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posted by DrR @ 4:41 PM
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CELOS Texas
Monday, August 24, 2009
Vitamin C: In Your Diet=Life Saving, As a Pill=Worthless
http://ping.fm/sKjlC
http://ping.fm/sKjlC
http://sites.google.com/a/clos.net/mini/opioid-sparing-effect-and-post-op-recovery
Opioid-sparing Effect and Post Op Recovery
Opioid-sparing effects of ketorolac and its correlation with the recovery of postoperative bowel function in colorectal surgery patients: a prospective randomized double-blinded study.
Chen JY, Ko TL, Wen YR, Wu SC, Chou YH, Yien HW, Kuo CD.
Department of Anesthesiology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.
Clin J Pain. 2009 Jul-Aug;25(6):485-9.
OBJECTIVES: Postoperative ileus (PI) is one of many common complications in major abdominal surgery. Postoperative Ileus results in patient discomfort, increased gastrointestinal leakage, prolonged hospital stay, and increased medical expenses. In this study, we have investigated the morphine-sparing effects of ketorolac and its correlation with the duration of Postoperative Ileus in patients with colorectal surgeries.
METHODS: We collected data from 102 patients who had received elective colorectal resection. The patients were randomly allocated into 2 groups and received intravenous patient-controlled analgesia (IVPCA) morphine (M group) or intravenous patient-controlled analgesia morphine plus ketorolac (M+K group). Time-scale morphine consumption (per 12 h), recovery of bowel functions (the first bowel movement and passage of flatus), pain scores, and opioid-related side effects were then recorded.
RESULTS:
Patients in the morphine plus ketorolac group received 18.3% less morphine than those in the morphine group within 72 postoperative hours.
The maximal opioid-sparing effects of ketorolac appeared in 12 to 24 postoperative hours.
The onset of the first bowel movement and passage of flatus was significantly less in the morphine plus ketorolac group than in the morphine group.
The morphine group showed a 5.25 times greater risk of inducing PI, a result comparable with the morphine plus ketorolac group in colorectal surgery patients.
DISCUSSION:
The addition of ketorolac to intravenous patient-controlled analgesia morphine has demonstrated
a clear opioid-sparing effect and benefits in regards to the shortening of the duration of bowel immobility.
We suggest that adding ketorolac to morphine intravenous patient-controlled analgesia be included in the multimodal postoperative rehabilitation program for the early restoration of normal bowel function.
Opioid-sparing Effect and Post Op Recovery
Opioid-sparing effects of ketorolac and its correlation with the recovery of postoperative bowel function in colorectal surgery patients: a prospective randomized double-blinded study.
Chen JY, Ko TL, Wen YR, Wu SC, Chou YH, Yien HW, Kuo CD.
Department of Anesthesiology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.
Clin J Pain. 2009 Jul-Aug;25(6):485-9.
OBJECTIVES: Postoperative ileus (PI) is one of many common complications in major abdominal surgery. Postoperative Ileus results in patient discomfort, increased gastrointestinal leakage, prolonged hospital stay, and increased medical expenses. In this study, we have investigated the morphine-sparing effects of ketorolac and its correlation with the duration of Postoperative Ileus in patients with colorectal surgeries.
METHODS: We collected data from 102 patients who had received elective colorectal resection. The patients were randomly allocated into 2 groups and received intravenous patient-controlled analgesia (IVPCA) morphine (M group) or intravenous patient-controlled analgesia morphine plus ketorolac (M+K group). Time-scale morphine consumption (per 12 h), recovery of bowel functions (the first bowel movement and passage of flatus), pain scores, and opioid-related side effects were then recorded.
RESULTS:
Patients in the morphine plus ketorolac group received 18.3% less morphine than those in the morphine group within 72 postoperative hours.
The maximal opioid-sparing effects of ketorolac appeared in 12 to 24 postoperative hours.
The onset of the first bowel movement and passage of flatus was significantly less in the morphine plus ketorolac group than in the morphine group.
The morphine group showed a 5.25 times greater risk of inducing PI, a result comparable with the morphine plus ketorolac group in colorectal surgery patients.
DISCUSSION:
The addition of ketorolac to intravenous patient-controlled analgesia morphine has demonstrated
a clear opioid-sparing effect and benefits in regards to the shortening of the duration of bowel immobility.
We suggest that adding ketorolac to morphine intravenous patient-controlled analgesia be included in the multimodal postoperative rehabilitation program for the early restoration of normal bowel function.
posted by DrR @ 3:33 PM
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http://ping.fm/m3mCE?pid=368070&id=1639571519
Xray of MGB by one of our patients that is aradiologist
Xray of MGB by one of our patients that is aradiologist
posted by DrR @ 3:14 PM
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Wednesday, August 19, 2009
http://ping.fm/tQhW6
Many Normal-Weight Teens Feel Fat, At a time when much of the Western world is focusing on obesity problems, even teens who are at a healthy weight may develop a distorted body image.
Many Normal-Weight Teens Feel Fat, At a time when much of the Western world is focusing on obesity problems, even teens who are at a healthy weight may develop a distorted body image.
posted by DrR @ 11:30 PM
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http://ping.fm/Z0Dzv
Changes in Weight, Waist Circumference and Compensatory Responses with Different Doses of Exercise among Sedentary, Overweight Postmenopausal Women
Conclusion
In this study of previously sedentary, overweight or obese, postmenopausal women we observed no difference in the actual and predicted weight loss with 4 and 8 KKW of exercise (72 and 136 minutes respectively)
Changes in Weight, Waist Circumference and Compensatory Responses with Different Doses of Exercise among Sedentary, Overweight Postmenopausal Women
Conclusion
In this study of previously sedentary, overweight or obese, postmenopausal women we observed no difference in the actual and predicted weight loss with 4 and 8 KKW of exercise (72 and 136 minutes respectively)
posted by DrR @ 11:21 PM
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http://ping.fm/njIuG
Why Exercise Won't Make You Thin, "In general, for weight loss, exercise is pretty useless," says Eric Ravussin, chair in diabetes and metabolism at Louisiana State University and a prominent exercise researcher. Many recent studies have found that exercise isn't as important in helping people lose weight as you hear so regularly in gym advertisements or on shows like The Biggest Loser — or, for that matter, from magazines like this one.
Why Exercise Won't Make You Thin, "In general, for weight loss, exercise is pretty useless," says Eric Ravussin, chair in diabetes and metabolism at Louisiana State University and a prominent exercise researcher. Many recent studies have found that exercise isn't as important in helping people lose weight as you hear so regularly in gym advertisements or on shows like The Biggest Loser — or, for that matter, from magazines like this one.
posted by DrR @ 11:13 PM
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Monday, August 17, 2009
http://sites.google.com/a/clos.net/mini/ulcers-gastritis-and-indigestion
Ulcers Gastritis and Indigestion
1. 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.
Ulcers Gastritis and Indigestion
1. 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.
posted by DrR @ 7:12 PM
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http://ping.fm/oueGj
Eating fatty food appears to take an almost immediate toll on both short-term memory and exercise performance, according to new research on rats and people....
Eating fatty food appears to take an almost immediate toll on both short-term memory and exercise performance, according to new research on rats and people....
posted by DrR @ 3:48 PM
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Friday, August 14, 2009
http://mgb.fm
5 New Scientific Studies Support the Mini-Gastric Bypass over other Weight Loss Surgery
*** Amazing New Findings! 3 New studies from the International Federation for Surgery of Obesity and Metabolic Diseases show: ***
A 5 year Randomized Controlled Prospective Trial: the Mini-Gastric Bypass better than the RNY gastric bypass.
In another randomized trial, the MGB out performed the lapBand and the Sleeve Gastrectomy in weight loss, quality of life
In another randomized trial of the treatment of diabetes the Mini-Gastric Bypass was roughly TWICE as effective as the Sleeve Gastrectomy
In Studies from ASMBS summer meetings:
New Lap band study showed failure to resolve diabetes in 60% of Diabetics and patients lost less than half of their excess weight.
In another study of 177 patients with type 2 diabetes who underwent RNY gastric bypass, remission of diabetes remained in only 57% at 8 years.
5 New Scientific Studies Support the Mini-Gastric Bypass over other Weight Loss Surgery
*** Amazing New Findings! 3 New studies from the International Federation for Surgery of Obesity and Metabolic Diseases show: ***
A 5 year Randomized Controlled Prospective Trial: the Mini-Gastric Bypass better than the RNY gastric bypass.
