Study Results
Results pending
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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Recruitment Status
COMPLETED
Total Enrollment
30 participants
Study Classification
OBSERVATIONAL
Study Start Date
2009-01-31
Study Completion Date
2009-12-31
Brief Summary
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A common late complication after gastric bypass surgery is marginal ulceration that is defined as ulcers at the margins of the gastrojejunostomy, mostly on the jejunal side. Most marginal ulcers respond to medical therapy and complicated or complex ulcer disease warrants operative intervention; specifically, perforated, penetrated, obstructing, bleeding and intractable marginal ulcers require surgical intervention.
Diverse operative strategies for addressing perforated marginal ulcers after gastric bypass have been described including I) Omental (Graham) patch repair, II) Revision of gastrojejunostomy, III) Irrigation and drainage, IV) any previous procedure with truncal vagotomy, V) Esophagojejunostomy, and VI) Reversal. We formally analyze our experience with the laparoscopic resection and repair of acutely perforated marginal ulcers after Roux-en-Y gastric bypass (RYGB), with or without concomitant resolution of technical risk factors for marginal ulceration.
Diverse operative strategies for addressing perforated marginal ulcers after gastric bypass have been described including I) Omental (Graham) patch repair, II) Revision of gastrojejunostomy, III) Irrigation and drainage, IV) any previous procedure with truncal vagotomy, V) Esophagojejunostomy, and VI) Reversal. We formally analyze our experience with the laparoscopic resection and repair of acutely perforated marginal ulcers after Roux-en-Y gastric bypass (RYGB), with or without concomitant resolution of technical risk factors for marginal ulceration.
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Detailed Description
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The epidemic of overweight and obesity in the United States of America along with its comorbidities continues to expand. Bariatric surgery has demonstrated to be the most effective and sustained method to control severe obesity and its comorbidities. For instance, type 2 diabetes mellitus was completely resolved in 76.8%, systemic arterial hypertension was resolved in 61.7%, dyslipidemia improved in 70% and obstructive sleep apnea-hypopnea syndrome was resolved in 85.7%. Furthermore, bariatric surgery significantly increases life expectancy (89%) and decreases overall mortality (30-40%), particularly deaths from diabetes, heart disease, and cancer. Lastly, preliminary evidence about downstream savings associated with bariatric surgery offset the initial costs in 2 to 4 years.
Since 2000, there has been a substantially progressive increase in bariatric surgery. In 2007, the ASMBS reported that 205,000 people had bariatric surgery in the United States from which approximately 80% of these were Gastric Bypass. Moreover, there is a mismatch between eligibility and receipt of bariatric surgery with just less than 1% of the eligible population being treated for morbid obesity through bariatric surgery. Along with the increasing number of elective primary weight loss procedures, up to 20% of post RYGB patients cannot sustain their weight loss beyond 2 to 3 years after the primary bariatric procedure. Thus, revisional surgery for poor weight loss and re-operations for technical or mechanical complications will rise in a parallel manner.
A common late complication after gastric bypass surgery is marginal ulceration that is defined as ulcers at the margins of the gastrojejunostomy, mostly on the jejunal side. Its incidence after RYGB ranges from as low as 0.6 to as high as 16%. After 1,040 laparoscopic RYGB surgeries, the incidence rate, in our hands, is 1.4% and mainly related to NSAID´s use. In observational cohort studies, the presence of specific technical factors - staple-line dehiscence or gastro-gastric fistula, enlarged pouch, foreign material and local ischemia - and environmental factors - tobacco, NSAID´s, alcohol consumption, and H pylori infection among others - have been associated with marginal ulceration however the exact etiopathogenesis has not been completely elucidated.
Similar to peptic ulcer disease, most marginal ulcers respond to medical therapy and complicated or complex ulcer disease warrants operative intervention. Specifically, perforated, penetrated, obstructing, bleeding and intractable marginal ulcers require surgical intervention.
