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.     

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.     

Omeprazole treatment of chronic duodenal ulceration

Omeprazole, a substituted benzimidazole, is an acid pump inhibitor, introduced for treatment of chronic duodenal ulceration. In a study of 116 patients with endoscopically documented chronic duodenal ulcers, omeprazole affected healing in 77 (66.3%) patients after two weeks and 106 (91.4%) patients after four weeks, with symptoms relief in 102 (88%) patients within the first week of treatment. There was significantly higher healing rate in females (p < 0.05) and diffuse ulceration rather than single ulcers (p < 0.05). In meta-analysis comparing omeprazole to other antiulcer drugs reported in this country, there was a significant higher healing rate (p < 0.01) and symptom relief (p < 0.01) in favour of omeprazole. It proved to be effective and safe for the short term treatment of chronic duodenal ulceration.     

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.     

Diagnostic yield of duodenal biopsy and aspirate in AIDS-associated diarrhea

OBJECTIVES: To evaluate the diagnostic yield of performing duodenal biopsies and aspirates in AIDS patients with chronic diarrhea. METHODS: Retrospective review of esophagogastroduodenoscopy (EGD) records from January 1993 to March 1995 to identify those patients who underwent EGD for evaluation of AIDS associated diarrhea and had a duodenal biopsy and/or aspirate. Biopsies were examined for pathogens using routine histology and special stains, viral culture, and electron microscopy. Duodenal aspirates were evaluated for ova and parasites. All patients had previous negative stool studies. Pathology laboratory charges (hospital and professional fees) for each test and charges per positive test were determined. RESULTS: Of the 57 patients included in this study, 56 had a duodenal biopsy and 42 had a duodenal aspirate. An established pathogen was identified in only 15 (26%) patients. One patient had both Mycobacterium avium complex and microsporidia. Pathogens were identified in seven patients by hematoxylin and eosin stain, in three patients by acid-fast bacillus stain, and in six patients by electron microscopy. No pathogens were identified with Gomori's methenamine silver stain (44 patients), duodenal aspirate for ova and parasites (46 patients), immunoperoxidase stains (4 patients), or viral culture (4 patients). Cryptosporidia were identified in six, microsporidia in five, Mycobacterium avium complex in three, and Giardia lamblia and adenovirus each in one patient. CONCLUSIONS: In this series, the diagnostic yield of EGD with duodenal biopsy and aspirate in AIDS associated diarrhea was low. Pathogens were identified in 26% of patients; predominantly Cryptosporidium organisms and microsporidia. The routine performance of aspiration of duodenal contents for parasite examination and staining of duodenal tissue with Gomori's methenamine silver stain for fungal identification are not recommended. One should consider obtaining tissue for electron microscopy whenever duodenal biopsies are performed. The utility of EGD in AIDS associated diarrhea may improve as more effective therapies become available.     

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.     

Seven-year follow-up of patients with duodenal ulcer disease

BACKGROUND: The activity of duodenal ulcer disease varies not only between patients but also from time to time within patients, and earlier studies have concluded that the disease 'burns out' in many cases. It was the aim of this study to examine duodenal ulcer disease activity over a long period, to determine whether the degree of activity is stable within the individual patient. METHODS: A cohort of 145 patients with a first-time duodenal ulcer diagnosed in our department between 1980 and 1985 were followed up for 7 years. The patients' self-reported use of acid-inhibitory drugs was taken as a measure of disease activity. RESULTS: Twenty-eight per cent of the patients had no or minimal ulcer symptoms during the 7 years after healing of the index ulcer, whereas 13% had maximal activity with frequent or continuous use of acid-inhibitory drugs every year or ulcer surgery. A total of 11 patients were operated on because of severe ulcer symptoms or complications to the ulcer disease. The disease activity during the first 2 years after diagnosis did not change much during the following 5 years in most of the patients. CONCLUSIONS: The course of duodenal ulcer disease during the first 2 years after diagnosis was a predictor of the long-term prognosis with a predictive value of approximately 70%, which may be considered satisfactory for decision-making in some clinical situations.     

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.     

