Mini-Gastric Bypass, Simple & Successful
HI all,
I had the mgb in Jan 04 with Dr. R. I have been having some hearburn and at times have difficulty swallowing (getting food down). I had and endoscopy this morning AND the gastroenterologist was very impressed with my mgb. I have a SMALL hernia that floats and anxiety causes tightening and it traps food. As stress decreases it has been a lot less. Said he is extremely impressed with my mgb and how my stomach looks. No sign of any damage to stomach etc. The nurse in the procedure room took done the information on the mgb and the website for her husband.
I initially lost 200 lbs and have gained back 15-20 lbs. I went from a size 28-30 to a size 6-8. I can live with that. Had dropped 10 lbs of the 20 I put on but just came back from a cruise. Felt like I ate a lot but those with me said no you take a lot on your plate and only sample each thing.
Had a friend that had a Roux Y a year before my mgb. She has sadly put back on most of her weight. Just wanted to thank Dr. R. for his good work and let you all know how it is 5 1/2 years out.
Blessings,
Susan
http://ping.fm/LGTSS The Mini-Gastric Bypass Out Performs Other Surgery!
The Mini-Gastric Bypass Out Performs Other Surgery at IFSO!
New Randomized Controlled Prospective studies to be presented in Paris (International Federation for the Surgery of Obesity and metabolic disorders. XIV World Congress
Paris, France August 26-29, 2009) show the MGB out performed the RNY, the LapBand and the Sleeve Gastrectomy.
Amazing New Findings! New studies to be presented at the Paris Meeting for the International Federation for Surgery of Obesity and Metabolic Diseases show that in a controlled prospective 5 year trial the MGB is better than the RNY gastric bypass.
In other studies the MGB out performed the Band and the Sleeve in weight loss, quality of life and in the treatment of diabetes.
Amazing New Findings! New studies to be presented at the Paris Meeting for the International Federation for Surgery of Obesity and Metabolic Diseases show that in a controlled prospective 5 year trial the MGB is better than the RNY gastric bypass.
In other studies the MGB out performed the Band and the Sleeve in weight loss, quality of life and in the treatment of diabetes.
http://ping.fm/hi5ngMGB Better than the Lap Band
MGB Better than the Lap Band and the Sleeve
2 years after surgery the Mini-Gastric Bypass had better results than other bariatric surgeries (Lapband or sleeve gastrectomy).
P-110 Comparison of Gastrointestinal Quality of Life Following Laparoscopic Mini-Gastric Bypass, Sleeve Gastrectomy and Adjustable Gastric Banding Surgery
Presenter: Y. H. Su (Min-Sheng General Hospital, Taoyuan, Taiwan)
Co-authors: K. Ser1, J. Chen1, W. Lee1
1Min-Sheng General Hospital Taoyuan Taiwan
Background
Laparoscopic Mini-Gastric Bypass (MGB), sleeve gastrectomy (LSG) and adjustable gastric banding (LAGB) surgeries are currently recommended procedures for morbid obesity.
Previous studies disclosed a significant improvement in the health-related and gastrointestinal quality of life among each specific surgery.
However, there has been no comparative data regarding the specific gastrointestinal quality of life between different procedures.
Methods
From October 2001 to Dec 2006, 640 consecutive patients with morbid obesity underwent different procedures
(Mini-Gastric Bypass: 423 patients;
sleeve gastrectomy: 110 patients;
LABG: 107 patients).
The mean body weight (BW), body mass index (BMI), and Gastrointestinal Quality Of Life Index were recorded and compared before operation and at 3, 6, 12 and 24 months after surgery.
Results
All procedures were completed laparoscopically and the three different surgeries were successful in weight loss in morbidly obese patients.
Patients underwent Mini-Gastric Bypass and sleeve gastrectomy had similar mean BW loss and BMI reduction at 1-year after surgery (27.9 kg/m2 and 23.7 kg/m2 respectively).
However, the BMI in sleeve gastrectomy and gastric banding groups began to increase after 1 year and only mini-gastric bypass group showed persistent and steady decrease in BMI.
The overall Gastrointestinal Quality Of Life Index improved significantly 2 years after Mini-Gastric Bypass (106.1 → 115.2; P < 0.05) between groups.
The adjustable gastric banding group only disclosed short-term benefit along with BW loss in one year, then the value returned to similar values before surgery.
Conclusion
The overall Gastrointestinal Quality Of Life Index improved significantly 2 years after Mini-Gastric Bypass.
