No association of coffee consumption with gastric ulcer, duodenal ulcer, reflux esophagitis, and non-erosive reflux disease: a cross-sectional study of 8,013 healthy subjects in Japan.

Probably due to caffeine-induced gastric acid secretion, negative effects of coffee upon various upper-gastrointestinal diseases have been precariously accepted, despite the inadequate epidemiological evidence. Our aim is to evaluate the effect of coffee consumption on four major acid-related diseases: gastric ulcer (GU), duodenal ulcer (DU), reflux esophagitis (RE), and non-erosive reflux disease (NERD) based on the large-scale multivariate analysis. Of the 9,517 healthy adults, GU, DU, and RE were diagnosed by endoscopy, and NERD was diagnosed by the symptoms of heartburn and regurgitation without esophageal erosion. Associations between coffee consumption and the four disorders were evaluated, together with age, gender, body mass index (BMI), Helicobacter pylori (HP) infection status, pepsinogen I/II ratio, smoking, and alcohol. We further performed meta-analysis using the random effects model to redefine the relationship between coffee intake and peptic ulcer disease. The eligible 8,013 study subjects comprised of 5,451 coffee drinkers and 2,562 non-coffee drinkers. By univariate analysis, age, BMI, pepsinogen I/II ratio, smoking, and alcohol showed significant associations with coffee consumption. By multiple logistic regression analysis, positively correlated factors with significance were HP infection, current smoking, BMI, and pepsinogen I/II ratio for GU; HP infection, pepsinogen I/II ratio, and current smoking for DU; HP non-infection, male, BMI, pepsinogen I/II ratio, smoking, age, and alcohol for RE; younger age, smoking, and female for NERD. The meta-analyses could detect any association of coffee consumption with neither GU nor DU. In conclusion, there are no significant relationship between coffee consumption and the four major acid-related upper gastrointestinal disorders.

Dietary phosphilipids and sterols protective against peptic ulceration.

The prevalence of duodenal ulceration in regions of developing countries with a stable diet is related to the staple food(s) in that diet. A higher prevalence occurs in areas where the diet is principally milled rice, refined wheat or maize, yams, cassava, sweet potato or green bananas, and a lower prevalence in areas where the staple diet is based on unrefined wheat or maize, soya, certain millets or certain pulses. Experiments using animal peptic ulcer models showed that the lipid fraction in foods from the staple diets of low prevalence areas gave protection against both gastric and duodenal ulceration, including ulceration due to non-steroidal anti-inflammatory drugs (NSAIDs), and also promoted healing of ulceration. The protective activity was found to lie in the phospholipid, sterol and sterol ester fractions of the lipid. Amongst individual phospholipids present in the phospholipid fraction, phosphatidyl ethanolamine (cephalin) and phosphatidyl choline (Lecithin) predominated. The sterol fraction showing activity contained ß-sitosterol, stigmasterol and an unidentified isomer of ß-sitosterol. The evidence shows that dietary phytosterols and phospholipids, both individually and in combination, have a protective effect on gastroduodenal mucosa. These findings may prove to be important in the prevention and management of duodenal and gastric ulceration including ulceration due to NSAIDs.

Seven-day intravenous low-dose omeprazole infusion reduces peptic ulcer rebleeding for patients with comorbidities.