In another randomized trial, the MGB out performed the lapBand and the Sleeve Gastrectomy in weight loss, quality of life
In another randomized trial of the treatment of diabetes the Mini-Gastric Bypass was roughly TWICE as effective as the Sleeve Gastrectomy
In Studies from ASMBS summer meetings:
New Lap band study showed failure to resolve diabetes in 60% of Diabetics and patients lost less than half of their excess weight.
In another study of 177 patients with type 2 diabetes who underwent RNY gastric bypass, remission of diabetes remained in only 57% at 8 years.
posted by DrR @ 7:13 PM
0 comments
5 New Scientific Studies Support the Mini-Gastric Bypass over other Weight Loss Surgery
*** Amazing New Findings! 3 New studies from the International Federation for Surgery of Obesity and Metabolic Diseases show: ***
A 5 year Randomized Controlled Prospective Trial: the Mini-Gastric Bypass better than the RNY gastric bypass.
In another randomized trial, the MGB out performed the lapBand and the Sleeve Gastrectomy in weight loss, quality of life
In another randomized trial of the treatment of diabetes the Mini-Gastric Bypass was roughly TWICE as effective as the Sleeve Gastrectomy
In Studies from ASMBS summer meetings:
New Lap band study showed failure to resolve diabetes in 60% of Diabetics and patients lost less than half of their excess weight.
In another study of 177 patients with type 2 diabetes who underwent RNY gastric bypass, remission of diabetes remained in only 57% at 8 years.
*** Amazing New Findings! 3 New studies from the International Federation for Surgery of Obesity and Metabolic Diseases show: ***
A 5 year Randomized Controlled Prospective Trial: the Mini-Gastric Bypass better than the RNY gastric bypass.
In another randomized trial, the MGB out performed the lapBand and the Sleeve Gastrectomy in weight loss, quality of life
In another randomized trial of the treatment of diabetes the Mini-Gastric Bypass was roughly TWICE as effective as the Sleeve Gastrectomy
In Studies from ASMBS summer meetings:
New Lap band study showed failure to resolve diabetes in 60% of Diabetics and patients lost less than half of their excess weight.
In another study of 177 patients with type 2 diabetes who underwent RNY gastric bypass, remission of diabetes remained in only 57% at 8 years.
posted by DrR @ 7:12 PM
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http://ping.fm/bwsEV Medical Student and MGB Patient talks about MGB and nutrition. On the web: www.clos.net Email: DrR@clos.net Tel: 702-714-0011
posted by DrR @ 6:41 PM
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Thursday, August 13, 2009
http://ping.fm/XbGvL
Surgeon Specialization
Surgeon specialization was inversely related to mortality rates
That is: More Specialized = Better Outcomes (Fewer Deaths)
Ann Surg. 2009 May;249(5):708-16.Click here to read Links
Comment in:
Ann Surg. 2009 May;249(5):717-8.
The impact of surgeon specialization on patient mortality: examination of a continuous Herfindahl-Hirschman index.
Hall BL, Hsiao EY, Majercik S, Hirbe M, Hamilton BH.
Department of Surgery, John Cochran Veterans Affairs Medical Center, St Louis, Missouri, USA. hallb@ wustl.edu
OBJECTIVE: To examine the effect of surgeon specialization on patient outcomes, controlling for volume.
BACKGROUND: There is great interest in the degree to which surgical specialization affects outcomes, particularly considering drives to measure and reward quality in healthcare. Although surgical specialization has been previously analyzed with respect to outcomes, most studies have treated it as a dichotomous variable based on academic credentials. We treat it here as a continuous variable defined quantitatively by procedural diversity.
METHODS: We used 2002 to 2005 patient data from the National Surgical Quality Improvement Program for the Department of Surgery, Barnes Jewish Hospital, St. Louis, Missouri. To quantitate procedural specialization, Herfindahl-Hirschman indices for surgeons were calculated using billing codes. These indices were calculated according to 3 different levels of procedural aggregation. Using conditional logit models, we examined the relationship between these indices and 30-day postoperative mortality rates.
RESULTS: Surgeon specialization was inversely related to mortality rates after adjusting for case volume when indices were calculated using medium procedural aggregation (odds ratio for mortality = 0.580 per 0.1 unit Herfindahl increase; P = 0.025) or low aggregation (odds ratio for mortality = 0.510 per 0.1 unit Herfindahl increase; P = 0.015). No relationship was observed at the high level of aggregation.
CONCLUSIONS: The procedural concentration component of surgical specialization is correlated with improved mortality rates independently of case volume.
Surgeon Specialization
Surgeon specialization was inversely related to mortality rates
That is: More Specialized = Better Outcomes (Fewer Deaths)
Ann Surg. 2009 May;249(5):708-16.Click here to read Links
Comment in:
Ann Surg. 2009 May;249(5):717-8.
The impact of surgeon specialization on patient mortality: examination of a continuous Herfindahl-Hirschman index.
Hall BL, Hsiao EY, Majercik S, Hirbe M, Hamilton BH.
Department of Surgery, John Cochran Veterans Affairs Medical Center, St Louis, Missouri, USA. hallb@ wustl.edu
OBJECTIVE: To examine the effect of surgeon specialization on patient outcomes, controlling for volume.
BACKGROUND: There is great interest in the degree to which surgical specialization affects outcomes, particularly considering drives to measure and reward quality in healthcare. Although surgical specialization has been previously analyzed with respect to outcomes, most studies have treated it as a dichotomous variable based on academic credentials. We treat it here as a continuous variable defined quantitatively by procedural diversity.
METHODS: We used 2002 to 2005 patient data from the National Surgical Quality Improvement Program for the Department of Surgery, Barnes Jewish Hospital, St. Louis, Missouri. To quantitate procedural specialization, Herfindahl-Hirschman indices for surgeons were calculated using billing codes. These indices were calculated according to 3 different levels of procedural aggregation. Using conditional logit models, we examined the relationship between these indices and 30-day postoperative mortality rates.
RESULTS: Surgeon specialization was inversely related to mortality rates after adjusting for case volume when indices were calculated using medium procedural aggregation (odds ratio for mortality = 0.580 per 0.1 unit Herfindahl increase; P = 0.025) or low aggregation (odds ratio for mortality = 0.510 per 0.1 unit Herfindahl increase; P = 0.015). No relationship was observed at the high level of aggregation.
CONCLUSIONS: The procedural concentration component of surgical specialization is correlated with improved mortality rates independently of case volume.
posted by DrR @ 10:26 PM
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Monday, August 10, 2009
ICISS: Dr. Rutledge's Contribution to Trauma Carehttp://ping.fm/vBbS7
Dr Rutledge: Inventor of ICISS (ICD based Injury Severity Score)
In 1993 Dr Rutledge published the first article describing
the use of ICD-9 codes as a means of predicting injury severity. (1) At the time the standard means of injury
severity scoring was the consensus derived ISS. Dr Rutledge’s invention was a data derived system
based upon analysis of actual injury outcomes that were quantitated from actual
trauma outcomes.
Although controversial at the time, (criticized by Champion,
MacKenzie and others) now 17 years later the ICISS stands as simple, well validated
and relatively inexpensive means of injury severity scoring, confirming Dr Rutledge’s
initial findings.(2-51)
Now 51 scientific articles later; Dr. Rutledge was right. Its hard changing people's minds.
Dr Rutledge: Inventor of ICISS (ICD based Injury Severity Score)
In 1993 Dr Rutledge published the first article describing
the use of ICD-9 codes as a means of predicting injury severity. (1) At the time the standard means of injury
severity scoring was the consensus derived ISS. Dr Rutledge’s invention was a data derived system
based upon analysis of actual injury outcomes that were quantitated from actual
trauma outcomes.
Although controversial at the time, (criticized by Champion,
MacKenzie and others) now 17 years later the ICISS stands as simple, well validated
and relatively inexpensive means of injury severity scoring, confirming Dr Rutledge’s
initial findings.(2-51)
Now 51 scientific articles later; Dr. Rutledge was right. Its hard changing people's minds.
posted by DrR @ 1:06 PM
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http://ping.fm/nJcDx
ICISS: Dr. Rutledge's Contribution to Trauma Care
Dr Rutledge: Inventor of ICISS (ICD based Injury Severity Score)
In 1993 Dr Rutledge published the first article describing the use of ICD-9 codes as a means of predicting injury severity. (1) At the time the standard means of injury severity scoring was the consensus derived ISS. Dr Rutledge’s invention was a data derived system based upon analysis of actual injury outcomes that were quantitated from actual trauma outcomes.
