Example: "I had surgery on April 16th, 2008 in Vegas and I think I have gastritis. What do I need to do?"
Dyspepsia is a pain or an uncomfortable feeling, usually located in the left upper middle part of your stomach. The pain might come and go, and can be made worse by certain foods (i.e. orange juice) and can be made better by Tums, Antacids and foods like Yogurt.
Dyspepsia, Gastritis, ulcer(s), indigestion, heartburn, acid stomach, upset stomach is the most common complication seen after the Mini-Gastric Bypass. It is seen in up to 5% of MGB patients similar to the rates seen in RNY Gastric Bypass (also see: Patel, Felix, Google Ulcer+RNY) patients.
Dyspepsia/Ulcer/Gastritis can lead to devastating complications such as bleeding and/or perforation which can be life threatening.
Because of this patients undergoing MGB should be well educated about the risks of Dyspepsia/Ulcer/Gastritis after MGB and follow advice to institute interventions to decrease the risks of Dyspepsia/Ulcer/Gastritis and to aggressively treat Dyspepsia/Ulcer/Gastritis when it occurs.
I. EDUCATION and AWARENESS
All MGB patients undergo an extensive preoperative education and testing procedure designed to aide them in understanding the risks of Dyspepsia/Ulcer/Gastritis, the interventions to decrease the incidence of Dyspepsia/Ulcer/Gastritis and the treatment of Dyspepsia/Ulcer/Gastritis in MGB post operative patients.
II. PREVENTATIVE MEASURES:
The MGB like the RNY and like Aspirin can increase the risk of Dyspepsia/Ulcer/Gastritis. Fortunately we know a list of factors to avoid to decrease this risk and interventions to recommend that can decrease the incidence of ulcers and gastritis.
Factors Associated with Ulcers/Gastritis
Age
Race
Gender
Heredity
Men have twice the risk of ulcers as women. Gastric ulcers peak at age 55 - 65.
Avoid:
Smoking: Gastric mucosal integrity is maintained by an interplay of some aggressive and defensive factors controlling apoptotic cell death and cell proliferation and smoking potentiates ulcer by disturbing this balance.
Alcohol
Coffee: Coffee consumption has a positive dose-response relation with active H. Pylori infection.
NSAIDS: Aspirin, Advil, Aleve, Ibuprofen and other NSAIDs (Non-steroidal anti-inflammatory drugs)
The use of NSAIDs increases the risk of peptic ulcer 300% to 500%.
Corticosteroids
Bisphosphonates are the primary agents used to treat osteoporosis. Although these agents are generally well tolerated, serious gastrointestinal adverse events, including hospitalization for gastrointestinal bleed, may arise.
Non-nitrogenous
Non-N-containing bisphosphonates:
* Etidronate (Didronel) - 1 (potency relative to that of etidronate)
* Clodronate (Bonefos, Loron) - 10
* Tiludronate (Skelid) - 10
Nitrogenous
N-containing bisphosphonates:
* Pamidronate (APD, Aredia) - 100
* Neridronate - 100
* Olpadronate - 500
* Alendronate (Fosamax) - 500
* Ibandronate (Boniva) - 1000
* Risedronate (Actonel) - 2000
* Zoledronate (Zometa, Aclasta) - 10000
Alendronate and Naproxen Are Synergistic for Development of Gastric Ulcers
David Y. Graham, MD; Hoda M. Malaty, MD, PhD Arch Intern Med. 2001;161:107-110.
Background Both alendronate sodium use and nonsteroidal anti-inflammatory drug use are associated with gastric ulcers. The aim of this study was to investigate whether alendronate and naproxen are synergistic as causes of gastric ulcers.
Methods We performed an endoscopist-blind, randomized, crossover, single-center comparison of 10 mg/d of alendronate sodium, 500 mg of naproxen sodium twice daily, or the combination taken orally for 10 days in volunteers aged 30 years or older. Videoendoscopy was used to evaluate the presence and degree of mucosal damage to the esophagus, stomach, or duodenal bulb before and after each treatment. There was a 1- to 4-week washout between evaluations.
Results Twenty-six healthy volunteers participated (18 women and 8 men), aged 30 to 50 years. Gastric ulcers were present in 2 subjects receiving ** alendronate (8%),** in 3 receiving ** naproxen (12%),** and in 10 receiving ** both (38%) ** (P<.05 for the combination vs either drug alone).
Conclusions Both alendronate and naproxen can cause gastric ulcers. The combination appears synergistic. Alendronate should be used with caution in those who simultaneously require nonsteroidal anti-inflammatory drugs.