BACKGROUND: Patients with comorbidities have an increased risk of ulcer rebleeding, especially within the 28 days after endoscopic therapy. Omeprazole infusion can prevent rebleeding after endoscopic therapy in patients with peptic ulcer bleeding. However, the optimal duration is uncertain, especially for those patients with comorbidities. OBJECTIVE: To determine whether prolonged low-dose intravenous omeprazole could reduce rebleeding for patients with comorbidities. DESIGN: A prospective randomized control study. SETTING: National Cheng Kung University, Tainan, Taiwan. PATIENTS: A total of 147 patients with comorbidities and peptic ulcer bleeding controlled by endoscopic hemostasis were enrolled. INTERVENTIONS: The enrolled patients were randomized into either the 7-day low-dose group or the 3-day high-dose group, who received 3.3 mg/h or 8 mg/h continuous omeprazole infusion, respectively. After omeprazole infusion, oral esomeprazole 40 mg every day was given. MAIN OUTCOME MEASUREMENTS: To compare the rebleeding rates within 28 days after gastroscopy between the 2 study groups. RESULTS: The 7-day cumulative rebleeding rate was similar between the 2 groups (9.5% vs 9.7%, P > .05), but the 7-day low-dose group had a lower risk of rebleeding between the 8th and 28th day compared with the 3-day high-dose group (0% vs 10.7%, P = .03; relative risk, 0.52 [95% CI, 0.43-0.63]). The Kaplan-Meier curves confirmed that the 7-day low-dose group had a significantly higher cumulative rebleeding-free proportion between the 8th and 28th day than the 3-day high-dose group (P = .02, log-rank test). CONCLUSIONS: In Asian patients, prolonged low-dose omeprazole infusion for 7 days may reduce peptic ulcer rebleeding during the first 28 days in patients with comorbidities.

Does adding misoprostol to standard intravenous proton pump inhibitor protocol improve the outcome of aspirin/NSAID-induced upper gastrointestinal bleeding?: a randomized prospective study.

Aspirin and nonsteroidal anti-inflammatory drug (NSAID)-induced gastrointestinal bleeding is recognized as an important health problem. We performed a single-center randomized clinical trial to compare the effect of high-dose intravenous proton pump inhibitor (omeprazole) alone (group 1) with omeprazole in combination with a low-dose prostaglandin analog (misoprostol; group 2) on clinical outcomes in patients with aspirin/NSAID-induced upper gastrointestinal bleeding. Additionally, we evaluated the contribution of Helicobacter pylori eradication therapy on the late consequences. Patients were recruited to the study if they had upper gastrointestinal bleeding with history of taking aspirin or other NSAIDs within the week before the onset of bleeding. All were evaluated in terms of probable risk factors. After the standard treatment protocol, patients with histologically proven H pylori infection were prescribed a triple eradication therapy for 14 days. The primary end points were recurrent bleeding, surgery requirement, and death rates before discharge and at the end of follow-up period. This study lasted for 2 years. A total of 249 patients with upper gastrointestinal bleeding were admitted, and 49.7% of these patients were users of aspirin/NSAIDs. There were 67 patients in group 1 and 56 in group 2. The distributions for gender, age, comorbidity, H pylori infection, and high-risk ulcer rate were similar in both groups. Among aspirin/NSAID users, endoscopy revealed duodenal ulcer in 47 (38.2%), gastric ulcer in 10 (8.1%), and erosive gastropathy in 33 (26.8%). The overall rebleeding occurred in 12.2%, death in 2.4% of the patients. The in-hospital death (P=.414), rebleeding (P=.925), and surgery (P=.547) rates were similar in both treatment groups. After the follow-up period of 3 months, overall rebleeding occurred in 4.1%, and death in 4.8% of the patients. The overall mortality rate was highest in those >65 years old, who were chronic low-dose aspirin users with comorbidity. One died of transfusion-related graft-versus-host disease. In this pilot study, we indicated that adding misoprostol (600 microg/day) to standardized proton pump inhibitor treatment did not improve or change the rebleeding or mortality rates of patients with upper gastrointestinal bleeding related to aspirin/NSAID use. Other prospective studies on higher doses of misoprostol are needed to establish the coeffect. One should bear in mind that all blood products must be irradiated before transfused to the host.

Retrospective review of the preoperative biliary and gastrointestinal evaluation for gastric bypass surgery.