The adjustable gastric banding group only had short-term benefit
At one year, the quality of life value and the Body Weight values returned to values before surgery.
With follow up of 2 years, the overall values all declined and the sleeve gastrectomy group had the worst result.
2 years after surgery the Mini-Gastric Bypass had better results than other bariatric surgeries (Lapband or sleeve gastrectomy).
However, each patient still should be individualized for the bariatric surgeries according to the patient’s decision.
http://ping.fm/I6R0JJul 31, 7:00 pm and Aug 01, 12:00 am Action Hero Makeover, Discovery Health
Gil Gerard, former Hollywood heartthrob, undergoes a lifesaving but controversial new gastric bypass procedure in order to reclaim his health and restart his career. Will this be the solution he's been looking for?
http://ping.fm/bu6BXMy surgery was on Sept 12, 2007. I can't believe it's almost 2 years. I think
Dr. Rutledge is wonderful and I suggest him to anyone considering weight loss
surgery. I was all set for a RouxNY when I felt it was not right. I did more
research and came across the Centers for weight loss surgery. They have all been
very helpful and friendly. After meeting Dr. Rutledge and the staff in
Henderson, I knew I had found what I wanted to do. I spent almost 6 months doing
my packet because I had to find funding for my surgery, and finally, I was able
to do it. The hospital staff and equipment was all up to date and they made
everything as convenient and comfortable as it could be (they were under
construction of some type at the time) I had a roommate in my room, which I
originally thought would be bad but it turned out good to have someone that
close who was in my same situation. My surgery was 28 minutes and he bypassed
about seven and a half feet.
http://ping.fm/tvojYWOW. Smiling from ear to ear. Today I joined the Onederland club.
I am 5.5 months out. Down 93 pounds. I don't look like my old self. I don't
feel like my old self. I don't eat like my old self. I am not addicted to food
like my old self. I am healthier than my old self. I am happier than my old
self. I don't miss my old self!
I have no regrets. It hasn't been and still is not always easy. I am still
learning and adjusting but oh my! I had fears about this before I did it. I,
however, was ever turning back from the decision.
I work out because I love it....no longer because it's the only way to gain
weight slower. I eat because my body needs food. I eat what I want. I don't
worry about obesity anymore. I don't dread a day when I will gain it all back.
I enjoy clothes shopping (although I don't do it much because I will be too
small for what I buy in a few weeks). I just passed my motorcycle test!
wooooot Yes I'm a biker chick now! I look hot on my ACE..hehe. I don't see
people looking at me anymore. I don't feel looked over at places because of my
weight.
Life is glorious in Onederland! Thank you is too mundane.
Barb
Dr. R
2/18/09
292 pre op
199 now
goal ..who knows...maybe 180..maybe 150 let's see
7 feet
34 min
5 foot 5 in
Laparoscopic Mini-Gastric Bypass Versus Roux-En-Y Gastric Bypass: 5-Year Results and Final Report of a Randomized Trial
Presenter: W. J. Lee (Min-Sheng General Hospital, Taoyuan, Taiwan)
Co-authors: J. Chen1, K. Ser1
1Min-Sheng General Hospital, Taoyuan, Taiwan
Background We had previously reported a randomized study evaluated the surgical morbidity and 2-year results of laparoscopic mini-gastric bypass (LMGBP) versus laparoscopic Roux-en-Y gastric bypass (LRYGBP). We now reported the final result after 5-year follow-up.
Methods 282 patients received LMGBP for the treatment of morbid obesity were recruited from our comprehensive obesity surgery center and compared with 40 patients received LRYGBP who were included in the previous randomized trial. Minimum follow-up was 5 years (from 5 to 8 years). The changes in body weight loss, BMI, quality of life and late complication were determined at follow-up. . Changes in quality of life were assessed using the Gastro-Intestinal Quality of Life Index (GIQLI).
Result There was no difference in preoperative clinical parameters between the two groups. All procedures were successfully carried out with no deaths in either group.
Surgical time was significantly longer for LRYGBP (205 minutes vs. 148 minutes for LMGBP, p < 0.05).
The complication rate was higher for LRYGBP (20% vs. 7.5%, p < 0.05).
Excess weight loss and mean BMI at 5 years for LRYGBP and LMGB were 60.1% vs. 72.1%, p = 0.072) and (29.2 vs. 27.1, p = 0.30) separately.
Post-operative GQILI increased significantly after operation in both groups without difference.
Late complications and revision rates were similar in the two groups.