COX-2 Selective cyclooxygenase-2 inhibitors (rofecoxib (Vioxx®) and celecoxib ( Celebrex®))
Diet and Ulcer: What You Eat Can Affect the Stomach and Your Gut
FIBER: Higher consumption of fruits and vegetables is associated with lower risk of ulcer
Total dietary fiber intake is inversely associated with the risk of ulcer
FRESH FRUITS AND VEGETABLES:
Grape seed extract may have antioxidative functions that have preventive action in ulcer disease (Grapes and Grape Juice)
Food sourced dietary vitamin C intake may protect against H. Pylori infection and ulcer and gastric cancer
"Emphasize fruits and vegetables. A diet rich in fresh fruits and vegetables, especially those high in vitamin C and beta carotene, has been shown to help protect against" H. Pylori infection and "stomach cancer. Look for deep green and dark yellow or orange fruits and vegetables, such as Swiss chard, bok choy, spinach, cantaloupe, mango, acorn or butternut squash, and sweet potatoes. Also try to eat vegetables from the cabbage family, including broccoli, brussels sprouts and cauliflower. Lycopene, a nutrient found in tomatoes and other red fruits and vegetables such as strawberries and red bell peppers, may be a particularly powerful anti-cancer chemical." From Mayo Clinic .com
FISH OIL:
Fish oil (FO) containing omega-3 polyunsaturated fatty acids may be protective of the stomach lining and prevent gastric ulcers. Fish oil causes a statistically significant increase both in mucus and phospholipid content of the gastric mucosal barrier. Fish oil showed a potent healing-promoting effect on acute gastric erosions and ulcers induced by indomethacin and significantly enhanced the mucus content of the mucosa.
H. pylori and Peptic Ulcer
Helicobacter pylori (H. pylori) is a type of bacteria. Researchers believe that H. pylori is responsible for the majority of peptic ulcers.
"The discovery of Helicobacter pylori, a spiral bacterium which lives in the inhospitable environment of the human stomach, must rank amongst the greatest medical triumphs of the twentieth century. The bacterium was discovered by two Australian doctors, Barry Marshall and Robin Warren in 1982. It took six long years for the medical profession to begin to acknowledge the importance of Marshall and Warren’s work and the first clinical treatment trial was conducted in 1987. Over half the planet’s population is reckoned to be carrying the bacteria and an estimated 5,000,000 cases of gastric cancer and duodenal ulcer occur annually as a result of the infection. From The Institute for Optimum Nutrition"
Helicobacter pylori, Yogurt and Probiotics
Probiotics: Lactobacillus- and Bifidobacterium Yogurt can improve the efficacy of therapy of Helicobacter pylori
"Helicobacter pylori infection, a highly prevalent pathogen, is a major cause of chronic gastritis and peptic ulcer and a risk factor for gastric malignancies. Antibiotics-based H. pylori eradication treatment is 90% effective. However, it is expensive and causes side effects and antibiotic resistance. Probiotics could present a low-cost, large-scale alternative solution to prevent or decrease H. pylori colonization. A literature search of the MEDLINE database (1966-2006) has been performed selecting all in vitro, animal, and human fully published English-language studies dealing with H. pylori and probiotics.
Lactobacillus- and Bifidobacterium-containing yogurt can suppress Helicobacter pylori. In a study of 138 patients were then randomly assigned to either a yogurt-plus-quadruple therapy or a quadruple therapy-only group. The yogurt-plus-quadruple therapy group had a higher H. pylori eradication rate than did the quadruple therapy-only group (intention-to-treat analysis: 90.8% compared with 76.6%, P < 0.05). 4-wk treatment with bacteria in yogurt can decrease H. pylori loads despite antimicrobial resistance, thus improving the efficacy of quadruple therapy in eradicating residual H. pylori.
Consumption of yogurt enriched with probiotics improves the eradication rate of Helicobacter pylori in peptic ulcer patients undergoing quadruple therapy after failed triple therapy, according to a study published in the American Journal of Clinical Nutrition (83, 4:864-69, 2006).
Probiotics had an in vitro inhibitory effect on H. pylori. Animal studies demonstrated that probiotic treatment is effective in reducing H. pylori-associated gastric inflammation. Seven of 9 human studies showed an improvement of H. pylori gastritis and decrease in H. pylori density after administration of probiotics. The addition of probiotics to standard antibiotic treatment improved H. pylori eradication rates (81% vs. 71%, with combination treatment vs. H. pylori-eradication treatment alone; chi(2)test: P=0.03). Probiotic treatment reduced H. pylori therapy-associated side effects (incidence of side effects: 23% vs. 46%, with combination therapy vs. H. pylori-eradication treatment alone; chi(2)test: P=0.04).
