcer. Even though there is no need for all criteria to be fulfilled, further studies are necessary to confirm the temporal relationship between H. pylori and peptic ulcer, and the biological gradient of H. pylori in relation to the gastric ulcer. Even so, there is a strong indication that most of the peptic ulcers, apart from those caused by non-steroid anti-inflammatory drugs and Zollinger-Ellison-like syndromes, are caused by H. pylori infection.     

Characterisation of macrophage inflammatory protein-5/human CC cytokine-2, a member of the macrophage-inflammatory-protein family of chemokines

The aim of this study was to determine the level of endogenous prostaglandin E2 (PGE2), prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) in the gastric and duodenal mucosa of patients with duodenal ulcer and duodenitis. Besides, the investigation aimed at determining the effect of smoking and infection by Helicobater pylori on prostaglandin synthesis. The investigation comprised 62 patients with duodenal ulcer, 46 patients with duodenitis and 44 controls. The results of our investigation indicate that the decreased prostaglandin synthesis in gastric and duodenal mucosa determined in patients with duodenal ulcer may have a considerable role in development of duodenal ulcer. Furthermore, the harmful effects of smoking on the gastric and duodenal mucosa may be mediated by the decreased prostaglandin synthesis in the gastric and duodenal mucosa. However, Helicobacter pylori seems to affect the development of duodenal ulcer through other mechanisms.     

Helicobacter pylori eradication as a surrogate marker for the reduction of duodenal ulcer recurrence

OBJECTIVES: An abundance of data exists documenting the association of H. pylori eradication with the reduction in duodenal ulcer recurrence. AIM: To evaluate the validity of using H. pylori eradication as a surrogate marker for the reduction in duodenal ulcer recurrence using rigorously controlled studies. METHODS: Three controlled clinical trials were conducted in patients with uncomplicated, active duodenal ulcers. Patients were treated with various combinations of omeprazole and amoxycillin. Ulcer healing and H. pylori eradication were assessed. For patients whose duodenal ulcer healed, duodenal ulcer recurrence was determined over a 6-month period in patients with H. pylori eradication and those remaining positive for H. pylori at least 4 weeks after treatment. To support the data obtained from these clinical trials, a search of the medical literature was conducted to identify additional human clinical trials in which duodenal ulcer recurrence rates were measured and categorized by H. pylori status at least 1 month post-treatment. RESULTS: In 11 controlled trials, the overall 6-18-month duodenal ulcer recurrence rate was 54% among patients remaining positive for H. pylori at least 4 weeks after treatment compared to 6% among patients with H. pylori eradication following treatment. This finding was corroborated by the uncontrolled trials, in which the duodenal ulcer recurrence rate was 64% among patients found to be H. pylori-positive and 6% for patients found to be H. pylori-negative at least 4 weeks after treatment. A time course of duodenal ulcer recurrence rates using pooled data from both controlled and uncontrolled studies demonstrated that duodenal ulcer recurrence rates for H. pylori-negative patients persisted for up to 4 years following treatment. Duodenal ulcer recurrence rates for H. pylori-positive patients increased for the first year, then levelled off. A comparison of the duodenal ulcer recurrence rates for different treatment regimens revealed that eradication regimens based on omeprazole plus antibiotics and bismuth plus antibiotics exhibited similar duodenal ulcer recurrence rates for H. pylori-positive and -negative patients. CONCLUSION: Regardless of treatment regimens, H. pylori eradication produced a consistent and significant reduction in duodenal ulcer recurrence. Therefore H. pylori eradication, 4 weeks post-therapy, can be used as a surrogate marker for reduced duodenal ulcer recurrence in investigational clinical trials.     

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.     

Long-term follow-up of childhood duodenal ulcers

PURPOSE: This study reports the long-term results in children who have duodenal ulcers diagnosed by endoscopy who were treated with H2-receptor antagonist. METHODS: The medical records of 32 children admitted into The Queen Mary Hospital with endoscopically proven duodenal ulcers between 1975 and 1988 were reviewed to evaluate the long-term outcome of childhood duodenal ulcers after initial treatment with H2-receptor antagonist (H2RA). Follow-up details were updated and patients who had been lost to follow-up were recalled. The age of the 22 boys and 10 girls at the time of diagnosis of the ulcers ranged from 3 to 16 years (mean, 11.8 yrs). The duration of follow-up ranged from 8.5 to 21 years (mean, 11.6 yrs). RESULTS: Their primary presentations included epigastric pain (n = 9, 28.0%); nonsteroidal antiinflammatory drug (NSAID)-induced gastrointestinal bleeding (GIB, n = 6, 18.7%); unprovoked GIB (n = 12, 37.5%); perforation (n = 4, 12.5%); and pyloric obstruction (n = 1, 3.0%). All 13 patients who had NSAID-induced ulcers (pain and bleeding) responded to H2RA therapy and required no further treatment. All 14 patients who had unprovoked ulcers who presented with pain or bleeding did not respond to H2RA treatment. Ulcer healing was achieved only after eradication of Helicobacter pylori with antibiotics (n = 8) or definitive surgery involving either truncal vagotomy and pyloroplasty (VP, n = 4) or proximal gastric vagotomy (PGV, n = 2). The patient who had gastric outlet obstruction had vagotomy and antrectomy. All four patients who had perforation were initially treated with patch repair, but two had persistent ulceration despite H2RA treatment and required PGV. Complications developed in none of the four patients who had PGV, whereas two of the four patients with VP had problems (diarrhea, n = 1; bezoar obstruction, n = 1). CONCLUSIONS: Unprovoked childhood duodenal ulcer is associated with significant long-term morbidity and requires continued follow-up. The majority of the ulcers are resistant to H2RA treatment alone and ultimately require either eradication of H. pylori or surgery. In the absence of obstruction, PGV may be enough to resolve the ulcer diathesis.     