Follow-up study disclosed an improvement of obesity-related clinical parameters in both groups without significant difference.
Conclusion This study demonstrates that LMGBP is an effective treatment for morbid obesity and can improve quality of life similar to LRYGBP. LMGBP is simpler and safer procedure than LRYGBP and no proven disadvantage after five year follow-up. LMGBP can be regarded as a simpler and safer alternative surgical procedure to LRYGBP.
Conclusion This study demonstrates that LMGBP is an effective treatment for morbid obesity and can improve quality of life similar to LRYGBP. LMGBP is simpler and safer procedure than LRYGBP and no proven disadvantage after five year follow-up. LMGBP can be regarded as a simpler and safer alternative surgical procedure to LRYGBP
Sleve Gastrectomy More Dangerous than MGB
Perforation and leaks(3.15%), intraluminal bleeding(2.72%) and hemoperitoneum(2.15%) were the more frequent complications, out of the total complication rate of 11.46%. Mortality was reported in 6/698(0.85%) patients, 3 of which received multiple reoperations and subsequently died of respiratory complications and sepsis.
Sleeve Gastrectomy more dangerous than MGB
Result The total study cohort contains more than 6000 patients. From January 2006 to December 2008, more than 500 sleeve gastrectomy procedures were performed in the 17 hospitals participating in the study. The mean body mass index (BMI) of all patients was 48.8 kg/m2. The BMI of patients undergoing SG was 54.5 kg/m2. In total, 73.8% of the patients were female and 26.2% of the patients were male. There were no significant differences between patients undergoing SG. The general complication rate after SG was 14.1%, and the surgical complication rate was 9.4%. The postoperative mortality rate was 1.4%.
Opiod Sparing Anesthesia in Mini-Gastric Bypass Using Dexmedetomidine, Ketamine and Remifentanil, Propofol Total Intravenous Anesthesia (TIVA)
Presenter: R. Rutledge (Centers for Laparocopic Obesity Surgery, Henderson, United States of America)
Background Anesthetic management of morbidly obese patients is problematic with particular concerns re: difficult airway, respiratory depression/failure and post operative nausea and vomiting (PONV). Opiod sparing techniques may allow improved management of these difficult patients.
Methods Mini-Gastric Bypass MGB patients were treated with either TIVA (remifentanil & propofol) with (TKD) or without (TNO) opiod sparing doses of supplemental ketamine (50-100 mg) and dexmedetomidine (100 μg IV over 10 minutes.) We compared post-anesthetic recovery analogue pain score (APS) and narcotic use (# of doses), post operative nausea and vomiting (PONV) and overall patient satisfaction.
Result Over a two year period 720 patients underwent MGB, 343 TKD patients and 377 TNO patients. The mean age 39 + 8, 85% female, mean BMI 45 + 7, mean operative time 39 + 5 min. No patient required reintubation for respiratory depression. In comparing the two groups the TKD patients had: significantly lower mean APS, fewer doses of rescue narcotics, a higher mean respiratory rate in recovery room, less PONV and higher levels of patient satisfaction.
Conclusion Morbidly obese patients present a serious anesthetic challenge to the surgeon and anesthesiologist. The short operative time of the Mini-Gastric Bypass (39 min) allows the use of opiod sparing techniques that decrease respiratory depression and PONV caused by narcotics. This decreases the need for narcotics, improves pain score, decrease PONV and improves overall patient satisfaction.
Laparoscopic gastric banding is a simple and safe ... Still, it results in overall < 50% of Excess Weight Loss in both short and long term follow up and is accompanied by a significant reoperation rate either due to complications or due to treatment failure. ** Thus, LAGB should no longer be considered as the procedure of choice for obesity and reliable selection criteria must be developed for its use if at all.***
Long-Term Results After Laparoscopic Gastric Banding for Morbid Obesity. 13 Years Follow Up in a Single University Unit
Presenter: A. Konstantinos (Bichat Claude Bernard Hospital, Paris, France)
Co-authors: A. Lasati1, K. Sandrine1, P. Mongol1, D. Chosidow 1, K. Sandrine1, R. Lara1, J. P. Marmuse1
1Bichat Claude Bernard Hospital Paris France
http://ping.fm/b4lz6I had the MGB in Florida under Dr. P almost 2 years ago. The steps
initially seemed daunting, but once I sat down and did it, it was
easy. It made me appreciate that there was a doctor who actually
wanted me informed about bariatric surgery and wasn't just ready to
operate when I paid the money. All of the claims on the CLOS website
were almost like "it's too good to do be true"... but I can say it has
been one of the best decisions of my life.