Long-term intake of products containing probiotic strains of probiotics may have a favorable effect on H. pylori infection in humans, particularly by reducing the risk of developing disorders associated with high degrees of gastric inflammation."
Other Dietary Factors/Supplements
Green tea,
Red wine,
Flavonoids,
Broccoli sprouts,
Garlic,
Probiotics and
Flavonoids are known to inhibit H. pylori colonization, decrease gastric inflammation by inhibiting cytokine and chemokine release, and repress precancerous changes
Studies have shown that "Red wine/ grapes and green tea are able to prevent H pylori-induced gastric epithelium damage."
Garlic
Capsaicin
Investigations have revealed that chili peppers and "capsaicin" are not the cause for ulcer formation but is a healing and protective agent. In contrast to what might be expected, Capsaicin does not stimulate but inhibits acid secretion. Capsaicin stimulates alkali, mucus secretions and particularly gastric mucosal blood flow which help in prevention and healing of ulcers. Capsaicin acts by stimulating afferent neurons in the stomach and signals for protection against injury. Chili and its pungent ingredient, capsaicin, have been shown to protect against experimental gastric mucosal injury induced by various necrotizing agents such as ethanol and aspirin and stress.
Chili protects against aspirin-induced gastroduodenal mucosal injury in humans.
Capsaicin, the pungent ingredient of chili, has a gastroprotective effect against experimental gastric mucosal injury in animals.
Such an effect has not, however, been documented in humans to date. Eighteen healthy volunteers with normal index endoscopies underwent two studies four weeks apart.
Each subject took 20 g chili orally with 200 ml water in one study and 200 ml water in another study.
In each case this was followed half an hour later by 600 mg aspirin BP with 200 ml water.
Endoscopy was repeated 6 hr later.
Gastroduodenal mucosal damage was assessed by a previously validated scoring system.
The median gastric injury score after chili was 1.5 compared to 4 in the control group (P < 0.05), demonstrating a gastroprotective effect of chili in human subjects.
Dig Dis Sci. 1995 Mar;40(3):580-3. Chili protects against aspirin-induced gastroduodenal mucosal injury in humans.
Yeoh KG, Kang JY, Yap I, Guan R, Tan CC, Wee A, Teng CH. Department of Medicine, National University Hospital, Singapore.
Gastroprotection induced by capsaicin in healthy human subjects.
AIM: To evaluate the gastro-protective effect of capsaicin against the ethanol- and indomethacin (IND)-induced gastric mucosal damage in healthy human subjects.
METHODS: The effects of small doses (1-8 microg/mL, 100 mL) of capsaicin on the gastric acid secretion basal acid output (BAO) and its electrolyte concentration, gastric transmucosal potential difference (GTPD), ethanol- (5 mL 300 mL/L i.g.) and IND- (3x25 mg/d) induced gastric mucosal damage were tested in a randomized, prospective study of 84 healthy human subjects.
The possible role of desensitization of capsaicin-sensitive afferents was tested by repeated exposures and during a prolonged treatment.
RESULTS: Intragastric application of capsaicin protected thestomach as seen by: decreased the gastric Basal Acid Output and enhanced "non-parietal" component, GTPD in a dose-dependent manner.
The stomach was protected from alcoholic damage to the lining of the stomach by a decrease of GTPD evoked by ethanol was inhibited by the capsaicin application, which was reproducible.
Gastric microbleeding induced by IND was inhibited by co-administration with capsaicin, but was not influenced by two weeks pretreatment with a daily capsaicin dose of 3x400 microg i.g.
CONCLUSION: Capsaicin in low concentration range protects against gastric injuries induced by ethanol or IND, which is attributed to stimulation of the sensory nerve endings.
World J Gastroenterol. 2005 Sep 7;11(33):5180-4.Gastroprotection induced by capsaicin in healthy human subjects.
Mózsik G, Szolcsányi J, Rácz I. First Department of Medicine, Medical and Health Center, University of Pécs, Hungary. gyula.mozsik@aok.pte.hu
Melatonin
Consider asking your Dr. about supplemental melatonin 5 milligrams every night and if having dyspepsia trying 5 milligrams three times a day for two weeks.
Melatonin, formed enzymatically from L-tryptophan, has been called "the most versatile and ubiquitous hormone molecule produced not only in all animals but also in some plants."
Melatonin is synthesized not only in the pineal gland, but also in gastrointestinal tract by enterochromaffin cells (EC) and it has a gastro-protective properties.