The etiological and pathogenetic characteristics of duodenal peptic ulcer in adolescents

Studied by endoscopy were 100 adolescents with diagnosed duodenal ulcer, as were 100 essentially healthy subjects and 90 ones of the same age presenting with primary chronic gastroduodenitis together with 60 adults who had duodenal ulcer. The following items were etiologic risk factors for duodenal ulcer, if combined, in the above adolescent series: Frequent episodes nervous of tension, hereditary predisposition and helicobacteriosis. In juveniles with duodenal ulcer, secretion and motility of the stomach appeared to be subjected to changes to a higher degree than it was in adult subjects with duodenal ulcer, while functions of the psychovegetative and immune systems were found to be less changeable in the former. In adolescents presenting with duodenal ulcer and primary chronic gastroduodenitis, the etiologic risk factors and pathogenetic changes were found out to be identical.     

Relationships between gastric acid secretion and recurrent duodenal ulcer after selective vagotomy and pyloroplasty in men

Relations between gastric acid secretion measurements and recurrence of duodenal ulcer within 1 to 4 years after selective vagotomy and pyloroplasty were evaluated in a series of 117 men. The discriminatory ability of spontaneous, histamine- and insulin-activated acid secretion measurements was significant and similar to that after truncal vagotomy and drainage. The measurements were of no practical value for the diagnosis of recurrent duodenal ulcer after vagotomy, but they provided a rationale for selective surgery in patients with duodenal ulcer and patients with recurrent duodenal ulcer after vagotomy.     

Surgical treatment of duodenal ulcer with chronic duodenal obstruction

Follow-up treatment results of 892 patients with duodenal ulcer (DU) are presented and the choice of surgical policy in its combination with chronic duodenal obstruction (CDO) in 307 (34.4%) patients is substantiated. Depending on peculiarities of DU, the kind and the stage of CDO, organ saving (140) or stomach resection (167) in combination with correction CDO interventions (287) were carried out. The course of the postoperative period was characterised by basic morphofunctional changes and by achievement of completeness of duodenal passage. Intermittent motor-evacuatory disorders were observed in 55 (17.9%) patients. Lethal outcome was in 1 case. Long-term functional results of the operations were studied in 267 patients. Excellent and good results were obtained in 66.3%, favorable-in 32.24% and unfavorable-in 1.44% of patients. The dependence of immediate and remote results of the operations on the effectiveness of the correction of associated CDO was established.     

Differential north to south gastric cancer-duodenal ulcer gradient in China. China Ulcer Study Group

There are suggestions that duodenal ulcer protects individuals from gastric cancer and that rice is ulcerogenic while wheat is gastro-protective. We aimed to examine the relationship of gastric cancer, duodenal and gastric ulcers in different geographical regions in China and identified dietary risk factors for duodenal ulcer and gastric cancer. The prevalence of peptic ulcer and gastric cancer among symptomatic patients in eight major cities, four each from the north and the south representing all the six defined regions of China were studied. Endoscopy and case records over a 10 year period were reviewed and cases of confirmed duodenal and gastric ulcer and gastric cancer, together with the total number of endoscopies performed per year, were recorded. Rates were expressed as cases/1000 endoscopies. Results were compared to another epidemiological study on diet and mortality in the same regions in China conducted at the same time. Duodenal ulcer rates were 2.4-fold higher in southern China than northern China, whereas gastric cancer rates were 1.6-fold higher in the north than in the south. Correlation studies showed for the first time an inverse linear relationship between the gastric cancer rates and the duodenal ulcer rates (r=-0.8076, P=0.015), as well as the duodenal ulcer: gastric ulcer ratios (r=-0.9133, P=0.002). Gastric ulcer rates were higher in southern China but did not correlate with the gastric cancer rates (r=0.1455, P=0.731). Duodenal ulcer rates were found to be related to daily rice intake (r=0.8554, P=0.029) and inversely related to daily wheat flour intake (r=-0.8472, P=0.033). Gastric cancer rates were not related to any dietary risk factors tested. We concluded there was an inverse relationship between gastric cancer rates and duodenal ulcer rates. Although duodenal ulceration and gastric cancer are both linked to Helicobacter pylori infection, the findings of this study indicate independent additional aetiological factors for the pathogenesis of these conditions. Dietary factors such as rice or wheat intake may play a role.     