BACKGROUND: The purpose of this study was to analyze the frequency and results of preoperative biliary and gastrointestinal (GI) evaluation of patients undergoing Roux-en-Y gastric bypass (RYGB). METHODS: Retrospective review of the preoperative evaluation of 144 consecutive RYGB patients. RESULTS: Cholecystectomy had already been performed in 43 (30%) patients; 22% of those patients with an intact gallbladder had cholelithiasis. Ten patients (7%) had an upper GI x-ray (UGI), and 94 patients (65%) had an esophagogastroduodenoscopy (EGD). Abnormalities were found in 40% of the UGIs and 84% of the EGDs. A total of 96 patients (67%) were tested for Helicobacter pylori; 11% were positive. Twenty-one patients (15%) underwent preoperative colonoscopy; 48% were abnormal, but most of the abnormalities were not clinically significant. Three patients had barium enema x-ray, which was normal in all cases. CONCLUSIONS: The preoperative biliary and GI evaluation of bariatric surgery patients should include a routine ultrasound of the gallbladder. Routine preoperative EGD will detect a significant number of abnormalities that should be treated, but should rarely alter the bariatric surgical procedure or result in denial of bariatric surgery. Many abnormalities will be asymptomatic. Patients should be routinely screened for H. pylori and, if positive, treated before bariatric surgery. Lower GI evaluation should be performed selectively based on the patient's symptoms, physical findings, and guidelines for colorectal cancer and polyp screening.

Duodenal ulcer in South Africa: home-pounded versus milled maize.

BACKGROUND: In South Africa there is suggestive evidence that home-pounded maize protects against duodenal ulceration. Therefore the purpose of the present paper was to test, in an animal model, whether oil from home-pounded maize gives protection against ulceration and whether this effect is present in commercially prepared maize oil. METHODS: Gastric ulceration was induced in rats with topical ethanol 1 h after giving oil prepared either from fresh-pounded or from commercially treated maize. The lengths of the linear ulcers produced were measured with a planimeter and summed in each rat. Control observations were made using arachis oil (which is known not to be ulceroprotective) and horse gram lipid (which is known to be strongly ulceroprotective). Statistical comparisons were performed mainly with the Mann-Whitney U-test, but also with reference to the normal distribution. Thin-layer chromatography (TLC) was performed on the oil from fresh maize, and the fractions similarly investigated for ulceroprotective activity. RESULTS: Fresh maize oil was strongly ulceroprotective (P = 0.0039), commercial maize oil was not (P = 0.2864). The active ingredient in the fresh maize oil was located in the fraction near the solvent front. CONCLUSION: These findings support the hypothesis that home-pounded maize protects against duodenal ulceration.

[Herbs and herbal preparations applied in the treatment of gastric hyperacidity, gastric and duodenal ulcer in cigarette smokers]. / Surowce i preparaty roslinne stosowane w leczeniu choroby wrzodowej zoladka i dwunastnicy u palaczy tytoniu.

The origins of gastric hyperacidity, gastric and duodenal ulcer appearance includes genetic predisposition, incorrect diet and unbalanced lifestyle, e.g. increased stress level, cigarette smoking. Herbal drugs have been proved to be very effective in treatment of hyperacidity, gastric and duodenal ulcer. They can be applied as drugs supplementing or enhancing the activity of synthetic medicines. Moreover, herbal drugs have been successfully applied inprophylactic of hyperacidity, gastric and duodenal ulcer. Herbal therapeutic preparations are administered as infusions from individual herbs, from mixtures of herbs, tinctures, herbal preparations. The most often used herbs include mucus: Lini semen, Psylli semen, Foenugraeci semen, Althaeae radix/folium, Sinapis albae semen; antiphlogistic volatile-oils: Chamomillae anthodium, Millefolii herba, moreover Glycyrrhizae radix, Aloe gel.

Duodenal ulcer prevalence: research into the nature of possible protective dietary lipids.

The varying geographical prevalence of duodenal ulceration has suggested a relationship to staple diet. Previous experiments on animal peptic ulcer models showed that certain foods, particularly the lipid fraction, are ulceroprotective. This paper reports experiments on animal models further to investigate the nature of the protective substances in the most active lipid, that of horse gram. The free fatty acids and triglycerides, sterols, sterol esters and phospholipids from horse gram were extracted and tested for protective activity on rat peptic ulcer models: the pyloric ligation model which is chronic, involving 14 days pre-feeding, and two acute models using ethanol or cysteamine to induce ulceration. The results showed that sterol esters, but not sterols, were protective in the pyloric ligation model. Sterols were protective in the acute models using ethanol-induced and cysteamine-induced ulceration. Phospholipids were protective in both types of model. The free fatty acids and triglycerides gave no protection using the pyloric ligation model. The presence of sterols, sterol esters and phospholipids in the lipid fraction of foods in staple diets may account for the low prevalence of duodenal ulcer in certain geographical areas, despite a uniformly high prevalence of Helicobacter pylori infection.