Although controversial at the time, (criticized by Champion, MacKenzie and others) now 17 years later the ICISS stands as simple, well validated and relatively inexpensive means of injury severity scoring, confirming Dr Rutledge’s initial findings.(2-51)
Over 10 years ago Dr. Rutledge wrote:
The Journal of Trauma: Injury, Infection, and Critical Care:
January 1998 - Volume 44 - Issue 1 - pp 41-49
Article
The End of the Injury Severity Score (ISS) and the Trauma and Injury Severity Score (TRISS): ICISS, an International Classification of Diseases, Ninth Revision-Based Prediction Tool, Outperforms Both ISS and TRISS as Predictors of Trauma Patient Survival, Hospital Charges, and Hospital Length of Stay
Rutledge, Robert MD; Osler, Turner MD; Emery, Sherry PhD; Kromhout-Schiro, Sharon PhD
Collapse Box
Abstract
Introduction: Since their inception, the Injury Severity Score (ISS) and the Trauma and Injury Severity Score (TRISS) have been suggested as measures of the quality of trauma care. In concept, they are designed to accurately assess injury severity and predict expected outcomes. ICISS, an injury severity methodology based on International Classification of Diseases, Ninth Revision, codes, has been demonstrated to be superior to ISS and TRISS. The purpose of the present study was to compare the ability of TRISS to ICISS as predictors of survival and other outcomes of injury (hospital length of stay and hospital charges). It was our hypothesis that ICISS would outperform ISS and TRISS in each of these outcome predictions.
Methods: "Training" data for creation of ICISS predictions were obtained from a state hospital discharge data base. "Test" data were obtained from a state trauma registry. ISS, TRISS, and ICISS were compared as predictors of patient survival. They were also compared as indicators of resource utilization by assessing their ability to predict patient hospital length of stay and hospital charges. Finally, a neural network was trained on the ICISS values and applied to the test data set in an effort to further improve predictive power. The techniques were compared by comparing each patient's outcome as predicted by the model to the actual outcome.
Results: Seven thousand seven hundred five patients had complete data available for analysis. The ICISS was far more likely than ISS or TRISS to accurately predict every measure of outcome of injured patients tested, and the neural network further improved predictive power.
Conclusion: In addition to predicting mortality, quality tools that can accurately predict resource utilization are necessary for effective trauma center quality-improvement programs. ICISS-derived predictions of survival, hospital charges, and hospital length of stay consistently outperformed those of ISS and TRISS. The neural network-augmented ICISS was even better. This and previous studies demonstrate that TRISS is a limited technique in predicting survival resource utilization. Because of the limitations of TRISS, it should be superseded by ICISS.
References
1. Rutledge R, Fakhry S, Baker C, Oller D. Injury severity grading in trauma patients: a simplified technique based upon ICD-9 coding. J Trauma 1993;35(4):497-506; discussion 506.
2. Rutledge R. Injury severity and probability of survival assessment in trauma patients using a predictive hierarchical network model derived from ICD-9 codes. J Trauma 1995;38(4):590-7; discussion 597.
3. Osler T, Rutledge R, Deis J, Bedrick E. ICISS: an international classification of disease-9 based injury severity score. J Trauma 1996;41(3):380-6; discussion 386.
4. Rutledge R, Hoyt DB, Eastman AB, Sise MJ, Velky T, Canty T, et al. Comparison of the Injury Severity Score and ICD-9 diagnosis codes as predictors of outcome in injury: analysis of 44,032 patients. J Trauma 1997;42(3):477-87; discussion 487.
5. Osler TM, Cohen M, Rogers FB, Camp L, Rutledge R, Shackford SR, et al. Trauma registry injury coding is superfluous: a comparison of outcome prediction based on trauma registry International Classification of Diseases-Ninth Revision (ICD-9) and hospital information system ICD-9 codes. J Trauma 1997;43(2):253-6; discussion 256.
6. Rutledge R, Osler T. The ICD-9-based illness severity score: a new model that outperforms both DRG and APR-DRG as predictors of survival and resource utilization. J Trauma 1998;45(4):791-799.
7. Osler TM, Rogers FB, Glance LG, Cohen M, Rutledge R, Shackford SR, et al. Predicting survival, length of stay, and cost in the surgical intensive care unit: APACHE II versus ICISS. J Trauma 1998;45(2):234-7; discussion 237.
8. Rutledge R, Osler T, Kromhout-Schiro S. Illness severity adjustment for outcomes analysis: validation of the ICISS methodology in all 821,455 patients hospitalized in North Carolina in 1996. Surgery 1998;124(2):187-94; discussion 194.
9. Rutledge R, Osler T, Emery S, Kromhout-Schiro S. The end of the Injury Severity Score (ISS) and the Trauma and Injury Severity Score (TRISS): ICISS, an International Classification of Diseases, ninth revision-based prediction tool, outperforms both ISS and TRISS as predictors of trauma patient survival, hospital charges, and hospital length of stay. J Trauma 1998;44(1):41-49.
10. Hannan EL, Farrell LS, Gorthy SF, Bessey PQ, Cayten CG, Cooper A, et al. Predictors of mortality in adult patients with blunt injuries in New York State: a comparison of the Trauma and Injury Severity Score (TRISS) and the International Classification of Disease, Ninth Revision-based Injury Severity Score (ICISS). J Trauma 1999;47(1):8-14.
11. West TA, Rivara FP, Cummings P, Jurkovich GJ, Maier RV. Harborview assessment for risk of mortality: an improved measure of injury severity on the basis of ICD-9-CM. J Trauma 2000;49(3):530-40; discussion 540.
12. Hannan EL, Farrell LS, Meaker PS, Cooper A. Predicting inpatient mortality for pediatric trauma patients with blunt injuries: a better alternative. J Pediatr Surg 2000;35(2):155-159.
13. Kim Y, Jung KY, Kim CY, Kim YI, Shin Y. Validation of the International Classification of Diseases 10th Edition-based Injury Severity Score (ICISS). J Trauma 2000;48(2):280-285.
14. Rogers FB, Osler TM, Shackford SR, Martin F, Healey M, Pilcher D, et al. Population-based study of hospital trauma care in a rural state without a formal trauma system. J Trauma 2001;50(3):409-13; discussion 414.
15. Osler TM, Rogers FB, Badger GJ, Healey M, Vane DW, Shackford SR, et al. A simple mathematical modification of TRISS markedly improves calibration. J Trauma 2002;53(4):630-634.
16. Meredith JW, Evans G, Kilgo PD, MacKenzie E, Osler T, McGwin G, et al. A comparison of the abilities of nine scoring algorithms in predicting mortality. J Trauma 2002;53(4):621-8; discussion 628.
17. Stephenson SCR, Langley JD, Civil ID. Comparing measures of injury severity for use with large databases. J Trauma 2002;53(2):326-332.
18. Kuhls DA, Malone DL, McCarter RJ, Napolitano LM. Predictors of mortality in adult trauma patients: the physiologic trauma score is equivalent to the Trauma and Injury Severity Score. J Am Coll Surg 2002;194(6):695-704.
19. Meredith JW, Kilgo PD, Osler TM. Independently derived survival risk ratios yield better estimates of survival than traditional survival risk ratios when using the ICISS. J Trauma 2003;55(5):933-938.
20. Meredith JW, Kilgo PD, Osler T. A fresh set of survival risk ratios derived from incidents in the National Trauma Data Bank from which the ICISS may be calculated. J Trauma 2003;55(5):924-932.
21. Kilgo PD, Osler TM, Meredith W. The worst injury predicts mortality outcome the best: rethinking the role of multiple injuries in trauma outcome scoring. J Trauma 2003;55(4):599-606; discussion 606.
22. Kim Y, Jung KY. Utility of the international classification of diseases injury severity score: detecting preventable deaths and comparing the performance of emergency medical centers. J Trauma 2003;54(4):775-780.
23. Stephenson S, Henley G, Harrison JE, Langley JD. Diagnosis based injury severity scaling: investigation of a method using Australian and New Zealand hospitalisations. Inj Prev 2004;10(6):379-383.
24. Kilgo PD, Meredith JW, Hensberry R, Osler TM. A note on the disjointed nature of the injury severity score. J Trauma 2004;57(3):479-85; discussion 486.
25. Kulla M, Fischer S, Helm M, Lampl L. [How to assess the severity of the multi-system trauma in the emergency-room -- a critical review]. Anasthesiol Intensivmed Notfallmed Schmerzther 2005;40(12):726-736.
26. Clarke JR, Ragone AV, Greenwald L. Comparisons of survival predictions using survival risk ratios based on International Classification of Diseases, Ninth Revision and Abbreviated Injury Scale trauma diagnosis codes. J Trauma 2005;59(3):563-7; discussion 567.
