sodium-bicarbonate and Helicobacter-Infections

The study tested whether pronase can improve endoscopic visibility and alter the accuracy of the CLO test for H. pylori detection.. A total of 160 patients were randomly assigned to receive one of five premedications for endoscopy: group A: dimethylpolysiloxane (DMPS) alone; group B: DMPS plus water (up to 100 ml); group C: pronase only, with 100 ml water; group D: pronase and sodium bicarbonate plus water up to 100 ml; group E: pronase, sodium bicarbonate, and DMPS, plus water up to 100 ml. Endoscopists, who were unaware of the premedication method administered, assessed visibility scores (range 1 - 4) for the antrum, lower gastric body, upper gastric body, and fundus. The higher the score, the less clear the visibility. The sum of scores from the four locations was defined as the total visibility score. A CLO test was also done during the endoscopy. One week after their endoscopy, patients in groups C, D, and E were scheduled for a (13)C-urea breath test (UBT).. Group E patients had a significantly lower total visibility score than those in the other four groups ( P < 0.05). Groups C and D had higher total visibility scores than the other three groups ( P < 0.05). The scores did not significantly differ between groups A and B. Based on the UBT results, the sensitivity and specificity of the CLO test were 92.6 % and 96.2 %, respectively.. Premedication as in group E provided the clearest endoscopic visibility. Without the application of DMPS, pronase alone cannot improve endoscopic visibility. Pronase does not influence H. pylori identification using the CLO test.

Topics: Adult; Breath Tests; Dimethylpolysiloxanes; Endoscopy, Gastrointestinal; Female; Helicobacter Infections; Helicobacter pylori; Humans; Image Enhancement; Male; Middle Aged; Predictive Value of Tests; Premedication; Pronase; Sodium Bicarbonate; Urea; Urease

Both proton pump inhibitor drug treatment and Helicobacter pylori infection cause hypergastrinaemia in man.. To determine whether eradicating H pylori is a means of reducing hypergastrinaemia during subsequent proton pump inhibitor treatment.. Patients with H pylori were randomised to treatment with either anti-H pylori or symptomatic treatment. One month later, all received four weeks treatment with omeprazole 40 mg/day for one month followed by 20 mg/day for six months. Serum gastrin concentrations were measured before and following each treatment.. In the patients randomised to anti-H pylori treatment, eradication of the infection lowered median fasting gastrin by 48% and meal stimulated gastrin by 46%. When gastrin concentrations one month following anti-H pylori/symptomatic treatment were used as baseline, omeprazole treatment produced a similar percentage increase in serum gastrin in the H pylori infected and H pylori eradicated patients. Consequently, in the patients in which H pylori was not eradicated, median fasting gastrin concentration was 38 ng/l (range 26-86) at initial presentation and increased to 64 ng/l (range 29-271) after seven months omeprazole, representing a median increase of 68% (p < 0.005). In contrast, in the patients randomised to H pylori eradication, median fasting gastrin at initial presentation was 54 ng/l (range 17-226) and was unchanged after seven months omeprazole at 38 ng/l (range 17-95).. Eradicating H pylori is a means of reducing the rise in gastrin during subsequent long term omeprazole treatment. In view of the potential deleterious effects of hypergastrinaemia it may be appropriate to render patients H pylori negative prior to commencing long-term proton pump inhibitor treatment.

Topics: Adult; Alginates; Aluminum Hydroxide; Amoxicillin; Antacids; Anti-Ulcer Agents; Drug Combinations; Drug Therapy, Combination; Esophagitis; Female; Gastrins; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Middle Aged; Omeprazole; Organometallic Compounds; Peptic Ulcer; Silicic Acid; Sodium Bicarbonate