The intestinal mucosa is not typically exposed to gastric acid, which is neutralized by the alkaline biliopancreatic secretions. The jejunal mucosa has no natural barriers; when exposed to gastric acid, it ulcerates easily. Capella \& Capella demonstrated that transecting the gastric segments significantly reduce staple-line dehiscence; this is the so-called divided gastric bypass. The incidence for gastro-gastric fistula (GGF) formation after undivided gastric bypass (GBP) was 23%, after a partially divided GBP was 19%, after a completely divided GBP was 2% and after complete transection with interposition of the jejunal limb was 0% (p \<0.001).
An unusually large gastric pouch (such as horizontal pouches, retained fundus, long lesser curvature based pouches or enlarged after initially being sized adequately) contain more acid-producing parietal cells. Increased acid production in the pouch carries the risk of developing marginal ulcers. Acid secretion in the small pouch after RYGB is virtually absent.
The anastomotic techniques influence the incidence of marginal ulcers. Capella \& Capella reported a consecutive series with significant decrement from 5.1% to 1.5% (p\< 0.001) after switching from a stapled to a hand-sewn anastomosis. Likewise, after changing from an inner layer of absorbable suture and an outer layer of nonabsorbable material to a double-layer of absorbable suture the incidence rate improved from 1.6% to 0%.
Local ischemia, in the immediate postoperative period, is probably secondary to technical reasons. Fundamental aspects for decreasing tension and local ischemia at the gastrojejunostomy are dissection of the tissues around the pouch without devascularizing the lesser curvature and complete mobilization of a well-perfused Roux limb.
NSAID´s inhibit prostaglandin synthesis 1) decreasing blood flow to the mucosa (mainly by PG subgroups E and I, which promotes vasodilatation), 2) increased adherence of neutrophils, 3) topical irritant effect, 4) impair of the repair/healing process, and 5) gastric-acid-related effects. In a retrospective cohort study, Wilson et al found NSAID´s consumption to correlate with the marginal ulcer development after RYGB. Numerous studies have identified NSAID´s use as a main risk factor for PUD; however, the precise relevance of NSAID´s as a factor in marginal ulcer development after RYGB is largely unknown.
In epidemiological, clinical and experimental studies, Tobacco has been identified as a major risk factor for peptic ulcer disease (PUD). Smoking carries an overall relative risk of 2.2 for developing PUD. A synergistic relationship for developing PUD exists between H pylori infection and smoking (2.3 vs. 6.1). Biological evidence suggests that smoking compromises the gastric mucosa barrier, decreases gastric emptying and increases gastric secretion. For marginal ulcer after RYGB, there are three cohort studies that showed positive correlation between smoking with developing anastomotic ulcer.
Helicobacter pylori (H pylori) infection carries an overall relative risk of 3.3 (95%CI, 2.6-4.4) for developing PUD. A synergistic relationship exists between H pylori infection and NSAID´s consumption for developing PUD with an overall risk of 3.5 (95%CI, 1.26-9.96) compared to either H pylori or NSAID´s negative individuals. Furthermore, a 61.1 (95%CI, 9.98-373) overall risk exist when compared to H pylori negative individuals not taking NSAID´s. For marginal ulcers after RYGB, three cohort studies have showed that H. pylori infection is not associated with the development of marginal ulcers. In Papasavas et al study, preoperative H. pylori testing with prophylactic eradication did not decrease the incidence of MU or erosive pouch gastritis.
The pathophysiological mechanisms of damage to the gastric mucosa of Ethanol and alcoholic beverages are poorly understood. There are scant retrospective epidemiological studies that determine if a relationship between alcohol consumption and PUD exists. Although alcohol is not associated with an increased risk of PUD, patients with PUD are advised to avoid alcoholic drinks. Basic science studies have showed that instillation of pure ethanol at lower concentrations (4-40% v/v) causes hemorrhagic gastritis in a dose-dependant fashion. Also a synergistic relationship exists between ethanol and NSAID´s, since both cause mucosal injury. On the other hand, there are no studies available about the effect of alcohol on marginal ulcer development after RYGB.