27. Hannan EL, Waller CH, Farrell LS, Cayten CG. A comparison among the abilities of various injury severity measures to predict mortality with and without accompanying physiologic information. J Trauma 2005;58(2):244-251.
28. Deutscher M. The responsibility to protect. Med Confl Surviv 2005;21(1):28-34.
29. Markogiannakis H, Sanidas E, Messaris E, Michalakis I, Kasotakis G, Melissas J, et al. Management of blunt hepatic and splenic trauma in a Greek level I trauma centre. Acta Chir Belg 2006;106(5):566-571.
30. Durham R, Pracht E, Orban B, Lottenburg L, Tepas J, Flint L, et al. Evaluation of a mature trauma system. Ann Surg 2006;243(6):775-83; discussion 783.
31. Clark DE, Ahmad S. Estimating injury severity using the Barell matrix. Inj Prev 2006;12(2):111-116.
32. Pressley JC, Trieu L, Kendig T, Barlow B. National injury-related hospitalizations in children: public versus private expenditures across preventable injury mechanisms. J Trauma 2007;63(3 Suppl):S10-S19.
33. Moore L, Lavoie A, Bergeron E, Emond M. Modeling probability-based injury severity scores in logistic regression models: the logit transformation should be used. J Trauma 2007;62(3):601-605.
34. Bergeron E, Simons R, Linton C, Yang F, Tallon JM, Stewart TC, et al. Canadian benchmarks in trauma. J Trauma 2007;62(2):491-497.
35. Tepas JJ, Leaphart CL, Celso BG, Tuten JD, Pieper P, Ramenofsky ML, et al. Risk stratification simplified: the worst injury predicts mortality for the injured children. J Trauma 2008;65(6):1258-61; discussion 1261.
36. Davie G, Cryer C, Langley J. Improving the predictive ability of the ICD-based Injury Severity Score. Inj Prev 2008;14(4):250-255.
37. Markogiannakis H, Sanidas E, Michalakis I, Manouras A, Melissas J, Tsiftsis D, et al. Predictive factors of operative or nonoperative management of blunt hepatic trauma. Minerva Chir 2008;63(3):223-228.
38. Burd RS, Ouyang M, Madigan D. Bayesian logistic injury severity score: a method for predicting mortality using international classification of disease-9 codes. Acad Emerg Med 2008;15(5):466-475.
39. Diggs BS, Mullins RJ, Hedges JR, Arthur M, Newgard CD. Proportion of seriously injured patients admitted to hospitals in the US with a high annual injured patient volume: a metric of regionalized trauma care. J Am Coll Surg 2008;206(2):212-219.
40. Moore L, Lavoie A, Le Sage N, Bergeron E, Emond M, Abdous B, et al. Consensus or data-derived anatomic injury severity scoring? J Trauma 2008;64(2):420-426.
41. Boufous S, Finch C, Hayen A, Williamson A. The impact of environmental, vehicle and driver characteristics on injury severity in older drivers hospitalized as a result of a traffic crash. J Safety Res 2008;39(1):65-72.
42. Wong SSN, Leung GKK. Injury Severity Score (ISS) vs. ICD-derived Injury Severity Score (ICISS) in a patient population treated in a designated Hong Kong trauma centre. McGill journal of medicine : MJM : an international forum for the advancement of medical sciences by students 2008;11(1):9-13.
43. Tepas JJ, Celso BG, Leaphart CL, Graham D. Application of International Classification Injury Severity Score to National Surgical Quality Improvement Program defines pediatric trauma performance standards and drives performance improvement. J Trauma 2009;67(1):185-8; discussion 188.
44. Glance LG, Osler TM, Mukamel DB, Meredith W, Wagner J, Dick AW, et al. TMPM-ICD9: a trauma mortality prediction model based on ICD-9-CM codes. Ann Surg 2009;249(6):1032-1039.
45. Smartt P, Chalmers D. Searching for ski-lift injury: An uphill struggle? J Sci Med Sport 2009;
46. Cinelli SM, Brady P, Rennie CP, Tuluca C, Hall TS. Comparative results of trauma scoring systems in fatal outcomes. Conn Med 2009;73(5):261-265.
47. Kim J, Shin SD, Im TH, Lee KJ, Ko SB, Park JO, et al. Development and Validation of the Excess Mortality Ratio-adjusted Injury Severity Score Using the International Classification of Diseases 10th Edition. Acad Emerg Med 2009;
48. McDonald G, Davie G, Langley J. Validity of police-reported information on injury severity for those hospitalized from motor vehicle traffic crashes. Traffic Inj Prev 2009;10(2):184-190.
49. Smartt P, Chalmers D. Obstructing the goal? Hospitalisation for netball injury in New Zealand 2000-2005. N Z Med J 2009;122(1288):62-75.
50. Leaphart CL, Graham D, Pieper P, Celso BG, Tepas JJ. Surgical quality improvement: a simplified method to apply national standards to pediatric trauma care. J Pediatr Surg 2009;44(1):156-159.
51. Millham F, Jain NB. Are there racial disparities in trauma care? World J Surg 2009;33(1):23-33.
ICISS: Dr. Rutledge's Contribution to Trauma Care
Dr Rutledge: Inventor of ICISS (ICD based Injury Severity Score)
In 1993 Dr Rutledge published the first article describing the use of ICD-9 codes as a means of predicting injury severity. (1) At the time the standard means of injury severity scoring was the consensus derived ISS. Dr Rutledge’s invention was a data derived system based upon analysis of actual injury outcomes that were quantitated from actual trauma outcomes.
Although controversial at the time, (criticized by Champion, MacKenzie and others) now 17 years later the ICISS stands as simple, well validated and relatively inexpensive means of injury severity scoring, confirming Dr Rutledge’s initial findings.(2-51)
Over 10 years ago Dr. Rutledge wrote:
The Journal of Trauma: Injury, Infection, and Critical Care:
January 1998 - Volume 44 - Issue 1 - pp 41-49
Article
The End of the Injury Severity Score (ISS) and the Trauma and Injury Severity Score (TRISS): ICISS, an International Classification of Diseases, Ninth Revision-Based Prediction Tool, Outperforms Both ISS and TRISS as Predictors of Trauma Patient Survival, Hospital Charges, and Hospital Length of Stay
Rutledge, Robert MD; Osler, Turner MD; Emery, Sherry PhD; Kromhout-Schiro, Sharon PhD
Collapse Box
Abstract
Introduction: Since their inception, the Injury Severity Score (ISS) and the Trauma and Injury Severity Score (TRISS) have been suggested as measures of the quality of trauma care. In concept, they are designed to accurately assess injury severity and predict expected outcomes. ICISS, an injury severity methodology based on International Classification of Diseases, Ninth Revision, codes, has been demonstrated to be superior to ISS and TRISS. The purpose of the present study was to compare the ability of TRISS to ICISS as predictors of survival and other outcomes of injury (hospital length of stay and hospital charges). It was our hypothesis that ICISS would outperform ISS and TRISS in each of these outcome predictions.
Methods: "Training" data for creation of ICISS predictions were obtained from a state hospital discharge data base. "Test" data were obtained from a state trauma registry. ISS, TRISS, and ICISS were compared as predictors of patient survival. They were also compared as indicators of resource utilization by assessing their ability to predict patient hospital length of stay and hospital charges. Finally, a neural network was trained on the ICISS values and applied to the test data set in an effort to further improve predictive power. The techniques were compared by comparing each patient's outcome as predicted by the model to the actual outcome.
Results: Seven thousand seven hundred five patients had complete data available for analysis. The ICISS was far more likely than ISS or TRISS to accurately predict every measure of outcome of injured patients tested, and the neural network further improved predictive power.
Conclusion: In addition to predicting mortality, quality tools that can accurately predict resource utilization are necessary for effective trauma center quality-improvement programs. ICISS-derived predictions of survival, hospital charges, and hospital length of stay consistently outperformed those of ISS and TRISS. The neural network-augmented ICISS was even better. This and previous studies demonstrate that TRISS is a limited technique in predicting survival resource utilization. Because of the limitations of TRISS, it should be superseded by ICISS.
References
1. Rutledge R, Fakhry S, Baker C, Oller D. Injury severity grading in trauma patients: a simplified technique based upon ICD-9 coding. J Trauma 1993;35(4):497-506; discussion 506.
2. Rutledge R. Injury severity and probability of survival assessment in trauma patients using a predictive hierarchical network model derived from ICD-9 codes. J Trauma 1995;38(4):590-7; discussion 597.