The enterochromaffin cells of the gastrointestinal (GI) tract secrete 400 times as much melatonin as the pineal gland.
Melatonin has been shown to act by ** scavenging free radicals,** ** protecting gut ** mucosa against various irritants and ** healing of various stomach ** and bowel lesions such as stomatitis, esophagitis, gastritis and peptic ulcer.
Melatonin is abundant in the gastrointestinal tract, has been shown to inhibit gastric acid secretion, augment Gastric Blood Flow and scavenge free radicals, resulting in the attenuation of stress-induced gastric ulcers.
Studies have shown that "nocturnal secretion of melatonin in subjects with asymptomatic infection of H. pylori is higher than in patients with ulcer-like dyspepsia and with duodenal ulcer disease.
** Lower nocturnal secretion of melatonin probably may play role in pathogenesis of upper digestive tract diseases."**
"In animal studies, melatonin protects against GI ulcerations, and randomized clinical trials suggest its efficacy in treating functional dyspepsia and irritable bowel syndrome.
Melatonin administration has been shown to protect against esophageal lesions in animals. Moreover, in a randomized, single-blind clinical trial of subjects with gastroesophageal reflux disease (GERD), the combination of melatonin with other natural supplements was found to be superior to omeprazole, a proton pump inhibitor (PPI)."
The effect of the melatonin on the life span of mice, rats and fruit flies has been studied using various approaches. It has been observed that in various strains of mice long-term administration of melatonin was followed by an increase in the mean life span.
In rats, melatonin treatment increased survival of male and female rats.
Melatonin and its precursor Trptophan significantly attenuate gastric mucosal lesions induced by aspirin. Melatonin and L-tryptophan, accelerate ulcer healing probably via interaction with MT2 receptors; this ulcer healing action is caused by an enhancement by melatonin of the microcirculation at the ulcer margin possibly mediated by COX-derived PG and NO because of overexpression of iNOS and gastrin, which exhibits trophic activity in the gastric mucosa and calcitonin gene related peptide (CGRP), released from sensory nerves, may also contribute to the ulcer healing action of melatonin.
Due to its anti-inflammatory and anti-oxidant properties, melatonin may be one of the most efficient protective factors preventing the development of acute gastric damage and accelerating healing of chronic gastric ulcers probably due to reduction in proinflammatory cytokine production, scavenging of the radical oxygen species and activation of COX-PG and NOS-NO systems as well as stimulating the afferent sensory nerves in the brain-gut axis.
Melatonin in gastroprotection against stress-induced acute gastric lesions and in healing of chronic gastric ulcers.
The degree of gastric damage following to exposition of the mucosa to noxious agents depends upon a balance between the factors promoting this damage and those activating the natural defense mechanisms.
Recent findings, presented in this review, provide evidence that melatonin prevents the formation of acute gastric lesions induced by stress and accelerates healing of chronic gastric ulcers due to increase in the activity of nitric oxide (NO) synthase (NOS)-NO and cyclooxygenase (COX)-prostaglandin E(2) (PGE(2)) systems resulting in the increase of mucosal blood flow and mucosal integrity.
Melatonin is produced and released into the circulation by the pineal gland and, in many times larger amounts, by the gastrointestinal tract.
Due to its anti-inflammatory and anti-oxidant properties, melatonin may be one of the most efficient protective factors preventing the development of acute gastric damage and accelerating healing of chronic gastric ulcers probably due to reduction in proinflammatory cytokine production, scavenging of the radical oxygen species and activation of COX-PG and NOS-NO systems as well as stimulating the afferent sensory nerves in the brain-gut axis.
J Physiol Pharmacol. 2006 Nov;57 Suppl 5:51-66.Melatonin in gastroprotection against stress-induced acute gastric lesions and in healing of chronic gastric ulcers. Konturek SJ, Konturek PC, Brzozowski T. Department of Clinical Physiology, Faculty of Medicine, Jagiellonian University Medical College, Cracow, Poland. mpkontur@cyf-kr.edu.pl
Treatment
Avoid Factors that Increase the Risk of Ulcers/Gastritis (See Above)
Utilize Factors/Supplements that Have Been Shown to Be Gastro-Protective (See Above)
Medical Therapy:
Antacids
(Tums Calcium Carbonate Oral, Adult Min/Max Dose: 400.0mg/5200.0mg
Antacids are attractive for rapid pain relief
Usual Adult Dose for Gastric Ulcer:
1250 to 3750 mg/day in 2 to 4 divided doses. This dose may be increased as needed and tolerated to decrease the abdominal discomfort.