Cocaine use is responsible for approximately 143,000 Emergency Department visits annually; 19% of American, between 18 to 25 years old, have used cocaine: more than 1% of the Americans use cocaine at least once a week; and approximately 50% of all drug-related deaths were secondary to Cocaine. The temporal association between smoking cocaine (crack) and GI tract manifestations include ulceration, perforation, visceral infarction, and retroperitoneal fibrosis. Most ulcer perforations are juxtapyloric or duodenal (D1) however jejunal location has been reported. The physiopathologic hypothesis includes the following mechanisms 1) cocaine blocks the re-uptake of norepinephrine leading to intense vasoconstriction (alpha-adrenergic receptors), mesenteric ischemia, focal tissue ischemia, coagulative necrosis and perforation; and 2) cocaine causes thrombus formation and platelet aggregation mediated by endogenous Thromboxane B2. A few retrospective cohort studies suggest that primary patch repair is the recommended therapeutic option for this type of ulcers. However, Shuster et al reported a high recurrence rate (42%) after omental patch repair compared to a definitive anti-ulcer procedure (0%). Little information exists about the association between crack and gastroduodenal ulcer perforations other than the temporal association reported in small retrospective cohort studies. In a communication, Dr Mason recalls two patients with perforated "stomach ulcers" associated with cocaine use.
The following Critically-Ill patients have a significant increased risk of stress-related mucosal disease (SRMD): 1) mechanical ventilation \> 48hrs conveys a 16-fold risk (p \< 0.001), 2) coagulopathy has a 4-fold risk (p \< 0.001), 3) shock carries a 3.7-fold risk (p= 0.08), 4) drop of intramural pH (from 8 to 6, 5), 5) increase of the number of risk factors (from 0 to 4), 6) recent major surgery, 7) major trauma, 8) severe burns, 9) head trauma, 10) hepatic or renal disease at admission, and 11) sepsis. SRMD encompasses stress-related injury (SRI), which is primarily erosion in the GI tract, and stress ulcer, which is a focal deep mucosal damage. The pathogenesis of SRMD has not being unraveled completely but there is strong evidence that hypoperfusion and reperfusion of the upper GI tract is the major cause. There is no literature available about marginal ulcer after RYGB associated to ICU or critically ill patients.
Diverse operative strategies for addressing perforated marginal ulcers after gastric bypass have been described including I) Omental (Graham) patch repair, II) Revision of gastrojejunostomy, III) Irrigation and drainage, IV) any previous procedure with truncal vagotomy, V) Esophagojejunostomy, and VI) Reversal.
Summarizing, there is scant information about late complications after gastric bypass especially after the widespread adoption of the laparoscopic approach and the modern anatomical construct of Roux-en-Y Gastric Bypass surgery.
Since 2000, there has been a substantially progressive increase in bariatric surgery. In 2007, the ASMBS reported that 205,000 people had bariatric surgery in the United States from which approximately 80% of these were Gastric Bypass. Moreover, there is a mismatch between eligibility and receipt of bariatric surgery with just less than 1% of the eligible population being treated for morbid obesity through bariatric surgery. Along with the increasing number of elective primary weight loss procedures, up to 20% of post RYGB patients cannot sustain their weight loss beyond 2 to 3 years after the primary bariatric procedure. Thus, revisional surgery for poor weight loss and re-operations for technical or mechanical complications will rise in a parallel manner.
A common late complication after gastric bypass surgery is marginal ulceration that is defined as ulcers at the margins of the gastrojejunostomy, mostly on the jejunal side. Its incidence after RYGB ranges from as low as 0.6 to as high as 16%. After 1,040 laparoscopic RYGB surgeries, the incidence rate, in our hands, is 1.4% and mainly related to NSAID´s use. In observational cohort studies, the presence of specific technical factors - staple-line dehiscence or gastro-gastric fistula, enlarged pouch, foreign material and local ischemia - and environmental factors - tobacco, NSAID´s, alcohol consumption, and H pylori infection among others - have been associated with marginal ulceration however the exact etiopathogenesis has not been completely elucidated.
Similar to peptic ulcer disease, most marginal ulcers respond to medical therapy and complicated or complex ulcer disease warrants operative intervention. Specifically, perforated, penetrated, obstructing, bleeding and intractable marginal ulcers require surgical intervention.