Membranous duodenal stenosis

The experience of our 16 patients treated for membranous duodenal stenosis is reported. Their treatment and course was analysed in a retrospective study. Eight patients were operated on within the first 16 days of life and in the remaining group surgery was performed at 1 month to 4 y of age. The presenting symptom leading to diagnosis was, in all but one case, non-bile-stained vomiting. Associated malformations were found in all but four patients, mostly morbus Down. The operative procedure performed was a partial excision of the duodenal membrane and a duodenoplasty in 10 patients, a duodenojejunostomy in 5 patients, and a duodenoplasty only in 1 patient. The postoperative course was without lethal complications. One late stricture in an anastomosis occurred. We conclude that in its presentation, duodenal stenosis differs from duodenal atresia, and can often be misinterpreted, resulting in a late diagnosis, and should be reported as a separate entity.     

Parietal cells in the duodenal bulb and their relation to Helicobacter pylori infection

AIM: To investigate the prevalence, and relation to Helicobacter pylori, of parietal cells in the duodenal bulb using a monoclonal antibody directed against H+,K(+)-ATPase (HK12.18). METHODS: Twenty six patients with duodenal ulcer disease and 16 healthy controls were studied. H pylori status was determined by gastric histology and culture and by the 13C-urea breath test. Four biopsy specimens were taken from the duodenal bulb and stained with HK12.18. The presence/absence and number of parietal cells in the duodenal bulb were assessed blindly by a histopathologist. RESULTS: The overall prevalence of parietal cells in the duodenal bulb was 31% (13/42) and was similar in patients with duodenal ulcer and in controls, and in H pylori positive and negative subjects. The median (range) number of parietal cells in the duodenal bulb was 7.5 (4-20) parietal cells/subject, and was similar in all four groups. CONCLUSIONS: The prevalence of parietal cells in the duodenal bulb (31%) is notably higher than previously reported in endoscopic studies, and is in keeping with reports from studies on necropsy/operative specimens. There was no difference in the prevalence or number of parietal cells in the duodenal bulb between patients with duodenal ulcer and controls, regardless of H pylori status. These findings suggest that parietal cells in the duodenal bulb do not contribute to the pathogenesis of duodenal ulcer.     

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.     

Total duodenal diversion in the treatment of complex peptic esophagitis

AIMS OF THE STUDY: The aims of this study was to report the results of total duodenal diversion in patients with complex peptic esophagitis (peptic stenosis, acquired short esophagus, columnar lined esophagus, previous surgery). PATIENTS-METHODS: Total duodenal diversion has been performed in 107 patients with complex peptic esophagitis. The standard procedure--including a troncular vagotomy, an antrectomy and a 70 cm Roux-en-Y gastro-jejunostomy--was used in 68 cases (64%). Technical adjustments were necessary in the 39 others patients. RESULTS: Two patients (1.8%) died postoperatively. Permanent healing of esophagitis was observed within 3 months in 88% of patients. Esophagitis healed in all patients operated with the standard technique. Three hours postprandial pH-monitoring was normal postoperatively in 92% of patients. Four anastomotic ulcers occurred in patients who did not have vagotomy. Among patients with columnar lined esophagus, one complete and six partial regressions were observed; no malignant degeneration was observed with a 210-patient-year follow-up. Among the 39 peptic stenoses, all except one (2.6%) resolved. Functional disorders occurred in 27% of patients within the first postoperative months; these disorders persisted in 14% of patients (Visick III or IV) after 3 years. The main disorders (dumping syndrome, anastomotic ulcer, diarrhea) were observed when a two-thirds distal gastrectomy has been performed to avoid the dangerous completion of vagotomy after a previous Heller's myotomy. CONCLUSION: These results suggest that total duodenal diversion is a suitable treatment of complex peptic esophagitis.     