Gaviscon
"In addition to the acid-neutralizing ingredients found in Gaviscon®, all Gaviscon® products contain "alginate". When chewed (Gaviscon tablets) or swallowed (Gaviscon liquid), the combination of the alginic acid and bicarbonate creates a foam barrier or "raft" that floats on the stomach acid. This raft foam barrier helps reduce the number of reflux episodes and provides longer lasting action against "heartburn" than other antacid products." From Gavison.com
* REGULAR-STRENGTH LIQUID
The usual dosage is 1 or 2 tablespoonfuls taken 4 times a day. Do not take more than 8 tablespoonfuls each 24 hours.
* EXTRA-STRENGTH LIQUID
The usual dosage is 2 to 4 teaspoonfuls taken 4 times a day. Do not take more than 16 teaspoonfuls each 24 hours.
* REGULAR AND EXTRA-STRENGTH TABLETS
The usual dosage is 2 to 4 tablets taken 4 times a day. Take the tablets after meals and at bedtime, or as needed. Do not take more than 16 tablets each 24 hours.
Metoclopramide
"Antiemetic use: Metoclopramide is commonly used to treat nausea and vomiting (emesis).
Prokinetic use: Metoclopramide increases peristalsis of the jejunum and duodenum, increases tone and amplitude of gastric contractions, and relaxes the pyloric sphincter and duodenal bulb. These prokinetic effects make metoclopramide useful in the treatment of gastric stasis (e.g. after gastric surgery or diabetic gastroparesis), It is also used in gastroesophageal reflux disease (GERD/GORD)." see Wikpedia Metaclopromide.
The recommended metoclopramide dosage for people being treated for GERD is 10 or 15 mg four times daily.
Proton Pump Inhibitors (PPIs)
Esomeprazole (Nexium®), Lansoprazole (Prevacid®), Omeprazole (Prilosec®), Pantoprazole (Protonix®), Rabeprazole (Aciphex®)
When dyspepsia/ulcer/gastritis occurs following MGB the etiology is almost always a marginal ulcer or gastritis. We routinely recommend Avoiding inciting factors, using gastroprotective supplements (see above) and the use of initial trial of high dose PPI (Proton Pump Inhibitors) usually over the counter Prilosec 20 mg tablets, 2 tabs three times a day for 2 weeks.
Table 1
Proton Pump Inhibitors
Adult Maximum Daily Acute Dose
DRUG
MAXIMUM DOSE
Esomeprazole
(Nexium®)
erosive esophagitis: 40 mg/day
GERD: 20 mg/day
H. pylori eradication: 40 mg/day
Lansoprazole
(Prevacid®)
duodenal ulcer: 15 mg/day
gastric ulcer: 30 mg/day
gastric ulcer associated with NSAIDs: 30 mg/day
GERD: 15 mg/day
H. pylori eradication:
triple therapy – 60 mg/day
dual therapy – 90 mg/day
hypersecretory conditions: 180 mg/day
erosive esophagitis: 30 mg/day
Omeprazole
(Prilosec®)
duodenal ulcer: 20 mg/day
gastric ulcer: 40 mg/day
H. pylori eradication:
triple therapy – 40 mg/day in divided doses
dual therapy – 40 mg/day
hypersecretory conditions: 360 mg/day
GERD, esophagitis: 20 mg/day
upper GI bleeding risk reduction (Zegerid® only): 40 mg/day
Pantoprazole
(Protonix®)
erosive esophagitis associated with GERD: 40 mg/day
hypersecretory conditions: 240 mg/day
Rabeprazole
(Aciphex®)
duodenal ulcer: 20 mg/day
hypersecretory conditions: 120 mg/day
H. pylori eradication: 40 mg/day
GERD: 20 mg/day
erosive esophagitis: 20 mg/day
From MEDICAID DRUG USE REVIEW CRITERIA FOR OUTPATIENT USE
Safety note: A few studies have linked PPIs to a higher risk of pneumonia and infection with a bacterium called C. difficile, and in December 2006 a study found that long–term use of PPIs may be associated with an increased risk of hip fractures. Talk with your doctor about these risks, especially if you must take a PPI over a long period of time.
People aged 65 and over, and people with chronic medical conditions, who take a PPI should get vaccinated against pneumonia and get a flu shot every year.
Bile Reflux Gastritis.
The Mini-Gastric Bypass is a Billroth II Loop Gastrojejunostomy, that is to say the stomach is connected to the side of the small intestine, to the "loop" of small bowel. Many physicians fear the risk that this will lead to a very high incidence of bile reflux gastritis. Bile is a normal part of the digestion in the gut. It is poweful detergent and can irritate the stomach, especially if there is some acid damage to the lining of the stomach from an acid ulcer or gastritis. In most MGB cases anti-ACID therapy resolves the ulcers and gastritis that follows the surgery but in some cases attention to the bile can be helpful as well.