Risk factors for peptic ulcer disease: a population based prospective cohort study comprising 2416 Danish adults.

BACKGROUND: No population based prospective cohort study has previously assessed the impact of multiple risk factors, including Helicobacter pylori infection, on the incidence of peptic ulcer disease (PUD). AIMS: To identify risk factors for PUD and estimate their relative impact on ulcer incidence. SUBJECTS: Random sample of 2416 Danish adults with no history of PU. METHODS: Sample members were interviewed in 1982 and 1994. PUs diagnosed within the observation period were verified through medical records. Information on psychosocial factors, lifestyle practices, and medication was obtained from a questionnaire completed at study entry. H pylori infection status was determined by ELISA. RESULTS: The main risk factors for PUD were H pylori infection (odds ratio 4.3 (95% confidence interval 2.2; 8.3)), tobacco smoking (3.8 (1.7; 9.8)), and use of minor tranquillisers (3.0 (1.4; 6.6)). Intake of non-steroid anti-inflammatory drugs did not affect the incidence of PUD (0.4 (0.1; 2.3)). In those with increased antibodies to H pylori, tobacco smoking (12.7 (2.8; 56.8)) and intake of spirits (2.4 (1.1; 5.4)) increased the risk of PUD whereas moderate leisure time physical activity (0.3 (0.2; 0.7)) protected against PUD. CONCLUSIONS: Tobacco smoking and H pylori infection are the main risk factors for PUD in Danish adults. Physical activity may protect against PUD in those infected with H pylori.

The gastrointestinal effects of nonselective NSAIDs and COX-2-selective inhibitors.

Nonsteroidal anti-inflammatory drugs (NSAIDs), which include aspirin, are among the most frequently prescribed medications worldwide. The main factor limiting use of NSAIDs is concern about their gastrointestinal (GI) side effects. The purpose of this article is to review the incidence, pathophysiology, and risk factors of GI side effects associated with NSAID therapy. Upper GI symptoms, such as dyspepsia, occur in 15% to 60% of NSAID users, twice as often as in individuals not taking NSAIDs. The prevalence of gastric or duodenal ulcers in patients taking NSAIDs regularly is approximately 15% to 30%. The annual incidence of NSAID-related clinical upper GI events (complicated and symptomatic ulcers) is approximately 2.5% to 4.5%, with the annual incidence of serious complications (severe bleeding, perforation, and obstruction) about 1% to 1.5%. A history of ulcer or GI complications, advanced age, concomitant anticoagulation therapy or corticosteroid use, and high-dose or multiple NSAID therapy are associated with an increased risk of GI events during NSAID therapy. The cyclooxygenase (COX)-2 specific inhibitors (coxibs) have been developed in order to improve the GI safety and tolerability profile of therapy with NSAIDs. In numerous clinical trials, coxibs have been shown to have efficacy similar to that of nonselective NSAIDs, but are associated with significantly fewer endoscopic ulcers. In addition, 2 large outcome trials indicated that coxibs can also reduce the incidence of clinically important GI events.

Operations for peptic ulcer disease: paradigm lost.