Minute early gastric cancers can be removed with endoscopic mucosal resection techniques. However, early detection of these minute cancers with endoscopy is still difficult. For this purpose, use of a dye is helpful. To increase visibility further, gastric mucus should be removed before endoscopic examination. In this study, the effectiveness of premedication with pronase for improving visibility during gastroendoscopy was investigated.. From January through July 1996, outpatients scheduled for gastroendoscopy were randomly assigned to oral premedication with the antifoam agent dimethylpolysiloxane alone (n=34), with dimethylpolysiloxane plus sodium bicarbonate (n=32), or with dimethylpolysiloxane, sodium bicarbonate, and pronase (n=34). All were given about 10 minutes before the start of endoscopy. After inserting the endoscope, the endoscopist gave visibility scores at conventional endoscopy and after methylene blue spraying.. Premedication with pronase significantly improved visibility before and after methylene blue spraying as compared with the two other groups pretreated without pronase. Pronase also significantly shortened the times for chromoendoscopic examination. Pronase had no significant effect on the culture of Helicobacter pylori.. Premedication with pronase improved endoscopic visualization during conventional endoscopy and chromoendoscopy. Its routine use at gastroendoscopy is therefore recommended.

Topics: Adult; Diagnosis, Differential; Dimethylpolysiloxanes; Female; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Image Enhancement; Male; Methylene Blue; Middle Aged; Premedication; Pronase; Sensitivity and Specificity; Sodium Bicarbonate; Stomach Neoplasms; Stomach Ulcer

Simpler, effective therapies to treat Helicobacter pylori infection are greatly needed. Omeprazole co-therapy apparently enhances effectiveness of some antimicrobials. Our objective in this study was to determine whether the apparent additional benefit provided by omeprazole to amoxicillin therapy could be equaled by a high dose of ranitidine plus sodium bicarbonate.. In a prospective randomized trial, we tested 1 g amoxicillin b.i.d. with either omeprazole 20 mg b.i.d., or high dose ranitidine (900 and 1800 mg) plus sodium bicarbonate tablets 650 t.i.d. (with meals) for 14 day.. Fifty-two patients with documented H. pylori infection and peptic ulcer completed therapy. The cure rate with omeprazole and amoxicillin was poor (46%), with the 95% confidence interval (CI) = 25-67%. Ranitidine plus sodium bicarbonate was also poor (39% cure) with the 95% CI = 21.5-59% (p > 0.57). Average compliance was more than 92% for all three groups. Side effects were experienced in only two patients (stomatitis and mild diarrhea).. Neither the omeprazole nor ranitidine plus bicarbonate plus amoxicillin therapies used here can be recommended for treatment of H. pylori infection.

Topics: Amoxicillin; Biopsy; Drug Administration Schedule; Drug Therapy, Combination; Female; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Omeprazole; Peptic Ulcer; Prospective Studies; Ranitidine; Reproducibility of Results; Sodium Bicarbonate

Potassium-competitive acid blockers and proton pump inhibitors/sodium bicarbonate can rapidly increase intragastric pH. In this study, we aimed to compare the clinical outcomes of tegoprazan-based and esomeprazole/sodium bicarbonate-based triple therapies in the treatment of Helicobacter pylori infection.. We retrospectively reviewed the data of patients with H. pylori infection treated with a 14-day tegoprazan-based triple therapy or 14-day esomeprazole/sodium bicarbonate-based triple therapy. The primary end point was the H. pylori eradication rate with first-line treatment in an intention-to-treat analysis. Secondary end points included the eradication rate with first-line therapy in the per-protocol analysis and adverse events associated with eradication therapy.. Of the 854 included patients, 435 were treated with tegoprazan-based therapy, and 419 received esomeprazole/sodium bicarbonate-based therapy. In the intention-to-treat population, no significant difference in eradication rate was detected between the tegoprazan-treated and esomeprazole/sodium bicarbonate-treated groups (78.6% [95% confidence interval (CI), 74.6-82.3%] vs 81.4% [95% CI, 77.4-84.9%], P = 0.313). The per-protocol analysis also revealed a similar eradication rate between groups (tegoprazan vs esomeprazole/sodium bicarbonate: 85.5% [95% CI, 81.8-87.5%] vs 87.8% [95% CI, 84.1-90.7%], P = 0.339). However, abdominal discomfort and diarrhea were more common in the esomeprazole/sodium bicarbonate-treated group than in the tegoprazan-treated group (abdominal discomfort: 1.1% vs 3.8%, P = 0.012; diarrhea: 9.9% vs 21.2%, P < 0.001).. The efficacy of the esomeprazole/sodium bicarbonate-based triple therapy for H. pylori eradication was comparable with that of the tegoprazan-based triple therapy. However, esomeprazole/sodium bicarbonate-based therapy exhibited a higher risk of abdominal discomfort and diarrhea than tegoprazan-based therapy.