The effect of H. pylori in perforation of duodenal ulcer

BACKGROUND/AIMS: H. pylori has been described as an opportunistic pathogen attracted by changes in the gastric mucosa caused by inflammation and ulceration. However, the role of H. pylori infection in the perforation of duodenal ulcers has not yet been clearly determined. The aim of this study was to assess the prevalence of H. pylori infection in patients undergoing laparotomy for repair of a perforated duodenal ulcer. METHODOLOGY: Patients who underwent surgery for a perforated duodenal ulcer in our Surgical Unit between January 1994 and July 1996 were included in this study. The study population consisted of eighteen patients with a mean age of 32.7 (21-48) years. All of the patients were male. Patients with chronic duodenal ulcer perforation and with no contraindications for definitive surgery, such as peritonitis, shock (blood pressure <90 mm Hg), age >60 years, or more than a 12-hour elapse from the time of perforation, were treated by bilateral truncal vagotomy and Weinberg pyloroplasty. The ulcer was excised with the pyloric ring. The cut was then extented by about 2 cm on both the gastric and duodenal sides. Two biopsies were taken from the antral mucosa by endoscopic biopsy forceps. The defect was closed transversely. The ulcer specimen and the antral biopsies were fixed separately in 10% formalin solution and sent to the department of Histopathology. The specimens were stained with Hematoxylin-Eosin and examined for H. pylori . Sections of the ulcer specimen were especially investigated for the presence of H. pylori through all layers of the ulcer. RESULTS: H. pylori was found in the antral biopsies of 16 patients (88.8%). In seven of the ulcer specimens (38.8%), H. pylori was present in the mucosa and also extended through the wall of the ulcer. H. pylori was positive in the antral biopsies of all patients with H. pylori present in the ulcer wall. CONCLUSIONS: In our study, H. pylori was present at a high ratio in the antral biopsies of patients with duodenal ulcer perforation. The presence of H. pylori throughout the ulcer wall to a considerable extent emphasizes the fact that eradication of H. pylori is important in the treatment of perforated duodenal ulcer.     

Use of duodenal drainage in the diagnosis of acalculous gallbladder disease

Because of overreliance on oral cholecystograms, we have re-evaluated a little used laboratory test, duodenal drainage. In a series of 56 patients with normal oral cholecystograms and upper GI series who underwent duodenal drainage and cholecystectomy, 53 (95%) were found to have positive microscopic examinations. We think duodenal drainage is a safe, simple test which should be used as an adjunct to history and physical examination and oral cholecystography. In regard to clinical follow-up, 96 per cent of patients followed were judged to have excellent-to-good results.     

The evaluation of pathogenic factors in duodenal ulcers

There were examined 90 patients with severe course of duodenal ulcer disease. In 83% of patients the atropinedependent reaction of acid production was noted, giving evidence the dominant influence of neural regulation on gastric secretion, in 17%--atropineresistant reaction, giving evidence the hormonal mechanism of regulation.     

Selective proximal vagotomy with duodenoplasty in the treatment of duodenal stenosis in patients with duodenal ulcer]

The results of surgical treatment of 118 patients with duodenal ulcer complicated with stenosis that have been operated on from 1981 to 1992 have been analysed. Selective proximal vagotomy (SPV) and duodenoplasty was performed in 58 (49.2%) patients (study group). SPV and gastroduodenal anastomosis by the method of Jabulay was performed in 60 (50.8%)-control group. The rate of postoperative morbidity in the study group-5.1%, in the control group-8.4%. The long-term follow up is from 1 year to 10 years (mean 5 + 0.6). The rate of recurrence of peptic ulcer is 8.6% in the study group and 10% in the control group. The modified scale (D. Johnson, 1976) was used for comparative evaluation of efficacy of two types of surgery. SPV and duodenoplasty was estimated in 175.1 points, that is 2.5 times less that SPV and gastroduodenal anastomosis (406.1 points). This demonstrates the advantages of SPV and duodenoplasty. The authors advocate SPV and duodenoplasty as a method of choice in the treatment of stenotic duodenal ulcer.     