The intestinal mucosa is not typically exposed to gastric acid, which is neutralized by the alkaline biliopancreatic secretions. The jejunal mucosa has no natural barriers; when exposed to gastric acid, it ulcerates easily. Capella \& Capella demonstrated that transecting the gastric segments significantly reduce staple-line dehiscence; this is the so-called divided gastric bypass. The incidence for gastro-gastric fistula (GGF) formation after undivided gastric bypass (GBP) was 23%, after a partially divided GBP was 19%, after a completely divided GBP was 2% and after complete transection with interposition of the jejunal limb was 0% (p \<0.001).
An unusually large gastric pouch (such as horizontal pouches, retained fundus, long lesser curvature based pouches or enlarged after initially being sized adequately) contain more acid-producing parietal cells. Increased acid production in the pouch carries the risk of developing marginal ulcers. Acid secretion in the small pouch after RYGB is virtually absent.
The anastomotic techniques influence the incidence of marginal ulcers. Capella \& Capella reported a consecutive series with significant decrement from 5.1% to 1.5% (p\< 0.001) after switching from a stapled to a hand-sewn anastomosis. Likewise, after changing from an inner layer of absorbable suture and an outer layer of nonabsorbable material to a double-layer of absorbable suture the incidence rate improved from 1.6% to 0%.
Local ischemia, in the immediate postoperative period, is probably secondary to technical reasons. Fundamental aspects for decreasing tension and local ischemia at the gastrojejunostomy are dissection of the tissues around the pouch without devascularizing the lesser curvature and complete mobilization of a well-perfused Roux limb.
NSAID´s inhibit prostaglandin synthesis 1) decreasing blood flow to the mucosa (mainly by PG subgroups E and I, which promotes vasodilatation), 2) increased adherence of neutrophils, 3) topical irritant effect, 4) impair of the repair/healing process, and 5) gastric-acid-related effects. In a retrospective cohort study, Wilson et al found NSAID´s consumption to correlate with the marginal ulcer development after RYGB. Numerous studies have identified NSAID´s use as a main risk factor for PUD; however, the precise relevance of NSAID´s as a factor in marginal ulcer development after RYGB is largely unknown.
In epidemiological, clinical and experimental studies, Tobacco has been identified as a major risk factor for peptic ulcer disease (PUD). Smoking carries an overall relative risk of 2.2 for developing PUD. A synergistic relationship for developing PUD exists between H pylori infection and smoking (2.3 vs. 6.1). Biological evidence suggests that smoking compromises the gastric mucosa barrier, decreases gastric emptying and increases gastric secretion. For marginal ulcer after RYGB, there are three cohort studies that showed positive correlation between smoking with developing anastomotic ulcer.
Helicobacter pylori (H pylori) infection carries an overall relative risk of 3.3 (95%CI, 2.6-4.4) for developing PUD. A synergistic relationship exists between H pylori infection and NSAID´s consumption for developing PUD with an overall risk of 3.5 (95%CI, 1.26-9.96) compared to either H pylori or NSAID´s negative individuals. Furthermore, a 61.1 (95%CI, 9.98-373) overall risk exist when compared to H pylori negative individuals not taking NSAID´s. For marginal ulcers after RYGB, three cohort studies have showed that H. pylori infection is not associated with the development of marginal ulcers. In Papasavas et al study, preoperative H. pylori testing with prophylactic eradication did not decrease the incidence of MU or erosive pouch gastritis.
The pathophysiological mechanisms of damage to the gastric mucosa of Ethanol and alcoholic beverages are poorly understood. There are scant retrospective epidemiological studies that determine if a relationship between alcohol consumption and PUD exists. Although alcohol is not associated with an increased risk of PUD, patients with PUD are advised to avoid alcoholic drinks. Basic science studies have showed that instillation of pure ethanol at lower concentrations (4-40% v/v) causes hemorrhagic gastritis in a dose-dependant fashion. Also a synergistic relationship exists between ethanol and NSAID´s, since both cause mucosal injury. On the other hand, there are no studies available about the effect of alcohol on marginal ulcer development after RYGB.