Several treatments have been found to aide in decreaseing the irritaion caused by the detergent bile in the stomach. Lowered recirculation of bile acids results in utilization of cholesterol to synthesize bile acid and reduced fat absorption.
1. Actigall (ursodeoxycholic acid)
which changes bile acid composition. This is less irritating than the patient's own bile acids on the gastric remnant. In a study by Stefaniwsky AB, Tint GS, Speck J, Shefer S, Salen G. "12 patients with symptomatic alkaline (bile) reflux gastritis were treated for 1 mo with placebo and for 1 mo with ursodeoxycholic acid, 1000 mg/day. Before treatment, all patients were symptomatic and manifested epigastric pain, nausea, and bilious vomiting. The gastric mucosa was erythematous, friable, and bile stained, and the histology revealed chronic inflammation. No significant change in symptoms was noted during administration of placebo. In contrast, ursodeoxycholic acid treatment resulted in a profound decrease in the intensity and frequency of pain and almost abolished nausea and vomiting. During bile acid therapy the proportion of ursodeoxycholic acid in gastric bile rose to 50% of total bile acids, whereas cholic and deoxycholic acids decreased and chenodeoxycholic acid remained unchanged."
2. Cholestyramine
Cholestyramine resin adsorbs 90+% of all bile salts tested. The addition of cholestyramine to duodenal contents inhibits their ulcerogenic action of bile in the stomach of rats challenged by bile and acid. "Cholestyramine protects the gastric mucosa from ulceration by blocking the barrier breaking action of bile salts" The recommended maintenance dose for all QUESTRAN powdered products is 2 to 4 packets or scoopfuls daily (8-16 grams anhydrous cholestyramine resin) divided doses. The recommended starting dose is 1 single-dose packet or 1 level scoopful, 1 to 2 times daily.
3. Fiber
Citrucel (cellulose) has been reported as the most active in capturing and inactivating biliary acids: this constitutes a cytoprotective action on the stomach mucosa. In a study by Paniagua M, Piñol F, and Cendan A. "50 patients with bile reflux gastritisreceived cellulose 5 g/day during three months. The results showed that total biliary acids in gastric content decreased at the end of treatment mostly in patients treated with cellulose..." "there was a an excellent response in pain, vomiting and heartburn after cellulose treatment."
4. Aluminum Containing Antacids
Aluminum Containing Antacids can bind bile acids.
Many antacids are available today that contain aluminum hydroxide.
* Aluminum carbonate (Basaljel)
* Aluminum hydroxide (ALternaGEL, Alu-Cap, Alu-Tab, Amphojel, Dialume, Nephrox)
* Aluminum hydroxide/magnesium carbonate (Duracid)
* Aluminum hydroxide/magnesium hydroxide (Alamag, Almacone, Aludrox, Gaviscon Liquid, Gelusil, Kudrox, Maalox, Magalox, Mintox, Mylanta, Rulox)
* Aluminum hydroxide/magnesium hydroxide/calcium carbonate (Tempo)
* Aluminum hydroxide/magnesium trisilicate (Alenic Alka, Gaviscon, Genaton, Foamicon)
5. Sucralfate Carafate
A drug used to treat ulcers. It adheres to proteins at the ulcer site and forms a protective coating over the ulcer. Sucralfate also binds bile acids and may be useful in treat bile reflux gastritis. The recommended adult oral dosage for duodenal ulcer is 1 g four times per day on an empty stomach.
6. Green and Leafy Vegetables
In a study by Kahlon TS, Chiu MC, Chapman MH at Western Regional Research Center, USDA-ARS, Albany, CA found that "relative to cholestyramine, in vitro bile acid binding was for the collard greens, kale, and mustard greens, 13%; broccoli, 10%; Brussels sprouts and spinach, 8%; green bell pepper, 7%; and cabbage, 5%.
"Steam cooking significantly improved the bile acid binding of collard greens, kale, mustard greens, broccoli, green bell pepper, and cabbage compared with previously observed bile acid binding values for these vegetables raw (uncooked).
"Inclusion of steam-cooked collard greens, kale, mustard greens, broccoli, green bell pepper, and cabbage in our daily diet as health-promoting vegetables should be emphasized. These green/leafy vegetables, when consumed regularly after steam cooking, would lower the risk of cardiovascular disease and cancer, advance human nutrition research, and improve public health."