3. Osler T, Rutledge R, Deis J, Bedrick E. ICISS: an international classification of disease-9 based injury severity score. J Trauma 1996;41(3):380-6; discussion 386.
4. Rutledge R, Hoyt DB, Eastman AB, Sise MJ, Velky T, Canty T, et al. Comparison of the Injury Severity Score and ICD-9 diagnosis codes as predictors of outcome in injury: analysis of 44,032 patients. J Trauma 1997;42(3):477-87; discussion 487.
5. Osler TM, Cohen M, Rogers FB, Camp L, Rutledge R, Shackford SR, et al. Trauma registry injury coding is superfluous: a comparison of outcome prediction based on trauma registry International Classification of Diseases-Ninth Revision (ICD-9) and hospital information system ICD-9 codes. J Trauma 1997;43(2):253-6; discussion 256.
6. Rutledge R, Osler T. The ICD-9-based illness severity score: a new model that outperforms both DRG and APR-DRG as predictors of survival and resource utilization. J Trauma 1998;45(4):791-799.
7. Osler TM, Rogers FB, Glance LG, Cohen M, Rutledge R, Shackford SR, et al. Predicting survival, length of stay, and cost in the surgical intensive care unit: APACHE II versus ICISS. J Trauma 1998;45(2):234-7; discussion 237.
8. Rutledge R, Osler T, Kromhout-Schiro S. Illness severity adjustment for outcomes analysis: validation of the ICISS methodology in all 821,455 patients hospitalized in North Carolina in 1996. Surgery 1998;124(2):187-94; discussion 194.
9. Rutledge R, Osler T, Emery S, Kromhout-Schiro S. The end of the Injury Severity Score (ISS) and the Trauma and Injury Severity Score (TRISS): ICISS, an International Classification of Diseases, ninth revision-based prediction tool, outperforms both ISS and TRISS as predictors of trauma patient survival, hospital charges, and hospital length of stay. J Trauma 1998;44(1):41-49.
10. Hannan EL, Farrell LS, Gorthy SF, Bessey PQ, Cayten CG, Cooper A, et al. Predictors of mortality in adult patients with blunt injuries in New York State: a comparison of the Trauma and Injury Severity Score (TRISS) and the International Classification of Disease, Ninth Revision-based Injury Severity Score (ICISS). J Trauma 1999;47(1):8-14.
11. West TA, Rivara FP, Cummings P, Jurkovich GJ, Maier RV. Harborview assessment for risk of mortality: an improved measure of injury severity on the basis of ICD-9-CM. J Trauma 2000;49(3):530-40; discussion 540.
12. Hannan EL, Farrell LS, Meaker PS, Cooper A. Predicting inpatient mortality for pediatric trauma patients with blunt injuries: a better alternative. J Pediatr Surg 2000;35(2):155-159.
13. Kim Y, Jung KY, Kim CY, Kim YI, Shin Y. Validation of the International Classification of Diseases 10th Edition-based Injury Severity Score (ICISS). J Trauma 2000;48(2):280-285.
14. Rogers FB, Osler TM, Shackford SR, Martin F, Healey M, Pilcher D, et al. Population-based study of hospital trauma care in a rural state without a formal trauma system. J Trauma 2001;50(3):409-13; discussion 414.
15. Osler TM, Rogers FB, Badger GJ, Healey M, Vane DW, Shackford SR, et al. A simple mathematical modification of TRISS markedly improves calibration. J Trauma 2002;53(4):630-634.
16. Meredith JW, Evans G, Kilgo PD, MacKenzie E, Osler T, McGwin G, et al. A comparison of the abilities of nine scoring algorithms in predicting mortality. J Trauma 2002;53(4):621-8; discussion 628.
17. Stephenson SCR, Langley JD, Civil ID. Comparing measures of injury severity for use with large databases. J Trauma 2002;53(2):326-332.
18. Kuhls DA, Malone DL, McCarter RJ, Napolitano LM. Predictors of mortality in adult trauma patients: the physiologic trauma score is equivalent to the Trauma and Injury Severity Score. J Am Coll Surg 2002;194(6):695-704.
19. Meredith JW, Kilgo PD, Osler TM. Independently derived survival risk ratios yield better estimates of survival than traditional survival risk ratios when using the ICISS. J Trauma 2003;55(5):933-938.
20. Meredith JW, Kilgo PD, Osler T. A fresh set of survival risk ratios derived from incidents in the National Trauma Data Bank from which the ICISS may be calculated. J Trauma 2003;55(5):924-932.
21. Kilgo PD, Osler TM, Meredith W. The worst injury predicts mortality outcome the best: rethinking the role of multiple injuries in trauma outcome scoring. J Trauma 2003;55(4):599-606; discussion 606.
22. Kim Y, Jung KY. Utility of the international classification of diseases injury severity score: detecting preventable deaths and comparing the performance of emergency medical centers. J Trauma 2003;54(4):775-780.
23. Stephenson S, Henley G, Harrison JE, Langley JD. Diagnosis based injury severity scaling: investigation of a method using Australian and New Zealand hospitalisations. Inj Prev 2004;10(6):379-383.
24. Kilgo PD, Meredith JW, Hensberry R, Osler TM. A note on the disjointed nature of the injury severity score. J Trauma 2004;57(3):479-85; discussion 486.
25. Kulla M, Fischer S, Helm M, Lampl L. [How to assess the severity of the multi-system trauma in the emergency-room -- a critical review]. Anasthesiol Intensivmed Notfallmed Schmerzther 2005;40(12):726-736.
26. Clarke JR, Ragone AV, Greenwald L. Comparisons of survival predictions using survival risk ratios based on International Classification of Diseases, Ninth Revision and Abbreviated Injury Scale trauma diagnosis codes. J Trauma 2005;59(3):563-7; discussion 567.
27. Hannan EL, Waller CH, Farrell LS, Cayten CG. A comparison among the abilities of various injury severity measures to predict mortality with and without accompanying physiologic information. J Trauma 2005;58(2):244-251.
28. Deutscher M. The responsibility to protect. Med Confl Surviv 2005;21(1):28-34.
29. Markogiannakis H, Sanidas E, Messaris E, Michalakis I, Kasotakis G, Melissas J, et al. Management of blunt hepatic and splenic trauma in a Greek level I trauma centre. Acta Chir Belg 2006;106(5):566-571.
30. Durham R, Pracht E, Orban B, Lottenburg L, Tepas J, Flint L, et al. Evaluation of a mature trauma system. Ann Surg 2006;243(6):775-83; discussion 783.
31. Clark DE, Ahmad S. Estimating injury severity using the Barell matrix. Inj Prev 2006;12(2):111-116.
32. Pressley JC, Trieu L, Kendig T, Barlow B. National injury-related hospitalizations in children: public versus private expenditures across preventable injury mechanisms. J Trauma 2007;63(3 Suppl):S10-S19.
33. Moore L, Lavoie A, Bergeron E, Emond M. Modeling probability-based injury severity scores in logistic regression models: the logit transformation should be used. J Trauma 2007;62(3):601-605.
34. Bergeron E, Simons R, Linton C, Yang F, Tallon JM, Stewart TC, et al. Canadian benchmarks in trauma. J Trauma 2007;62(2):491-497.
35. Tepas JJ, Leaphart CL, Celso BG, Tuten JD, Pieper P, Ramenofsky ML, et al. Risk stratification simplified: the worst injury predicts mortality for the injured children. J Trauma 2008;65(6):1258-61; discussion 1261.
36. Davie G, Cryer C, Langley J. Improving the predictive ability of the ICD-based Injury Severity Score. Inj Prev 2008;14(4):250-255.
37. Markogiannakis H, Sanidas E, Michalakis I, Manouras A, Melissas J, Tsiftsis D, et al. Predictive factors of operative or nonoperative management of blunt hepatic trauma. Minerva Chir 2008;63(3):223-228.
38. Burd RS, Ouyang M, Madigan D. Bayesian logistic injury severity score: a method for predicting mortality using international classification of disease-9 codes. Acad Emerg Med 2008;15(5):466-475.
39. Diggs BS, Mullins RJ, Hedges JR, Arthur M, Newgard CD. Proportion of seriously injured patients admitted to hospitals in the US with a high annual injured patient volume: a metric of regionalized trauma care. J Am Coll Surg 2008;206(2):212-219.
40. Moore L, Lavoie A, Le Sage N, Bergeron E, Emond M, Abdous B, et al. Consensus or data-derived anatomic injury severity scoring? J Trauma 2008;64(2):420-426.