The prevalence of esophagitis in patients with duodenal ulcer or ulcer-like dyspepsia

OBJECTIVE: It has been reported that 30-72% of patients with duodenal ulcer disease also have esophagitis. However, many of these reports included patients who had severe or complicated ulcer disease, so that the high prevalence may reflect pyloric stenosis or gastric hyper-secretion. The objective of this study was to determine the prevalence of esophagitis in unselected patients with duodenal ulcer disease or ulcer-like dyspepsia. METHOD: A prospective study of endoscopic and histological esophagitis in consecutive patients with either duodenal ulcer disease or with ulcer-like dyspepsia. RESULTS: Of 27 patients with duodenal ulcer disease, 33% had endoscopic esophagitis, 26% had histological esophagitis, and 48% had esophagitis by either criterion. Of 66 patients with ulcer-like dyspepsia, 35% had endoscopic esophagitis, 47% had histological esophagitis, and 62% had esophagitis by either criterion. Esophagitis was independent of patients' Helicobacter pylori status. CONCLUSIONS: Esophagitis is common in patients with duodenal ulcer disease, and the prevalence is similar in patients with ulcer-like dyspepsia. In addition to causing heartburn, esophagitis may also be cause ulcer-like epigastric pain. Concomitant esophagitis may account for the persisting or recurring dyspepsia that has been reported in up to one-third of duodenal ulcer patients after successful eradication of H. pylori.     

Circadian gastric acidity in Helicobacter pylori positive ulcer patients with and without gastric metaplasia in the duodenum

BACKGROUND: The presence of gastric metaplasia allows helicobacter pylori to colonise the duodenum and this condition is thought to be acquired as a response to acid hypersecretion. This functional disorder, however, is present only in a subgroup of duodenal ulcer patients and, in addition, surface gastric metaplasia has been frequently found in the proximal duodenum of normal subjects and patients with non-ulcer dyspepsia, who cannot be certainly considered as acid hypersecretors. AIMS: To clarify the role of acid in inducing gastric type epithelium in the duodenum. This study aimed at assessing whether the pattern of circadian gastric acidity differs between H pylori positive duodenal ulcer patients with and without duodenal gastric metaplasia. PATIENTS: Seventy one patients with duodenal ulcer confirmed by endoscopy and who were found to be positive for H pylori infection by histology on antrum biopsy specimens were enrolled into this study. METHODS: Gastric type epithelium in the duodenum was found in 49 of 71 ulcer patients (69%). Continuous 24 hour gastric pH metry was performed in 50 healthy subjects and in the two subgroups of duodenal ulcer patients with and without gastric metaplasia in the duodenum. Gastric acidity was calculated for 24 hours (1700-1659), night (2000-0759) and day-time (0800-1959). RESULTS: Ulcer patients without gastric metaplasia showed a significantly higher gastric acidity (p < 0.001) than controls for every time interval considered, while the ulcer subgroup with gastric metaplasia was more acid than healthy subjects (p < 0.001) during the whole 24 hour period and the daytime. There was no difference between the two subgroups of duodenal ulcer patients with and without gastric metaplasia during the various time segments analysed. CONCLUSION: The findings confirm that the circadian gastric acidity of duodenal ulcer patients is higher than that of controls. As there is no difference in gastric pH between duodenal ulcer patients with and without gastric metaplasia, gastric hyperacidity is not specific to patients with duodenal gastric metaplasia. It is probable that this histological change is a non-specific response to mucosal injury resulting from various factors and not exclusively to acid.     

Catecholamine concentrations in biopsied gastroduodenal tissue specimens of patients with duodenal ulcer

We measured dopamine and norepinephrine concentrations in the biopsied gastroduodenal mucosa obtained from 12 ulcer-free dyspeptic patients, nine patients with active duodenal ulcer, and eight patients with inactive (or healed) duodenal ulcer using a high-performance liquid chromatography with electrochemical detection method. Biopsy specimens were taken from endoscopically normal-appearing mucosa in the gastric body and antrum as well as in the duodenal bulb. Additional specimens were obtained from the outer edge of the ulcer margin in patients with active duodenal ulcer. The mean (+/- SD) mucosal dopamine concentrations in the gastric body and duodenum (7.6 +/- 2.8 and 6.8 +/- 2.6 pg/mg tissue) obtained from patients with inactive duodenal ulcer were significantly (P < 0.05) lower than those from dyspeptic patients (13.6 +/- 6.9 and 10.9 +/- 3.5 pg/mg tissue, respectively). In contrast, no significant differences were observed in the mean norepinephrine concentrations in these gastroduodenal tissues among the three study groups. However, the mean mucosal norepinephrine concentration in the outer edge of duodenal ulcer (86.2 +/- 125.6 pg/mg tissue) was significantly (P < 0.05 and 0.01) reduced as compared with that in the ulcer-free area of duodenum obtained from patients with inactive duodenal ulcer (257.1 +/- 188.2 pg/mg tissue) and from dyspeptic patients (276.8 +/- 138.3 pg/mg tissue). The results suggest that an alteration in the catecholaminergic system may be associated with one of the pathogenic factors of duodenal ulcer.