Over the past several decades, the pharmacologic and endoscopic treatment of peptic ulcer disease (PUD) has dramatically improved. To determine the effects of these and other changes on the operative management of PUD, we reviewed our surgical experience with gastroduodenal ulcers over the past 20 years. A computerized surgical database was used to analyze the frequencies of all operations for PUD performed in two training hospitals during four consecutive 5-year intervals beginning in 1980. Operative rates for both intractable and complicated PUD were compared with those for other general surgical procedures and operations for gastric malignancy. In the first 5-year period (1980 to 1984), a yearly average of 70 upper gastrointestinal operations were performed. This experience included 36 operations for intractability, 15 for hemorrhage, 12 for perforation, and seven for obstruction. During the same time span, 13 resections were performed annually for gastric malignancy. By the most recent 5-year interval (1994 to 1999), the total number of upper gastrointestinal operations had declined by 80% (14 cases), although the number of operations for gastric cancer had changed only slightly. Operations decreased most markedly for patients with intractability, but the prevalence of operations for bleeding, obstruction, and perforation was also decreased. We conclude that improved pharmacologic and endoscopic approaches have progressively curtailed the use of operative therapy for PUD. Elective surgery is now rarely indicated, and emergency operations are much less common. This changed paradigm poses new challenges for training and suggests different approaches for practice.

Fermented milk products are associated to ulcer disease. Results from a cross-sectional population study.

BACKGROUND: Prevalence of peptic ulcer disease has been associated to diet. Some dietary factors seem to have bactericidal effect which may modify the risk of peptic ulcer disease. The objective was to analyze associations between dietary habits and peptic ulcers. DESIGN: A cross sectional population study. SUBJECTS: One thousand, one hundred and thirty-five subjects out of 11700 randomly invited men and women, aged 46-67 y, participating in a diet and disease study during 1991-1993. The study population comprised of 764 cases with reported peptic ulcer, 142 with dyspeptic symptoms and 229 randomly selected controls. METHODS: X-ray examinations and endoscopies were reviewed and 332 out of 764 peptic ulcer cases were verified. Mean daily intake of foods and nutrients were assessed with a combined 7d menu book and a quantitative food frequency questionnaire, including dietary supplements. RESULTS: Subjects with verified ulcer had lower intake of fermented milk products and vegetables and higher intake of milk, meat and bread than controls. Intake of total fat, saturated and monounsaturated fatty acids and linolenic acid were higher in the ulcer group. Higher intake of fermented milk products, by quintiles showed a decreased ulcer risk; odds ratio 0.82 (0.71-40.95), adjusted for covariates below. Higher intake of milk, by quintiles, was associated with an increased risk of ulcer; odds ratio 1.17 (1.03-1.32). Smoking, foreign ethnicity and being unmarried or divorced were covariates associated to ulcer. CONCLUSION: This study indicates the multifactorial etiology of peptic ulcer including dietary factors. High intake of fermented milk products was associated with decreased risk for ulcer, whereas increased risk was noted for high milk intake.

Epidemiology and prevention of non-steroidal anti-inflammatory drug effects in the gastrointestinal tract.

Lesions of the gastric, duodenal and intestinal mucosae are found in large numbers of patients using non-steroidal anti-inflammatory drugs (NSAIDs); however, no markers have yet been isolated to identify patients at risk for developing gastrointestinal problems or to predict which patients with lesions are at risk for developing catastrophic complications. There appears to be a poor correlation between the presence of ulcer disease and the appearance of symptoms while patients are using NSAIDs. The ideal treatment--namely, withdrawal from NSAIDs--may not always be practicable in patients who require the analgesic benefit of these otherwise generally innocuous agents. It is incumbent on the clinician to identify the agent most appropriate for the needs of the individual, and to supplement NSAID therapy, where appropriate, with a means of preventing or minimizing adverse effects. Four classes of drugs are used to prevent NSAID-related gastric mucosal damage: histamine (H2)-receptor antagonists (ranitidine, cimetidine, nizatidine, famotidine); gastric acid-pump inhibitor (omeprazole); barrier agent (sucralfate); and prostaglandin analogue (misoprostol). The current therapies (H2 antagonists and barriers) have not lived up to their promise for preventing gastroduodenal erosion. Moreover, such protection as they provide is limited to the duodenal mucosa; they afford no protection to the gastric mucosa. Preliminary data indicate that an acid pump inhibitor may be useful, but large-scale studies have yet to be reported. Acute and long-term studies of the prostaglandin analogue misoprostol have shown that this agent has an important role as an adjunctive therapy to prevent both gastric and duodenal ulceration due to NSAIDs.