41. Boufous S, Finch C, Hayen A, Williamson A. The impact of environmental, vehicle and driver characteristics on injury severity in older drivers hospitalized as a result of a traffic crash. J Safety Res 2008;39(1):65-72.
42. Wong SSN, Leung GKK. Injury Severity Score (ISS) vs. ICD-derived Injury Severity Score (ICISS) in a patient population treated in a designated Hong Kong trauma centre. McGill journal of medicine : MJM : an international forum for the advancement of medical sciences by students 2008;11(1):9-13.
43. Tepas JJ, Celso BG, Leaphart CL, Graham D. Application of International Classification Injury Severity Score to National Surgical Quality Improvement Program defines pediatric trauma performance standards and drives performance improvement. J Trauma 2009;67(1):185-8; discussion 188.
44. Glance LG, Osler TM, Mukamel DB, Meredith W, Wagner J, Dick AW, et al. TMPM-ICD9: a trauma mortality prediction model based on ICD-9-CM codes. Ann Surg 2009;249(6):1032-1039.
45. Smartt P, Chalmers D. Searching for ski-lift injury: An uphill struggle? J Sci Med Sport 2009;
46. Cinelli SM, Brady P, Rennie CP, Tuluca C, Hall TS. Comparative results of trauma scoring systems in fatal outcomes. Conn Med 2009;73(5):261-265.
47. Kim J, Shin SD, Im TH, Lee KJ, Ko SB, Park JO, et al. Development and Validation of the Excess Mortality Ratio-adjusted Injury Severity Score Using the International Classification of Diseases 10th Edition. Acad Emerg Med 2009;
48. McDonald G, Davie G, Langley J. Validity of police-reported information on injury severity for those hospitalized from motor vehicle traffic crashes. Traffic Inj Prev 2009;10(2):184-190.
49. Smartt P, Chalmers D. Obstructing the goal? Hospitalisation for netball injury in New Zealand 2000-2005. N Z Med J 2009;122(1288):62-75.
50. Leaphart CL, Graham D, Pieper P, Celso BG, Tepas JJ. Surgical quality improvement: a simplified method to apply national standards to pediatric trauma care. J Pediatr Surg 2009;44(1):156-159.
51. Millham F, Jain NB. Are there racial disparities in trauma care? World J Surg 2009;33(1):23-33.
posted by DrR @ 1:02 PM
0 comments
ICISS: Dr. Rutledge's Contribution to Trauma Care (ICISS) (http://ping.fm/PQNma)
posted by DrR @ 12:33 PM
0 comments
Sunday, August 09, 2009
Mini-Gastric-Bypass : Mini-Gastric Bypass, Simple & Successful (http://ping.fm/qdKDD)
posted by DrR @ 12:40 AM
0 comments
MD Consult - Laparoscopic Roux-en-Y versus mini-gastric bypass for the treatment of morbid obesity: a prospective randomized controlled clinical trial. (abstract) - Annals of surgery - Medical Journal (http://ping.fm/VS2sN)
posted by DrR @ 12:31 AM
0 comments
Julia commented
"I had my surgery 3.5 yrs ago, lost 160 lbs, and 99% of the time I have had no problems..but every once in a while.. I still get a lovely wake up call at 3 or 4 am with bile spewing out my nose and throat in that lovely luminous yellow. I know how to calm it down now but it's always a jolt, very uncomfortable and painful. I feel it usually happens after a high stress experience. Thanks for posting this..it was a good refresher."
"I had my surgery 3.5 yrs ago, lost 160 lbs, and 99% of the time I have had no problems..but every once in a while.. I still get a lovely wake up call at 3 or 4 am with bile spewing out my nose and throat in that lovely luminous yellow. I know how to calm it down now but it's always a jolt, very uncomfortable and painful. I feel it usually happens after a high stress experience. Thanks for posting this..it was a good refresher."
posted by DrR @ 12:17 AM
0 comments
Saturday, August 08, 2009
" I also had a problem with my band:erosion. I had my first surgery to put it in Brazil, 1999. I had to remove it here in New York, March, 2007 by Dr. D G, at North Shore Hospital. Since then I have gained all the weight back. I almost died with the removal surgery. Could someone help me?
posted by DrR @ 11:27 PM
0 comments
CLOS Mail - Comment posted on "Failed (Slipped) LAP-BAND® Patient 1 Day Post Op" - drr@clos.net (http://ping.fm/eBeyQ)
posted by DrR @ 11:25 PM
0 comments
http://sites.google.com/a/clos.net/minibikinix/
Mini-Bikini X (MBX): 1/2 an MGB (Sleeve Gastrectomy/No Bypass) Done with NOTES
10 Things You Need to Know about
the new Mini-Bikini X (MBX) Sleeve Gastrectomy
** Think Thin ** It's a Sensational Feeling
1. The Mini-Bikini X is a short simple outpatient same day surgery weight loss procedure using leading edge technology.
2. The Mini-Bikini X (MBX) is designed for lighter weight women who are concerned about the 5 tiny scars on the abdomen from a Mini-Gastric Bypass
and who want to wear a bikini (2 piece swimsuit) after surgery,
3. The Mini-Bikini X (MBX) is for women who want a short simple outpatient same day surgery.
4. The MBX surgical procedure is 1/2 of the Mini-Gastric Bypass, it is a Sleeve Gastrectomy WITHOUT the Bypass portion of the MGB.
5. For cosmetic reasons: The operating ports are placed either transvaginally or through the umbilicus (naval) with one or 2 additional ports, less than the size of a pencil eraser head added as needed.
6. Since there is no Bypass, the Mini-Bikini X (MBX) Sleeve Gastrectomy patients can expect less than half the weight loss seen after Bypass surgery.
7. Since the weight loss is expected to be less than half that seen in the Mini-Gastric Bypass, the MBX (Mini-Bikini X) is only for
lighter weight female patients that are intently focused upon the cosmetic result of the surgery
8. Heavier patients are much better served by choosing the Mini-Gastric Bypass,
a short, simple and reversible procedure, that is also a much more powerful and durable weight loss procedure than
the Mini-Bikini X (MBX) Sleeve Gastrectomy.
For example in a recent study comparing the MGB to a Sleeve,
the cure rate of diabetics was 90% for the MGB patients and 50% for Sleeve Gastrectomy patients,
i.e. the Sleeve is roughly 1/2 the MGB.
9. The Mini-Bikini X (MBX) Sleeve Gastrectomy surgery is performed using Natural Orifice Transluminal Endoscopic Surgery (NOTES)
via the vagina (click for more info) or the umbilicus (naval) using the new SILS™ Port Multiple Instrument Access Port so that female patients can expect
excellent cosmetic results by avoiding the ports usually used in Laparoscopic Bypass Surgery.
UC San Diego Center claimed this “Scarless” Surgery, is the "future of U.S. surgery."
10. You can call (702-215-9550) or Email (DrR@clos.net) Dr. Rutledge for more information.
Nothing Feels Better than ** Thin, ** Imagine
Mini-Bikini X (MBX): 1/2 an MGB (Sleeve Gastrectomy/No Bypass) Done with NOTES
10 Things You Need to Know about
the new Mini-Bikini X (MBX) Sleeve Gastrectomy
** Think Thin ** It's a Sensational Feeling
1. The Mini-Bikini X is a short simple outpatient same day surgery weight loss procedure using leading edge technology.
2. The Mini-Bikini X (MBX) is designed for lighter weight women who are concerned about the 5 tiny scars on the abdomen from a Mini-Gastric Bypass
and who want to wear a bikini (2 piece swimsuit) after surgery,
3. The Mini-Bikini X (MBX) is for women who want a short simple outpatient same day surgery.
4. The MBX surgical procedure is 1/2 of the Mini-Gastric Bypass, it is a Sleeve Gastrectomy WITHOUT the Bypass portion of the MGB.
5. For cosmetic reasons: The operating ports are placed either transvaginally or through the umbilicus (naval) with one or 2 additional ports, less than the size of a pencil eraser head added as needed.
6. Since there is no Bypass, the Mini-Bikini X (MBX) Sleeve Gastrectomy patients can expect less than half the weight loss seen after Bypass surgery.
7. Since the weight loss is expected to be less than half that seen in the Mini-Gastric Bypass, the MBX (Mini-Bikini X) is only for
lighter weight female patients that are intently focused upon the cosmetic result of the surgery
8. Heavier patients are much better served by choosing the Mini-Gastric Bypass,
a short, simple and reversible procedure, that is also a much more powerful and durable weight loss procedure than
the Mini-Bikini X (MBX) Sleeve Gastrectomy.