I was 355 pounds and miserable. I was proud of what I did, but I
wasn't proud of myself. My back was hurting and I knew if I didn't
get my weight down, I would be facing yet a second back operation.
On August 28th of 2007 I had the surgery and each day has been an
incredible journey. I went from 355 pounds, size 48 pants to 180
pounds and 34 pants.
There are times I wish I was a multi-millionaire and I'd pay for all
my obese friends to have the same life changing experience.
My biggest let down was that our insurance refused to cover it. We
pulled the money out of retirement savings but my theory was this...
"If like keeps like this, I'm not sure I'll even make it to retirement
age. Even if I do, I'm not going to enjoy it. So let's just bite
the bullet now."
I can say unequivocally, that every day of the last 2 years I haven't
had one minute of regret of doing the MGB. Go for it! It'll change
your life.
Les
My monthly progress
01/28/09 = 232
02/28/09 = 215 and 14.25 Inches Down
03/28/09 = 207 and 23.5 Inches Down
04/28/09 = 199 and 29.5 Inches Down
05/28/09 = 194 and 31 Inches Down
06/28/09 = 188 and 37.25 Inches Down
07/17/09 = 186 and 37.25 Inches Down
Karen
January 28, 2009
Dr R in Vegas
7 Feet Bypass
52 Minutes I Think?
276 High / 232 Pre-op / 186 Now / 125 Goal
My monthly progress
01/28/09 = 232
02/28/09 = 215 and 14.25 Inches Down
03/28/09 = 207 and 23.5 Inches Down
04/28/09 = 199 and 29.5 Inches Down
05/28/09 = 194 and 31 Inches Down
06/28/09 = 188 and 37.25 Inches Down
07/17/09 = 186 and 37.25 Inches Down
Karen
January 28, 2009
Dr R in Vegas
7 Feet Bypass
52 Minutes I Think?
276 High / 232 Pre-op / 186 Now / 125 Goal
Hi Gina,
This was easy since I already had this as part of my contact letter here you go:
Started 279
One week -12 lbs. 267
One month -26 lbs. 253
Two months -37 lbs. 242
Three months -49 lbs. 230
Four months -59 lbs. 220
Five months -72 lbs. 207
Six months -80 lbs 199
Seven months -90 lbs. 189
Eight months -96 lbs. 183
Nine months -102 lbs. 177
Ten months -109 lbs. 170
Eleven months -115 lbs. 164
Twelve months -118 lbs. 161
Thirteen Months -121 lbs. 158
Fourteen Months -124 lbs. 155
Fifteen Months -125 lbs. 154
Sixteen Months -129.5 149.5
Seventeen Months -134 lbs. 145
Eighteen Months -136 lbs. 143
Nineteen Months -139 lbs. 140
Twenty Months -140.5 138.5
Twenty-one Months -141.5 lbs. 137.5
Twenty-two Months -141 lbs. 138
Twenty-three Months -141 lbs. 138
Two Years -145 lbs. 134
Two and ½ yrs -148 lbs. 131
Three Years -146 lbs. 133
Sunday is my three year anniversary! WooHoo!
Regie in FL
7/19/2006
Dr. D
5'3", 6'bp
Flaxseed consumption influences endogenous hormone concentrations in postmenopausal women.
Hutchins AM, Martini MC, Olson BA, Thomas W, Slavin JL.
Department of Food Science and Nutrition, University of Minnesota, St. Paul, MN 55108, USA.
Lignans, similar in structure to endogenous sex steroid hormones, may act in vivo to alter hormone metabolism and subsequent cancer risk.
The objective of this study was to examine effects of dietary intake of a lignan-rich plant food (flaxseed) on serum concentrations of endogenous hormones and binding proteins (estrone, estrone sulfate, 17 beta-estradiol, sex hormone-binding globulin, progesterone, prolactin, dehydroepiandrosterone sulfate, dehydroepiandrosterone, androstenedione, testosterone, and free testosterone) in postmenopausal women.
This randomized, crossover trial consisted of three seven-week feeding periods, during which 28 postmenopausal women, aged 52-82 yr, consumed their habitual diets plus 0, 5, or 10 g of ground flaxseed. Serum samples collected during the last week of each feeding period were analyzed for serum hormones using standard diagnostic kits.