Cocaine use is responsible for approximately 143,000 Emergency Department visits annually; 19% of American, between 18 to 25 years old, have used cocaine: more than 1% of the Americans use cocaine at least once a week; and approximately 50% of all drug-related deaths were secondary to Cocaine. The temporal association between smoking cocaine (crack) and GI tract manifestations include ulceration, perforation, visceral infarction, and retroperitoneal fibrosis. Most ulcer perforations are juxtapyloric or duodenal (D1) however jejunal location has been reported. The physiopathologic hypothesis includes the following mechanisms 1) cocaine blocks the re-uptake of norepinephrine leading to intense vasoconstriction (alpha-adrenergic receptors), mesenteric ischemia, focal tissue ischemia, coagulative necrosis and perforation; and 2) cocaine causes thrombus formation and platelet aggregation mediated by endogenous Thromboxane B2. A few retrospective cohort studies suggest that primary patch repair is the recommended therapeutic option for this type of ulcers. However, Shuster et al reported a high recurrence rate (42%) after omental patch repair compared to a definitive anti-ulcer procedure (0%). Little information exists about the association between crack and gastroduodenal ulcer perforations other than the temporal association reported in small retrospective cohort studies. In a communication, Dr Mason recalls two patients with perforated "stomach ulcers" associated with cocaine use.
The following Critically-Ill patients have a significant increased risk of stress-related mucosal disease (SRMD): 1) mechanical ventilation \> 48hrs conveys a 16-fold risk (p \< 0.001), 2) coagulopathy has a 4-fold risk (p \< 0.001), 3) shock carries a 3.7-fold risk (p= 0.08), 4) drop of intramural pH (from 8 to 6, 5), 5) increase of the number of risk factors (from 0 to 4), 6) recent major surgery, 7) major trauma, 8) severe burns, 9) head trauma, 10) hepatic or renal disease at admission, and 11) sepsis. SRMD encompasses stress-related injury (SRI), which is primarily erosion in the GI tract, and stress ulcer, which is a focal deep mucosal damage. The pathogenesis of SRMD has not being unraveled completely but there is strong evidence that hypoperfusion and reperfusion of the upper GI tract is the major cause. There is no literature available about marginal ulcer after RYGB associated to ICU or critically ill patients.
Diverse operative strategies for addressing perforated marginal ulcers after gastric bypass have been described including I) Omental (Graham) patch repair, II) Revision of gastrojejunostomy, III) Irrigation and drainage, IV) any previous procedure with truncal vagotomy, V) Esophagojejunostomy, and VI) Reversal.
Summarizing, there is scant information about late complications after gastric bypass especially after the widespread adoption of the laparoscopic approach and the modern anatomical construct of Roux-en-Y Gastric Bypass surgery.
Conditions
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Ulcer Disease After Gastric Bypass
Marginal Ulcer
Perforated Marginal Ulcer
Acutely Perforated Marginal Ulcer
Study Design
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Observational Model Type
COHORT
Study Time Perspective
RETROSPECTIVE
Study Groups
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perforated ulcer after gastric bypass
No interventions assigned to this group
Eligibility Criteria
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Inclusion Criteria
* Laparoscopic repair of perforated marginal ulcer after RYGB
Exclusion Criteria
* Perforated marginal ulcers after other bariatric procedures
* Repair by open approach
* Missing records and/or unreachable patients with scant information for analysis
* Repair by open approach
* Missing records and/or unreachable patients with scant information for analysis
Minimum Eligible Age
18 Years
Maximum Eligible Age
65 Years
Eligible Sex
ALL
Accepts Healthy Volunteers
No
Sponsors
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University of California, San Francisco
OTHER
Sponsor Role
lead
Responsible Party
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UCSF Fresno / ALSA Medical Group, Inc. Minimally Invasive Surgery Program
Principal Investigators
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Francisco M Tercero, MD
Role: STUDY_DIRECTOR
Research Associate, University of California San Francisco
Kelvin D Higa, MD
Role: PRINCIPAL_INVESTIGATOR
Professor of Surgery, University of California San Francisco
Locations
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UCSF Fresno Center for Medical Education and Research
Fresno, California, United States
Site Status
Countries
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United States
References
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Higa KD, Boone KB, Ho T, Davies OG. Laparoscopic Roux-en-Y gastric bypass for morbid obesity: technique and preliminary results of our first 400 patients. Arch Surg. 2000 Sep;135(9):1029-33; discussion 1033-4. doi: 10.1001/archsurg.135.9.1029.