Other Gastroprotective Agents:
Amino Acids:
7. Taurine
Protective effect of taurine against alendronate-induced gastric damage in rats.
Sener G, Sehirli O, Cetinel S, Midillioğlu S, Gedik N, Ayanoğlu-Dülger G. Fundam Clin Pharmacol. 2005 Feb;19(1):93-100.
Alendronate (Fosamax) causes serious gastrointestinal adverse effects.
The aim of this study was to investigate whether taurine, a semi-essential amino acid and an antioxidant, improves the alendronate-induced gastric injury.
Rats were administered 20 mg/kg Alendrolate by gavage for 4 days, either alone or following treatment with Taurine (50 mg/kg, i.p.).
On the last day of treatment, following drug administration, pylorus ligation was performed and 2 h later, rats were killed and stomachs were removed.
Gastric acidity and tissue ulcer index values, lipid peroxidation and glutathione (GSH) levels, myeloperoxidase (MPO) activity as well as the histologic appearance of the stomach tissues were determined.
Chronic oral administration of Alendrolate induced significant gastric damage, increasing lipid peroxidation, MPO activity and collagen content, as well as decreasing tissue GSH levels.
Treatment with Taurine prevented the damage and also the changes in biochemical parameters.
Findings of the present study suggest that Alendrolate induces oxidative gastric damage by a local irritant effect, and that Taurine ameliorates this damage by its antioxidant and/or membrane-stabilizing effects.
Modulation of indomethacin-induced gastric injury by spermine and taurine in rats.
Motawi TK, Abd Elgawad HM, Shahin NN. J Biochem Mol Toxicol. 2007;21(5):280-8.
This study investigated the involvement of neutrophil infiltration, nitric oxide (NO) generation, and oxidative stress in indomethacin-induced ulcer and the possible gastroprotective potentials of taurine, known for antioxidant effects.
Rats were allocated into a normal control group, ulcer control group (received a single dose of indomethacin 40 mg-kg p.o.), and ulcer group pretreated with taurine (250 mg-kg i.p. for three consecutive days before ulcer induction).
6 h after indomethacin administration, and the gastric juice, serum, and mucosal tissue were used for gastric injury evaluation.
Taurine significantly ameliorated the indomethacin-induced gastric lesions in glandular mucosa.
Taurine was able to decrease the elevated levels of gastric myeloperoxidase, conjugated diene, and serum NO. The lowered tissue NO content was markedly elevated by taurine.
The antioxidant action of taurine was illustrated by restoration of the depressed content of glutathione, normalization of the inhibited activities of glutathione reductase, and superoxide dismutase.
These results suggest that taurine confers significant gastroprotection against indomethacin-induced gastric injury
Effect of taurine on ulcerogenic response and impaired ulcer healing induced by monochloramine in rat stomachs.
Kato S, Umeda M, Takeeda M, Kanatsu K, Takeuchi K. Aliment Pharmacol Ther. 2002 Apr;16 Suppl 2:35-43.
BACKGROUND: It is well known that neutrophil-derived hypochlorous acid interacts with ammonia (NH4OH) to generate monochloramine (NH2Cl) and that NH2Cl irritates the gastric mucosa and impairs ulcer healing.
AIM: To examine the effect of taurine, a hypochlorous acid scavenger, on the mucosal ulcerogenic and the impaired healing response induced by NH2Cl in rat stomachs, in comparison with those of methionine and glycine.
METHODS AND RESULTS: Under anaesthesia, oral administration of NH2Cl (120 mmol/L) produced severe lesions in male Sprague-Dawley rat stomachs.
Taurine (10-100 mg/kg) given p.o. 30 min prior to NH2Cl dose-dependently prevented these lesions in response to NH2Cl.
This action was mimicked by methionine (3-30 mg/kg) but not by glycine (10-100 mg/kg).
Under urethane anaesthesia, mucosal exposure to NH4OH (120 mmol/L) caused a marked reduction of potential difference (PD) in the ex vivo chambered stomachs after induction of ischaemia, resulting in severe lesions.
These ulcerogenic and PD responses by NH4OH plus ischaemia were also mitigated by taurine and methionine, but not glycine, applied to the chamber 20 min before the onset of NH4OH plus ischaemia.
Moreover, oral administration of 100% ethanol produced severe haemorrhagic lesions in rat stomachs, all of which rapidly healed within 7 days after lesion induction.
Daily administration of NH2Cl (20 mmol/L) significantly delayed the healing of these lesions, but recovery of this impaired healing response was obtained by concurrent administration of taurine.
Both taurine and methionine showed a potent scavenging effect against NH2Cl in vitro.