Duodenal bicarbonate secretion: eradication of Helicobacter pylori and duodenal structure and function in humans

BACKGROUND & AIMS: Eradication of Helicobacter pylori expedites duodenal ulcer healing and prevents recurrences. Most patients with duodenal ulcers have impaired proximal duodenal mucosal bicarbonate secretion (DMBS). In patients with inactive, healed duodenal ulcers and normal subjects, the effect of H. pylori infection on DMBS and proximal duodenal secretory function and structure were examined. METHODS: DMBS was quantitated before and after eradication of H. pylori. Mucosal structure (duodenal bulb histopathology) and function (DMBS at rest and stimulated, effect of active vs. healed ulcer and of age) were determined in patients with duodenal ulcers and normal subjects. RESULTS: In patients with duodenal ulcers, H. pylori eradication normalized proximal DMBS. Histological examination of duodenal biopsy samples was comparable in patients with duodenal ulcers and normal subjects without apparent relationship between inflammation and DMBS. Significantly impaired DMBS occurred in response to all agonists tested (luminal acid, prostaglandin E2, and cephalic-vagal stimulation) in patients with duodenal ulcers, suggesting a generalized secretory defect. Neither the presence of active (vs.inactive) ulcer nor age significantly affected bicarbonate secretion. CONCLUSIONS: In patients with duodenal ulcers, eradication of H. pylori normalized proximal DMBS and may thereby reduce ulcer recurrences. Altered DMBS in patients with duodenal ulcers was unrelated to histopathologic abnormalities. Impaired bicarbonate secretion in patients with duodenal ulcers could be caused by a cellular and/or physiological regulatory transport defect possibly related to H. pylori.     

Seasonal behaviour of healed duodenal ulcer

Incidence of peptic ulcer is more in people living at higher altitude and similarly relapse of healed duodenal ulcer is more in winter season. Seasonal behaviour of healed duodenal ulcer with or without maintenance therapy with H2 blockers was studied among subjects residing around Shimla (approximate altitude 7000 feet above mean sea level). Sixty-four subjects of endoscopically healed duodenal ulcer were alternatively advised placebo (32 subjects) and ranitidine 150 mg (32 subjects) at bed time as maintenance therapy for period of one year. Subjects were reviewed endoscopically and evaluated for H pylori by rapid urease test, every months or earlier if symptomatic. Relapse rate was analysed among 60 subjects at the end of one year. Cumulative relapse rate was found 60% in ranitidine group and 100% in placebo group. In ranitidine group percentage of relapse to number of endoscopic examinations was 21.4% throughout the year, but in placebo group during winter and spring season relapse was 87.5% of endoscopic examination whereas 57.2% during summer and fall season. Incidence of duodenal ulcer relapse without maintenance therapy was more in winter and spring season (October to March) as compared to summer and fall (April to September), whereas intermittent seasonal treatment is efficacious in prevention of duodenal ulcer relapse and also improves cost benefit ratio of ulcer treatment.     

Risk of recurrent biliary tract disease after cholecystectomy in patients with duodenal diverticula

OBJECTIVE: To determine if the presence of duodenal diverticula predisposes to the development of common bile duct stones. DESIGN: Cohort study; median follow-up, 10.0 years (25th and 75th percentiles, 5.2 and 16.1 years, respectively). SETTING: Tertiary care center. PATIENTS: One hundred fifty-seven patients with radiologically diagnosed duodenal diverticula who had undergone cholecystectomy from 1950 through 1987 and were asymptomatic at the initiation of follow-up. MAIN OUTCOME MEASURES: All patients were followed up for evidence of recurrent biliary tract disease to the following end points: (1) evidence of choledocholithiasis demonstrated by radiologic surgical, or biochemical means and (2) clinical or biochemical evidence of biliary pancreatitis. RESULTS: Of the 157 patients in the study cohort, 13 patients were categorized as having had recurrent biliary tract disease. Using the Kaplan-Meier survivorship method, the cumulative probabilities of recurrent biliary tract disease in patients with radiologically diagnosed duodenal diverticula were 3.6% at 5 years (95% confidence interval, 0.5-6.9), 5.5% at 10 years (95% confidence interval, 1.5-9.4), and 10.2% at 15 years (95% confidence interval, 3.8-16.7). Age, common bile duct exploration and choledochotomy, and the presence of common bile duct dilatation were not found to be significantly associated with recurrence based on a univariate analysis of risk factors by means of the log-rank statistic. CONCLUSIONS: For patients with radiologically diagnosed, second-portion duodenal diverticula, the risk of developing recurrent bile duct stones after cholecystectomy is lower than has been suggested in previous studies. In the absence of concurrent choledocholithiasis, sphincterotomy or biliary bypass at the time of cholecystectomy seems unwarranted.     

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.