The flaxseed diets significantly reduced serum concentrations of
17 beta-estradiol by 3.26 pg/ml (12.06 pmol/l) and
estrone sulfate by 0..09 ng/ml (0.42 nmol/l) and increased prolactin by 1.92 micrograms/l (0.05 IU/ml).
Serum concentrations of androstenedione, estrone, sex hormone-binding globulin, progesterone, testosterone, free testosterone, dehydroepiandrosterone, and dehydroepiandrosterone sulfate were not altered with flaxseed feeding.
In this group of postmenopausal women, consuming flaxseed in addition to their habitual diets influenced their endogenous hormone metabolism by decreasing serum 17 beta-estradiol and estrone sulfate and increasing serum prolactin concentrations.
Nutr Cancer. 2001;39(1):58-65.
Hello Everyone.
Some of you know my story. My main regret is getting the lap band. After 2 years with it in I had a revision to MGB and I now weigh 330. I am going in for an MGB revision on July 29th. I still have not heard about anyone having surgery that week. Anyone out there for July 29th?
Thanks,
Van
Merry, you do what you think will work for you. If you can stick to the Weight Watchers diet and lose the weight, then by all means do it. I have tried Weight Watchers, Jenny Craig, Nutri-System, Medifast, etc., and I gained the weight back every single time. I became very discouraged because personally, my weight came off very slowly and I was still so large that it was very difficult to effectively exercise. I was embarrassed to go to the gym and would always say, "I'll go when I've lost a little more weight." My joints hurt from arthritis so badly that it was difficult to walk, and especially when I would develop plantar fasciitis. I had to wear orthotics in my shoes, had cortisone injections into the plantar fascia, and would always give up the fight. I didn't mention that hypertension and diabetes also played a big role in my lack of motivation. I was SO tired all the time. I would take a nap every day between 2 and 3 p.m...you
could set your watch by it! Now, I can go all day long and feel fantastic.
Looking back at my lifetime struggle with weight, there was only one time that I actually lost a significant amount. I worked for Richard Simmons as an instructor at the Anatomy Asylum in Aurora, CO. I had gotten a job there working in the nursery to help pay for my membership, as we were a young couple with three small children and my husband was attending graduate school, and money was tight. As I was losing weight, I was asked to train so I could teach the "overweight" aerobic classes. Some of the women in that class weighed close to 400 pounds, so naturally the routine was simpler and less demanding. I was able to work out 3-4 times a week for an hour, sometimes twice a day, and I did lose around 40 pounds; however, it wasn't just the exercise that caused the weight loss, it was because I put myself on a 500 calorie-a-day diet eating some type of protein bar for two meals a day, then a salad with a little tuna or grilled chicken for
dinner. Heck, I would have lost weight on the diet alone, without the exercise...I was REALLY hungry all the time. Surprisingly, I found myself expecting our 4th child after losing from 180 down to 139-ish and guess what...I gained every single pound back during my high-risk pregnancy where I was put on complete bed rest for 6 months. And, after that pregnancy, I weighed more than I ever had.
Yes, the weight loss does slow down with the MGB, but what I found was the initial large amount of weight I lost was very encouraging and motivating. I can walk, jog, and have just started Pilates, which I absolutely LOVE. A year ago, I couldn't perform any of these activities.
I don't know what diet you could go on where in 12 months' time you would lose 100 pounds or more (depending on your beginning weight and length of bypass) without feeling hungry and having uncontrollable cravings. For me, losing my craving for food has been the biggest blessing of all. At 7 to 8 months out, you will start craving some of the bad "old" foods you were used to eating, but this is the period of time where you need to train yourself to eat good foods! This surgery is a tool, and you still need to change your thinking when it comes to food. I have to say that this "tool" is very powerful and it certainly hasn't taken much effort on my part. I keep plenty of veggies cut up in the fridge to nibble on, as well as fresh fruit. Last night I cut up a cantaloupe and half a watermelon, and I always have grapes, apples, or strawberries for when I get a sweet tooth and feel that craving for a little sugar. I also find when I
increase the protein in my diet, I lose that craving for sugar and I also lose better.
Bottom line, this surgery has been a blessing and Dr. Rutledge has given me a second lease on life. I am so happy and feel SO fantastic...I can't sing his praises enough! BUT, it is you who has to feel good about your decision, and we will all support you either way!
Best wishes,
Holly
Ulcers Gastritis and Indigestion Dyspepsia (Indigestion) After the Mini-Gastric Bypass (Also see Gastritis, ulcer(s), indigestion, heartburn, acid stomach, upset stomach, unsettled stomach, stomachache ..., also see Bile Reflux, Esophageal Reflux, GERD Gastro Esophageal Reflux Disease...