Reference Type
BACKGROUND
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BACKGROUND
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BACKGROUND
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BACKGROUND
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BACKGROUND
Cremieux PY, Buchwald H, Shikora SA, Ghosh A, Yang HE, Buessing M. A study on the economic impact of bariatric surgery. Am J Manag Care. 2008 Sep;14(9):589-96.
Reference Type
BACKGROUND
Santry HP, Gillen DL, Lauderdale DS. Trends in bariatric surgical procedures. JAMA. 2005 Oct 19;294(15):1909-17. doi: 10.1001/jama.294.15.1909.
Reference Type
BACKGROUND
Flum DR, Khan TV, Dellinger EP. Toward the rational and equitable use of bariatric surgery. JAMA. 2007 Sep 26;298(12):1442-4. doi: 10.1001/jama.298.12.1442. No abstract available.
Reference Type
BACKGROUND
Meguid MM, Glade MJ, Middleton FA. Weight regain after Roux-en-Y: a significant 20% complication related to PYY. Nutrition. 2008 Sep;24(9):832-42. doi: 10.1016/j.nut.2008.06.027.
Reference Type
BACKGROUND
Nguyen NT. Reoperations and revisions in bariatric surgery. Surg Endosc. 2007 Nov;21(11):1907-8. doi: 10.1007/s00464-007-9572-6. Epub 2007 Sep 8. No abstract available.
Reference Type
BACKGROUND
Sapala JA, Wood MH, Sapala MA, Flake TM Jr. Marginal ulcer after gastric bypass: a prospective 3-year study of 173 patients. Obes Surg. 1998 Oct;8(5):505-16. doi: 10.1381/096089298765554061.
Reference Type
BACKGROUND
Higa KD, Boone KB, Ho T. Complications of the laparoscopic Roux-en-Y gastric bypass: 1,040 patients--what have we learned? Obes Surg. 2000 Dec;10(6):509-13. doi: 10.1381/096089200321593706.
Reference Type
BACKGROUND
Sanyal AJ, Sugerman HJ, Kellum JM, Engle KM, Wolfe L. Stomal complications of gastric bypass: incidence and outcome of therapy. Am J Gastroenterol. 1992 Sep;87(9):1165-9.
Reference Type
BACKGROUND
Capella JF, Capella RF. Staple Disruption and Marginal Ulceration in Gastric Bypass Procedures for Weight Reduction. Obes Surg. 1996 Feb;6(1):44-49. doi: 10.1381/096089296765557259.
Reference Type
BACKGROUND
Capella JF, Capella RF. Gastro-gastric fistulas and marginal ulcers in gastric bypass procedures for weight reduction. Obes Surg. 1999 Feb;9(1):22-7; discussion 28. doi: 10.1381/096089299765553674.
Reference Type
BACKGROUND
Jordan JH, Hocking MP, Rout WR, Woodward ER. Marginal ulcer following gastric bypass for morbid obesity. Am Surg. 1991 May;57(5):286-8.
Reference Type
BACKGROUND
Sacks BC, Mattar SG, Qureshi FG, Eid GM, Collins JL, Barinas-Mitchell EJ, Schauer PR, Ramanathan RC. Incidence of marginal ulcers and the use of absorbable anastomotic sutures in laparoscopic Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2006 Jan-Feb;2(1):11-6. doi: 10.1016/j.soard.2005.10.013.
Reference Type
BACKGROUND
Lublin M, McCoy M, Waldrep DJ. Perforating marginal ulcers after laparoscopic gastric bypass. Surg Endosc. 2006 Jan;20(1):51-4. doi: 10.1007/s00464-005-0325-0. Epub 2005 Dec 7.
Reference Type
BACKGROUND
St Jean MR, Dunkle-Blatter SE, Petrick AT. Laparoscopic management of perforated marginal ulcer after laparoscopic Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2006 Nov-Dec;2(6):668. doi: 10.1016/j.soard.2006.09.011. No abstract available.