CONCLUSIONS: (1) NH2Cl generated either exogenously or endogenously damages the gastric mucosa and impairs the healing response;
(2) taurine exerts a prophylactic effect against the deleterious effects of NH2Cl, mainly due to its scavenging action against NH2Cl; and
(3) this effect of taurine may be useful for treatment of gastritis associated with Helicobacter pylori infection.
Effect of taurine on gastric oxidative stress and hemorrhagic erosion in brain ischemic rats.
Hung CR. Chin J Physiol. 2006 Jun 30;49(3):152-9.
The effect of taurine on gastric hemorrhage and mucosal erosion in the brain ischemia is unknown.
The aim of the research was to study the involvement of gastric oxidative stress in hemorrhagic erosion produced in brain ischemia rats.
The protective effect of taurine on this erosion model was evaluated.
Male Wistar rats were deprived of food for 24 h. Under chloral hydrate -anesthesia, bilateral carotid artery ligation was performed 12, 18 and 21 h after removal of food to obtain 12, 6 and 3 h of brain ischemia duration.
The pylorus and carotid esophagus of rats also were ligated. The stomachs were then irrigated for 3 h with normal saline or simulated gastric juice containing 100 mM HCl plus 17.4 mM pepsin and 54 mM NaCl. The stomach was dissected. Gastric samples were harvested. The rat brain was dissected for examination of ischemia by using triphenyltetrazolium chloride staining method.
Changes in gastric ulcerogenic parameters, such as decreased mucosal GSH level as well as enhanced gastric acid back-diffusion, mucosal lipid peroxide generation, histamine concentration, luminal hemoglobin content and mucosal erosion in gastric samples were measured.
The results indicated that bilateral carotid artery ligation could produce severe brain ischemia in rats.
Moreover, a brain ischemia- duration-dependent exacerbation of various ulcerogenic parameters also was observed in these rats.
Intraperitoneal taurine (0-300 mg/kg) dose-dependently ameliorated gastric oxidative stress and hemorrhagic erosion in brain ischemia rats.
Taken together, brain ischemia could produce gastric oxidative stress and hemorrhagic erosions that was ameliorated by taurine through stimulation of GSH biosynthesis and inhibition of oxidative stress.
Taurine ameliorates water avoidance stress-induced degenerations of gastrointestinal tract and liver. Zeybek A, Ercan F, Cetinel S, Cikler E, Sağlam B, Sener G. Dig Dis Sci. 2006 Oct;51(10):1853-61.
We investigated the role of taurine, is a potent free radical scavenger, on water avoidance stress-induced degeneration of the gastric, ileal, and colonic mucosa and liver parenchyma.
Wistar rats were exposed to chronic water avoidance stress (water avoidance stress group) 2 hr daily for 5 days. After exposing animals to chronic water avoidance stress (water avoidance stress + taurine group), 50 mg/kg taurine was injected IP for 3 days. Control animals received vehicle solution only.
The stomach, ileum, colon, and liver samples were investigated under light microscope for histopathologic changes.
To demonstrate the topography of the luminal mucosa of the stomach, ileum, and colon, scanning electron microscope was used and for hepatocyte ultastructure transmission electron microscope was used. Malondialdehyde (MDA, a biomarker of oxidative damage) and glutathione (GSH, a biomarker of protective oxidative injury) levels were also determined in all tissues.
In the water avoidance stress group, the stomach epithelium showed ulceration in some areas, dilatations of the gastric glands, and degeneration of gastric glandular cells; prominent congestion of the capillaries was apparent.
In the water avoidance stress group, severe vascular congestion was observed along with degeneration of ileal and colonic epithelium.
Prominent vascular congestion and dilated sinusoids, activated Kupffer cells, dilated granular endoplasmic reticulum membranes, and focal pyknotic nuclei were observed in liver parenchyma. MDA levels (stomach, P < 0.01; ileum, colon, and liver P < 0.05) were increased and GSH levels (P < 0.01) were decreased in all tissues in the water avoidance stress group compared with the control group.
The morphology of gastric, ileal, and colonic mucosa and liver parenchyma in the water avoidance stress + taurine group (stomach and ileum, P < 0.05; colon and liver, P < 0.01) showed a significant amelioration when compared to the water avoidance stress group. Increased MDA and decreased GSH levels in the water avoidance stress group were ameliorated with taurine treatment.
Based on the results, taurine supplementation effectively attenuates the oxidative damage of gastrointestinal mucosa and liver because of water avoidance stress induction possibly by its antioxidant effects.
posted by DrR @ 9:49 PM
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