Effects of compound U74500A in animal models of gastric and duodenal ulceration.

Pretreatment with U74500A (up to 0.65 mg/100 g) failed to affect gastric lesions induced by 100% EtOH gavage in Sprague-Dawley rats. Topical application of U74500A did not reduce lesions induced by 40% EtOH in ex vivo gastric chamber preparations. However, pretreatment of rats with U74500A (0.65 g/100 g per os) reduced the incidence and severity of experimental duodenal ulcer induced by cysteamine HCl, and duodenal ulcer induced by cysteamine-HCl plus GABA. These results show U74500A to have powerful and specific antiduodenal ulcer actions. Pharmacologic analysis of organ-bath preparations of the small intestine show this compound to reduce intestinal contractility to applied cholinergic and serotonergic agonists. However, relaxations induced by electrical or nicotinic ganglionic stimulation were unaffected. U74500A itself caused concentration-dependent contractions.

The economic consequences of NSAID-induced gastropathy: the French context.

The costs of treating gastroduodenal ulcers caused by nonsteroidal anti-inflammatory drugs (NSAIDs) are shown to increase the total cost of NSAID treatment to the Assurance-Maladie, the French national health insurance system. This increased cost is termed the iatrogenic cost factor, and is defined as the ratio of the shadow price of an NSAID to its reimbursed cost. The shadow price is calculated from estimates of the incidence of NSAID-induced gastropathies, the cost of the drug, and the hospital and ambulatory costs of treating the gastropathies. The resulting iatrogenic cost factors are estimated as 1.36 for naproxen, 1.48 for sulindac, 1.65 for diclofenac, 1.67 for piroxicam, 2.00 for ketoprofen, and 2.12 for etodolac.

Natural history of duodenal ulcer detected by the gastric mass surveys in men over 40 years of age.

In a gastric mass survey with photofluorography performed on 10,605 male office workers over 40 years of age, 456 cases of duodenal ulcer (4.3%) were detected. These cases were scheduled to be followed up every 6 months with endoscopy and without any anti-ulcer drugs. Two hundred and seventy-six of the cases, including 169 cases with craters and 107 cases with scars, were followed up for 2 years. Forty-one of 169 craters (24.3%) had healed, and 21 of 107 scars (19.6%) had relapsed at 6 months. At 24 months 36 of 169 craters (21.3%) had healed, and 31 of 107 scars (29.0%) had relapsed. Sixty-four and a half per cent of the ulcers that showed crater at entry remained at the crater stage, and 62.6% of ulcer scars at entry remained healed at every endoscopy during the trial period. With regard to the cases' background, cigarette smoking adversely affected the natural history of the duodenal ulcer. However, years after onset, previous treatment, history of overt bleeding, and alcohol and coffee consumption did not affect the present ulcer activity.

Smoking, alcohol, coffee, and familial factors: any associations with peptic ulcer disease? A clinically and radiologically prospective study.

In the period between 1980 and 1983 smoking habits, alcohol consumption, coffee drinking, and familial occurrences of peptic ulcers were studied in patients with gastric or duodenal ulcer in North Norway. The results were compared with those in two control groups matched for sex and age but without anamnestically known previous peptic ulcer disease. Statistically significant increased familial occurrences of peptic ulcer were found in relatives of patients both with gastric and with duodenal ulcer, compared with the control group. Furthermore, significantly more smokers were found in the two groups of patients than in the control groups. Patients with duodenal ulcers smoked more than those with gastric ulcer. Both the consumption of coffee and that of alcohol, however, were significantly reduced in the ulcer patients compared with their controls. Therefore, both familial factors and smoking habits appear to have some relationship or even play etiologic roles in the development of peptic ulcer disease, at least in the northern part of Norway. Coffee drinking and intake of alcohol seem to be of no importance. Both tobacco smoking and familial accumulation of peptic ulcers increased the relative risks of getting both gastric and duodenal ulcer as compared with 'non-exposed' persons. Furthermore, a positive correlation was found in men between the quantity of smoking and the risk of developing duodenal ulcer.