For example in a recent study comparing the MGB to a Sleeve,
the cure rate of diabetics was 90% for the MGB patients and 50% for Sleeve Gastrectomy patients,
i.e. the Sleeve is roughly 1/2 the MGB.
9. The Mini-Bikini X (MBX) Sleeve Gastrectomy surgery is performed using Natural Orifice Transluminal Endoscopic Surgery (NOTES)
via the vagina (click for more info) or the umbilicus (naval) using the new SILS™ Port Multiple Instrument Access Port so that female patients can expect
excellent cosmetic results by avoiding the ports usually used in Laparoscopic Bypass Surgery.
UC San Diego Center claimed this “Scarless” Surgery, is the "future of U.S. surgery."
10. You can call (702-215-9550) or Email (DrR@clos.net) Dr. Rutledge for more information.
Nothing Feels Better than ** Thin, ** Imagine
posted by DrR @ 11:14 PM
0 comments
Wednesday, August 05, 2009
Ok, it has been almost a month since I last posted and almost that in me reading the posts. I have been so busy with work and my 9 kids that time flew by so fast.
First off let me say thank you Dr. R for the surgery. As of 3 days before my 4th month mark I was down 80 lbs. Yep folks reading that correctly. As of today I am down 82. My friend walked up behind me and said oh it is you, I didn't recognize you from behind. Wow that really made me feel good.
I don't have any side effects, and have more energy that I used to, which is weird since I am not sure how I was functioning with my previous weight. You see I have 10 kids, 9 of which live at home, work a full time job and manage a house. I also sell candles on the side and occasionlly baby sit my friends 4 kids. So I have a busy life. But my blood pressure is normal and I feel good.
I know it is a hard decision and the money seems like a lot, I was in everyone's shoes. I looked into this back in 2004 and didn't get it done until this year. You have to decide if your life is worth it. Mine was and is. I can chase my kids and I don't feel like I am an embarassement to them (at least not as big of one) and even though my husband loved and loves me for me, I don't feel so awkward around his work and the comments he used to get.
Bottom line is I am so happy. I am about a little over 1/2 way to my goal, but I am confident I will not only get there but I will enjoy the journey there. Every time I weigh myself I get so happy and amazed that it has moved down yet again.
Thank you again Dr. R. You and the staff are the BEST!!!!!
Laura
April 1, 2009
305/297/215/150
First off let me say thank you Dr. R for the surgery. As of 3 days before my 4th month mark I was down 80 lbs. Yep folks reading that correctly. As of today I am down 82. My friend walked up behind me and said oh it is you, I didn't recognize you from behind. Wow that really made me feel good.
I don't have any side effects, and have more energy that I used to, which is weird since I am not sure how I was functioning with my previous weight. You see I have 10 kids, 9 of which live at home, work a full time job and manage a house. I also sell candles on the side and occasionlly baby sit my friends 4 kids. So I have a busy life. But my blood pressure is normal and I feel good.
I know it is a hard decision and the money seems like a lot, I was in everyone's shoes. I looked into this back in 2004 and didn't get it done until this year. You have to decide if your life is worth it. Mine was and is. I can chase my kids and I don't feel like I am an embarassement to them (at least not as big of one) and even though my husband loved and loves me for me, I don't feel so awkward around his work and the comments he used to get.
Bottom line is I am so happy. I am about a little over 1/2 way to my goal, but I am confident I will not only get there but I will enjoy the journey there. Every time I weigh myself I get so happy and amazed that it has moved down yet again.
Thank you again Dr. R. You and the staff are the BEST!!!!!
Laura
April 1, 2009
305/297/215/150
posted by DrR @ 11:48 PM
0 comments
Lactose Intolerance
http://ping.fm/ICtuL
# What is lactose intolerance?
# What causes lactose intolerance?
# Who is at risk for lactose intolerance?
# What are the symptoms of lactose intolerance?
# How is lactose intolerance diagnosed?
# How is lactose intolerance managed?
# What other products contain lactose?
# Points to Remember
# Hope through Research
# For More Information
http://ping.fm/ICtuL
# What is lactose intolerance?
# What causes lactose intolerance?
# Who is at risk for lactose intolerance?
# What are the symptoms of lactose intolerance?
# How is lactose intolerance diagnosed?
# How is lactose intolerance managed?
# What other products contain lactose?
# Points to Remember
# Hope through Research
# For More Information
posted by DrR @ 10:08 PM
0 comments
http://ping.fm/KUbZA
Definition
By Mayo Clinic staff
Clostridium difficile, often called C. difficile or "C. diff," is a bacterium that can cause symptoms ranging from diarrhea to life-threatening inflammation of the colon. Illness from C. difficile most commonly affects older adults in hospitals or in long term care facilities and typically occurs after use of antibiotic medications. ...
Definition
By Mayo Clinic staff
Clostridium difficile, often called C. difficile or "C. diff," is a bacterium that can cause symptoms ranging from diarrhea to life-threatening inflammation of the colon. Illness from C. difficile most commonly affects older adults in hospitals or in long term care facilities and typically occurs after use of antibiotic medications. ...
posted by DrR @ 10:05 PM
0 comments
http://ping.fm/ql4Mm
From Medscape Medical News
Common Misconceptions May Result in Misdiagnosis of Clostridium difficile Infection
Laurie Barclay, MD
From Medscape Medical News
Common Misconceptions May Result in Misdiagnosis of Clostridium difficile Infection
Laurie Barclay, MD
posted by DrR @ 10:03 PM
0 comments
Tuesday, August 04, 2009
Hello all, my name is Renee, I have posted on here a few times, but I have been reading every single post for a couple of months now. I am in the Temecula area of So. Cal. I was wondering if anyone here could recommend a very supportive primary care physician in my neck of the woods. Also I was wondering if there are any patients of Dr. R. that live in my area that i could add to my support team, right now, it is just my hubby, he is VERY supportive, but sometimes it helps to talk to someone who "gets it". I am going to start my packet now, so if anyone wants to be a contact for me, I would SO MUCH appreciate it! Thanks!
P.S. I had the Lap Band surgery last November, i have had so many problems with it that it has been deflated for most of the time that I have had it, so I am very excited about getting this out of my body and starting fresh with the MGB. I wish I had known about this long before I went through all of the mess! If there are any pre-banded converted to MGB's that would like to be a contact, I have some specific questions regarding the removal/switch :)
P.S. I had the Lap Band surgery last November, i have had so many problems with it that it has been deflated for most of the time that I have had it, so I am very excited about getting this out of my body and starting fresh with the MGB. I wish I had known about this long before I went through all of the mess! If there are any pre-banded converted to MGB's that would like to be a contact, I have some specific questions regarding the removal/switch :)
posted by DrR @ 7:35 PM
0 comments
Hi David
I had surgery 5 months ago with Dr R.
I am down 70 lbs and feel great! Blood pressure is better, no cholesterol meds, no more sleep apnea, I am buying new cloths and getting compliments on how great I look since losing weight.
My Mother is the only person that mentioned thinning hair.
I do not have a lot to lose as I am going bald. I cut my hair short for the summer and maybe it will grow back in.
But really, who cares! the weight loss, and health and just feeling great and being able to keep up with my kids has all been great.
Thinning hair and being normal weigh looks muck better than thinning hair and overweight!
Good luck with the surgery
Joe
Dr R 2/25/09 7ft
306/248/190
I had surgery 5 months ago with Dr R.
I am down 70 lbs and feel great! Blood pressure is better, no cholesterol meds, no more sleep apnea, I am buying new cloths and getting compliments on how great I look since losing weight.
My Mother is the only person that mentioned thinning hair.
I do not have a lot to lose as I am going bald. I cut my hair short for the summer and maybe it will grow back in.
But really, who cares! the weight loss, and health and just feeling great and being able to keep up with my kids has all been great.
Thinning hair and being normal weigh looks muck better than thinning hair and overweight!
Good luck with the surgery
Joe
Dr R 2/25/09 7ft
306/248/190
posted by DrR @ 7:33 PM
0 comments
Ok, it has been almost a month since I last posted and almost that in me reading the posts. I have been so busy with work and my 9 kids that time flew by so fast.
First off let me say thank you Dr. R for the surgery. As of 3 days before my 4th month mark I was down 80 lbs. Yep folks reading that correctly. As of today I am down 82. My friend walked up behind me and said oh it is you, I didn't recognize you from behind. Wow that really made me feel good.
I don't have any side effects, and have more energy that I used to, which is weird since I am not sure how I was functioning with my previous weight. You see I have 10 kids, 9 of which live at home, work a full time job and manage a house. I also sell candles on the side and occasionlly baby sit my friends 4 kids. So I have a busy life. But my blood pressure is normal and I feel good.