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.
Hospitalization before and after mini-gastric bypass surgery,
The mini-gastric bypass (MGB) was developed to address some of the limitations of the Roux-en-Y gastric bypass (“RNY”). The RNY has recently been reported to increase the need for hospitalization for complications after RNY surgery.
To determine the rates and indications for inpatient hospital use before and after MGB in comparison to similar rates in RNY.
The study is a self reported retrospective study of patients from across the United States receiving MGB in Centers for Excellence in Laparoscopic Obesity Surgery (“CELOS”) hospitals from 2000 to 2005.
Complications and hospitalization in the year before and in the 1 to 5years after MGB.
1069 patients who underwent MGB were selected for study. The rate of hospitalization in the year following MGB was 67% of the rate in the year preceding MGB (11% vs. 17%, P
Hospitalization before and after mini-gastric bypass surgery, Abstract
The mini-gastric bypass (MGB) was developed to address some of the limitations of the Roux-en-Y gastric bypass (“RNY”). The RNY has recently been reported to increase the need for hospitalization for complications after RNY surgery.
To determine the rates and indications for inpatient hospital use before and after MGB in comparison to similar rates in RNY.
The study is a self reported retrospective study of patients from across the United States receiving MGB in Centers for Excellence in Laparoscopic Obesity Surgery (“CELOS”) hospitals from 2000 to 2005.
Complications and hospitalization in the year before and in the 1 to 5years after MGB.
1069 patients who underwent MGB were selected for study. The rate of hospitalization in the year following MGB was 67% of the rate in the year preceding MGB (11% vs. 17%, P<0.001). The most common reasons for admission prior to MGB were general medical problems (38%) obstetric and Gynecological issues (36%), orthopedic problems (16%), gallbladder surgery (9%) and renal stones in 2%. The most common reasons for hospital admission after MGB were complications from surgery (29%), gallbladder surgery (20%), renal stones (14%), plastic surgery procedures (11%), appendectomy (9%), Gynecologic issues (9%) and orthopedic problems (6%). Thus while MGB complications made up a third of hospital readmissions following MGB surgery the over all hospitalization rates declined significantly.
Previous studies have demonstrated that hospitalization after RNY gastric bypass increases remarkably (20% per year). The present study shows that hospitalization following MGB instead of rising, as reported with RNY, decreases by a third. The MGB has been shown to be a short, safe successful weight loss surgery in previous work. The present study supports the MGB as a low risk procedure that decreases the need for hospitalization.
Dr. Rutledge, I am sure u don't remember me- I was gpingbto have surgery with you but broke mynleg which left me out of the running(so to speak) atva chance of having anMGB. I had ryn 2 years later(differentsurgeon) and have ended up with serious problems. my colon was knicked-peritonitis,bled out 2x,reap failure2-4x,comas, high grade fevers,holes didn't heal for over 18 months( 14 of that in a hospital. I still have extreme pain and difficulty when of comesbtoeating..any suggestions? I'm tired of not being able to eat a meal because it will make me feel nautios after and maybe get sick. I do this every day after day. just want some relief
Dear Dr. Rutledge,
I had lap band surgery 3 years ago and an unhappy with my choice. I have had no problems with the band, other than I cannot lose weight, and am gaining. It varies in it's tightness from hour to hour.
I met a patient of yours this weekend, Robyn R. She recommended you to me.
My question is, how much would it cost for you to remove my lap band, and do a mini gastric bypass? I am an otherwise healthy 56 year old woman. I weight 228 and am 5'6". I love in CA.
I am still paying for my lap band. It cost $17,600. I chose the wrong surgery and the wrong surgeon. He berates me whenever I go in for a fill or a visit, therefore, I don't want to go.
Please let me know if this is a possibility. I have a lot of friends who got lap band too, who are unhappy also. Thank you for your time.
Nina
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
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.
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.
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
http://sites.google.com/a/clos.net/mini/ulcers-gastritis-and-indigestionUlcers Gastritis and Indigestion Dyspepsia (Indigestion) After the Mini-Gastric Bypass (Also see Gastritis, ulcer(s), indigestion, heartburn, acid stomach, upset stomach, unsettled stomach, stomachache ..., also see Bile Reflux, Esophageal Reflux, GERD Gastro Esophageal Reflux Disease...
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.
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.
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.