Topics: Anti-Bacterial Agents; Bicarbonates; Diarrhea; Esomeprazole; Helicobacter Infections; Helicobacter pylori; Humans; Retrospective Studies; Sodium Bicarbonate

Acid hydrolysis of components from the diet in the stomach require the presence of an acid and a hydrolysing agent. The acid involved is hydrochloric acid. The present mechanism of hydrochloric acid production in the stomach is demonstrated to be incompatible with measured intracellular or intercellular concentrations of the relevant ions. An alternative set of chemical reactions whereby hydrochloric acid is formed in the stomach is presented. The hydrolysing agent is identified and a mechanism of transfer of chemical compounds into the metabolism is described. The hypothesis demonstrates that some of chemical compounds produced in the stomach can induce conditions such as asthma and that the conditions of osteoporosis and hemochromatosis can be linked to the function of the stomach. Possible treatments for these and other conditions such as stomach acidity and anaemia are proposed.

Topics: Adult; Ammonia; Antacids; Asthma; Bicarbonates; Calcium Chloride; Calcium Phosphates; Chlorides; Digestion; Ferric Compounds; Ferrous Compounds; Gastric Acid; Gastric Juice; Gastric Mucosa; Gastritis; Gastrointestinal Contents; Helicobacter Infections; Helicobacter pylori; Hemochromatosis; Humans; Hydrolysis; Ion Transport; Metabolic Diseases; Models, Biological; Models, Chemical; Nitrous Oxide; Osteoporosis; Parietal Cells, Gastric; Sodium Bicarbonate; Stomach

We studied the effects of famotidine, sodium bicarbonate, and citric acid on the 13C-urea breath test (UBT).. Helicobacter pylori-infected volunteers received a UBT, 40 mg of famotidine at bedtime, and a second UBT (pudding test meal, 648 mg NaHCO3 tablet then 125 mg of urea in 200 ml of water containing 650 mg of NaHCO3). Experiment 2 consisted of four UBTs. Two were standard citric acid UBTs with 75 mg of urea and 2 g citric acid and two were sequential bicarbonate-citric acid UBTs. Sequential UBTs consisted of administration of a 648 mg bicarbonate tablet with 50 g of Polycose in 200 ml of water. Five minutes later, 125 mg of 13C-urea was given in 75 ml of water containing 650 mg of NaHCO3. Breath samples were collected after 15 minutes. Then, to acutely acidify the stomach, 4 g of citric acid was given in 200 ml of water. A second breath sample was collected 15 minutes after the citric acid. The standard UBTs were done before and after 6 days of famotidine (40 mg b.i.d.). Sequential UBTs were done after 1 and 6 days of famotidine therapy. Gastric biopsies for histology, culture, and mucosal cytokines were assessed before and after 6 days of famotidine.. Eighteen subjects participated, 10 in each experiment; seven had endoscopy with biopsy. Famotidine/ bicarbonate resulted an approximately 50% fall in UBT values (p = .021) with 10% becoming negative. The gastric pH increased from 5.1 +/- 0.5 to 6.7 +/- 0.2 (p = .03) although no pH value predicted the occurrence of false negative results. Under famotidine acid suppression, NaHCO3 reduced the delta over baseline (DOB) by 63% (p = .021). This was reversed with citric acid. Histology showed a H2-receptor antagonist-associated increase in the depth of gastric corpus inflammation.. H2-receptor antagonists differ from proton pump inhibitors as high intragastric pH may cause a reduction in urease activity, unrelated to a reduced bacterial load and reversed by citric acid.

Topics: Adolescent; Adult; Aged; Biopsy; Breath Tests; Citric Acid; Endoscopy, Gastrointestinal; False Negative Reactions; Famotidine; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Histamine H2 Antagonists; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Sodium Bicarbonate; Urea