Reference Type
BACKGROUND
Chin EH, Hazzan D, Sarpel U, Herron DM. Multimedia article. Laparoscopic repair of a perforated marginal ulcer 2 years after gastric bypass. Surg Endosc. 2007 Nov;21(11):2110. doi: 10.1007/s00464-007-9486-3. Epub 2007 Aug 18.
Reference Type
BACKGROUND
Wheeler AA, de la Torre RA, Fearing NM. Laparoscopic repair of perforated marginal ulcer following Roux-en-Y gastric bypass: a case series. J Laparoendosc Adv Surg Tech A. 2011 Jan-Feb;21(1):57-60. doi: 10.1089/lap.2010.0402. Epub 2011 Jan 19.
Reference Type
BACKGROUND
Nguyen NT, Hinojosa MW, Gray J, Fayad C. Reoperation for marginal ulceration. Surg Endosc. 2007 Nov;21(11):1919-21. doi: 10.1007/s00464-007-9538-8. Epub 2007 Aug 19. No abstract available.
Reference Type
BACKGROUND
Patel RA, Brolin RE, Gandhi A. Revisional operations for marginal ulcer after Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2009 May-Jun;5(3):317-22. doi: 10.1016/j.soard.2008.10.011. Epub 2008 Nov 6.
Reference Type
BACKGROUND
Hata JA, DeMaria EJ, Portenier DD, et al. Marginal ulcer after 1,792 laparoscopic Roux-en-Y gastric bypass (LRYGB) procedures: incidence, medical and surgical treatment and complications. Surg Obes Relat Dis 2008; 4:308-9 (abstract).
Reference Type
BACKGROUND
Madan AK, DeArmond G, Ternovits CA, Beech DJ, Tichansky DS. Laparoscopic revision of the gastrojejunostomy for recurrent bleeding ulcers after past open revision gastric bypass. Obes Surg. 2006 Dec;16(12):1662-8. doi: 10.1381/096089206779319400.
Reference Type
BACKGROUND
Silver R, Levine MS, Williams NN, Rubesin SE. Using radiography to reveal chronic jejunal ischemia as a complication of gastric bypass surgery. AJR Am J Roentgenol. 2003 Nov;181(5):1365-7. doi: 10.2214/ajr.181.5.1811365. No abstract available.
Reference Type
BACKGROUND
Ruutiainen AT, Levine MS, Williams NN. Giant jejunal ulcers after Roux-en-Y gastric bypass. Abdom Imaging. 2008 Sep-Oct;33(5):575-8. doi: 10.1007/s00261-007-9344-8.
Reference Type
BACKGROUND
Wallace JL. Pathogenesis of NSAID-induced gastroduodenal mucosal injury. Best Pract Res Clin Gastroenterol. 2001 Oct;15(5):691-703. doi: 10.1053/bega.2001.0229.
Reference Type
BACKGROUND
Ben-Meir A, Sonpal I, Patterson L, et al. Cigarette smoking, but not NSAID or alcohol use of comorbidities, is associated with anastomotic ulcer in Roux-en-Y gastric bypass (RYGB) patients. Surg Obes Relat Dis 2005;1: 263-4.
Reference Type
BACKGROUND
Kurata JH, Nogawa AN. Meta-analysis of risk factors for peptic ulcer. Nonsteroidal antiinflammatory drugs, Helicobacter pylori, and smoking. J Clin Gastroenterol. 1997 Jan;24(1):2-17. doi: 10.1097/00004836-199701000-00002.
Reference Type
BACKGROUND
Schreiber H, Ben-Meir A, Sonpal I, et al. Cigarette smoking, but not the presence of H.pylori, is associated with anastomotic ulcers in Roux-en-Y gastric bypass patients. Surg Obes Relat Dis 2005;1:257.
Reference Type
BACKGROUND
Huang JQ, Sridhar S, Hunt RH. Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease: a meta-analysis. Lancet. 2002 Jan 5;359(9300):14-22. doi: 10.1016/S0140-6736(02)07273-2.
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Related Links
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http://www.fresno.ucsf.edu/surgery/
"Click here for more information about the department sponsor´s web site"
Other Identifiers
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U1111-1113-0006
Identifier Type: OTHER
Identifier Source: secondary_id
CMC IRB No. 2008091
Identifier Type: -
Identifier Source: org_study_id
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