I know it is a hard decision and the money seems like a lot, I was in everyone's shoes. I looked into this back in 2004 and didn't get it done until this year. You have to decide if your life is worth it. Mine was and is. I can chase my kids and I don't feel like I am an embarassement to them (at least not as big of one) and even though my husband loved and loves me for me, I don't feel so awkward around his work and the comments he used to get.
Bottom line is I am so happy. I am about a little over 1/2 way to my goal, but I am confident I will not only get there but I will enjoy the journey there. Every time I weigh myself I get so happy and amazed that it has moved down yet again.
Thank you again Dr. R. You and the staff are the BEST!!!!!
Laura
April 1, 2009
305/297/215/150
First off let me say thank you Dr. R for the surgery. As of 3 days before my 4th month mark I was down 80 lbs. Yep folks reading that correctly. As of today I am down 82. My friend walked up behind me and said oh it is you, I didn't recognize you from behind. Wow that really made me feel good.
I don't have any side effects, and have more energy that I used to, which is weird since I am not sure how I was functioning with my previous weight. You see I have 10 kids, 9 of which live at home, work a full time job and manage a house. I also sell candles on the side and occasionlly baby sit my friends 4 kids. So I have a busy life. But my blood pressure is normal and I feel good.
I know it is a hard decision and the money seems like a lot, I was in everyone's shoes. I looked into this back in 2004 and didn't get it done until this year. You have to decide if your life is worth it. Mine was and is. I can chase my kids and I don't feel like I am an embarassement to them (at least not as big of one) and even though my husband loved and loves me for me, I don't feel so awkward around his work and the comments he used to get.
Bottom line is I am so happy. I am about a little over 1/2 way to my goal, but I am confident I will not only get there but I will enjoy the journey there. Every time I weigh myself I get so happy and amazed that it has moved down yet again.
Thank you again Dr. R. You and the staff are the BEST!!!!!
Laura
April 1, 2009
305/297/215/150
posted by DrR @ 7:31 PM
0 comments
Monday, August 03, 2009
http://content.nejm.org/cgi/content/short/361/5/445
Perioperative Safety in the Longitudinal Assessment of Bariatric Surgery
The Longitudinal Assessment of Bariatric Surgery (LABS) Consortium
ABSTRACT
Background To improve decision making in the treatment of extreme obesity, the risks of bariatric surgical procedures require further characterization.
Methods We performed a prospective, multicenter, observational study of 30-day outcomes in consecutive patients undergoing bariatric surgical procedures at 10 clinical sites in the United States from 2005 through 2007. A composite end point of 30-day major adverse outcomes (including death; venous thromboembolism; percutaneous, endoscopic, or operative reintervention; and failure to be discharged from the hospital) was evaluated among patients undergoing first-time bariatric surgery.
Results There were 4776 patients who had a first-time bariatric procedure (mean age, 44.5 years; 21.1% men; 10.9% nonwhite; median body-mass index [the weight in kilograms divided by the square of the height in meters], 46.5). More than half had at least two coexisting conditions. A Roux-en-Y gastric bypass was performed in 3412 patients (with 87.2% of the procedures performed laparoscopically), and laparoscopic adjustable gastric banding was performed in 1198 patients; 166 patients underwent other procedures and were not included in the analysis. The 30-day rate of death among patients who underwent a Roux-en-Y gastric bypass or laparoscopic adjustable gastric banding was 0.3%; a total of 4.3% of patients had at least one major adverse outcome. A history of deep-vein thrombosis or pulmonary embolus, a diagnosis of obstructive sleep apnea, and impaired functional status were each independently associated with an increased risk of the composite end point. Extreme values of body-mass index were significantly associated with an increased risk of the composite end point, whereas age, sex, race, ethnic group, and other coexisting conditions were not.
Conclusions The overall risk of death and other adverse outcomes after bariatric surgery was low and varied considerably according to patient characteristics. In helping patients make appropriate choices, short-term safety should be considered in conjunction with both the long-term effects of bariatric surgery and the risks associated with being extremely obese.
Perioperative Safety in the Longitudinal Assessment of Bariatric Surgery
The Longitudinal Assessment of Bariatric Surgery (LABS) Consortium
ABSTRACT
Background To improve decision making in the treatment of extreme obesity, the risks of bariatric surgical procedures require further characterization.
Methods We performed a prospective, multicenter, observational study of 30-day outcomes in consecutive patients undergoing bariatric surgical procedures at 10 clinical sites in the United States from 2005 through 2007. A composite end point of 30-day major adverse outcomes (including death; venous thromboembolism; percutaneous, endoscopic, or operative reintervention; and failure to be discharged from the hospital) was evaluated among patients undergoing first-time bariatric surgery.
Results There were 4776 patients who had a first-time bariatric procedure (mean age, 44.5 years; 21.1% men; 10.9% nonwhite; median body-mass index [the weight in kilograms divided by the square of the height in meters], 46.5). More than half had at least two coexisting conditions. A Roux-en-Y gastric bypass was performed in 3412 patients (with 87.2% of the procedures performed laparoscopically), and laparoscopic adjustable gastric banding was performed in 1198 patients; 166 patients underwent other procedures and were not included in the analysis. The 30-day rate of death among patients who underwent a Roux-en-Y gastric bypass or laparoscopic adjustable gastric banding was 0.3%; a total of 4.3% of patients had at least one major adverse outcome. A history of deep-vein thrombosis or pulmonary embolus, a diagnosis of obstructive sleep apnea, and impaired functional status were each independently associated with an increased risk of the composite end point. Extreme values of body-mass index were significantly associated with an increased risk of the composite end point, whereas age, sex, race, ethnic group, and other coexisting conditions were not.
Conclusions The overall risk of death and other adverse outcomes after bariatric surgery was low and varied considerably according to patient characteristics. In helping patients make appropriate choices, short-term safety should be considered in conjunction with both the long-term effects of bariatric surgery and the risks associated with being extremely obese.
posted by DrR @ 9:47 PM
0 comments
http://sites.google.com/a/clos.net/mini/ulcers-gastritis-and-indigestion
Ulcers Gastritis and Indigestion
1. 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.
Ulcers Gastritis and Indigestion
1. 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.
posted by DrR @ 7:32 PM
0 comments
http://ping.fm/duXjn
Lack of Vitamin D in Children 'Shocking'
LiveScience.com
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LiveScience Staff
LiveScience.com livescience Staff
livescience.com – Mon Aug 3, 9:26 am ET
About 70 percent of U.S. children have low levels of vitamin D, which puts them at higher risk for bone and heart disease, researchers said today.
"We expected the prevalence of vitamin D deficiency would be high, but the magnitude of the problem nationwide was shocking," said Dr. Juhi Kumar of Children's Hospital at Montefiore Medical Center.
Cases of rickets, a bone disease in infants caused by low vitamin D levels, have also been increasing, other research shows.
The new finding, from a nationwide study, adds to growing evidence that children as well as many adults also lack the vitamin.
Lack of Vitamin D in Children 'Shocking'
LiveScience.com
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Buzz up!248 votes
* Send
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* Share
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LiveScience Staff
LiveScience.com livescience Staff
livescience.com – Mon Aug 3, 9:26 am ET
About 70 percent of U.S. children have low levels of vitamin D, which puts them at higher risk for bone and heart disease, researchers said today.
"We expected the prevalence of vitamin D deficiency would be high, but the magnitude of the problem nationwide was shocking," said Dr. Juhi Kumar of Children's Hospital at Montefiore Medical Center.
Cases of rickets, a bone disease in infants caused by low vitamin D levels, have also been increasing, other research shows.
The new finding, from a nationwide study, adds to growing evidence that children as well as many adults also lack the vitamin.
posted by DrR @ 7:04 PM
0 comments
http://ping.fm/ctasm
Low Vitamin D Levels Pose Large Threat To Health; Overall 26 Percent Increased Risk Of Death
ScienceDaily (Aug. 12, 2008) — Researchers at Johns Hopkins are reporting what is believed to be the most conclusive evidence to date that inadequate levels of vitamin D, obtained from milk, fortified cereals and exposure to sunlight, lead to substantially increased risk of death....
Low Vitamin D Levels Pose Large Threat To Health; Overall 26 Percent Increased Risk Of Death
ScienceDaily (Aug. 12, 2008) — Researchers at Johns Hopkins are reporting what is believed to be the most conclusive evidence to date that inadequate levels of vitamin D, obtained from milk, fortified cereals and exposure to sunlight, lead to substantially increased risk of death....
posted by DrR @ 7:02 PM
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