A retrospective analysis of the correlation of patients' description of melena with...
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A1308 AGA ABSTRACTS 5968 H.PYLORI ERADICATION IS NOT ABLE TO PREVENT THE ATHEROSCLEROSIS ASSOCIATED WITH HOMOCYSTEINE. Daisuke Shirasaka, Nobuo Aoyama, Toshiyuki Sakai, Takahiro Ikemura, Masanori Sakashita, Kohei Kuroda, Shuji Maekawa, Casmir Wambura, Shigeyuki Ebara, Takashi Inoue, Masaki Miyamoto, Masato Kasuga, Kobe Univ Sch of Med, Kobe, Japan. Background: In an environment of increased gastric juice pH which are associated with Helicobacter pylori infection, the folate absorption may be reduced and this result in increase the blood concentration of homocysteine (Hey) which is known to be a risk factor for atherosclerosis. H.pylori eradication decreases gastric juice pH, however, it is not clear that the folate absorption and the blood concentration of Hcy are changed after H.pylori eradication and this result in the prevention of atherosclerosis. Materials and Methods: Thirty patients, who had received H.pylori eradi- cation and found to be H.pylori negative after eradication, participated in this study. In the morning before breakfast, gastric juice samples aspirated through the suction channel of the endoscope and blood samples were obtained, before and after H.pylori eradication. Gastric juice pH, the blood concentration of folic acid (FA), vitamin BI2 (BI2), and Hey were mea- sured. Results: Gastric juice pH decreased after eradication (mean pH 3.89::!:2.79 and 1.92::!: 1.69, p<0.05). FA and BI2 had no change (mean FA [ng/ml] 6.6::!:3.4 and 6.8::!:2.9, mean BI2 [pg/m!] 49±230 and 454::!:212). However, Hey increased after H.pylori eradication (mean Hcy [umol/L] 1O.8±S.3 and II.7::!:6.0, p<0.05). Conclusions: H.pylori eradication in- creased the blood concentration of Hey and is not able to reduce the risk factor for atherosclerosis associated with homocysteine. 5969 A RETROSPECTIVE ANALYSIS OF THE CORRELATION OF PATIENTS' DESCRIPTION OF MELENA WITH GASTROENTER· OLOGISTS' INTERPRETATION AND THE PRESENCE OF UP- PER GASTROINTESTINAL TRACT LESIONS. Archana K. Shyamsunder, Atenodoro Ruiz, Ramprasad Dandillaya, Marie L. Borum, George Washington Univ, Washington, DC. INTRODUCTION Melena usually correlates with an upper gastrointestinal (GI) source of bleeding. Since stool is not always available for direct observation by a physician, reliance upon a patient's stool description may be necessary. This is a retrospective analysis of the correlation of patients' description of black and/or taITY stool with (1) gastroenterologists' inter- pretation, and (2) presence of an upper GI source of blood loss. METH- ODS A retrospective chart review of consecutive consults between January 1998 and June 1999 performed by the university gastroenterology service was conducted. All consults for the evaluation of melena were selected for analysis. Consults with incomplete or unclear stool description were ex- cluded. Patients' and gastroenterologists' description of the stool were recorded. Results of the GI evaluation were also recorded. Data were analyzed to correlate patients' description of black and/or tarry stool with (1) gastroenterologists' interpretation, and (2) upper GI lesions. RESULTS Of 519 consults, 77 were obtained for evaluation of melena, 9 were excluded due to incomplete data, leaving 68 for study inclusion. The mean age of the population was 5S years (range 23-94). In 44 (6S%) a gastro- enterologist identified the stool as melena. In 7 (1O%)a gastroenterologist did not identify the stool as melena. In the remaining 17 (2S%), there was no clear description of the stool by a gastroenterologist. Of the SI cases in which a gastroenterologist's description of stool was available, 44(86%) correlated with the patient's description. Review of esophagogastroduode- noscopy (EGO) results revealed that 49 (72%) had demonstrable upper GI lesions. Nine (13%) EGOs did not identify a lesion. In 2 cases, an EGO was not performed because the stool color was attributed to the consumption of Peptobismol and in I case an EGO was not completed due to clinical instability. In the remaining 7 (10%), results of the EGO were unavailable. In 8 of the 9 cases in which there was a negative EGO, a colonoscopy was performed and lower GI lesions were identified in 7. CONCLUSIONS In the majority of cases, patients' description of black and/or taITY stools is reliable and correlates with a gastroenterologist's interpretation and the presence of an upper GI source of blood loss. Decisions regarding diag- nostic evaluation can be based upon patients' description of melena. 5970 GASTRIC SECRETORY FUNCTION IN CATS WITH HELICO- BACTER PYLORI ASSOCIATED GASTRITIS. Kenneth W. Simpson, Dalit Strauss-Ayali, Reinhard K. Straubinger, Eu- genio Scanziani, Patrick L. McDonough, Alix F. Straubinger, Yung-FU Chang, Maria I. Esteves, Fox G. James, Cyntia Domeneghini, Naila Arebi, John Calam, Cornell Univ, Ithaca, NY; Univ of Milan, Milan, Italy; MIT, Boston, MA; Imperial Coli, London, United Kingdom. Background & Aims: The pathogenesis of gastric secretory abnormalities in people with H. pylori infection is unclear. This study evaluated gastric secretory function and the mucosal inflammatory response in cats with naturally acquired H. pylori infection. Methods: Twenty H. pylori infected and 19 Helicobacter-itee cats were evaluated. Gastric secretory function was assessed by measuring pentagastrin stimulated acid secretion, fasting plasma gastrin, and antral mucosal gastrin and somatostatin immunoreac- tivity. The mucosal inflammatory response was evaluated by light micros- copy, and by RT-PCR of the proinflammatory cytokines IL-I a, IL-l {3, IL-8 and TNF-ain gastric mucosa. Results: Gastric secretory function was GASTROENTEROLOGY Vol. 118, No.4 similar in both infected and uninfected cats. Mononuclear inflammation, lymphoid follicle hyperplasia, atrophy, and fibrosis were observed primal- ily in H. pylori infected cats, with the pylorus most severely affected. Neutrophilic and eosinophilic infiltrates, epithelial dysplasia, and up-reg- ulation of mucosal IL-l {3and IL-8 were observed solely in infected cats. There was no relationship of bacterial colonization density or gastric inflammation to gastric acid output or plasma gastrin concentrations. Con- clusions:H. pylori infection in cats is associated with pylorus dominant gastritis, up-regulation of mucosal IL-I {3and IL-8 and marked lymphoid follicle hyperplasia, but normal gastric secretory function. Our findings argue against a direct effect of urease or other H. pylori associated factors on the gastric secretory-axis in the cat. 5971 GASTROINTESTINAL PERMEABILITY TO ACUTE DOSES OF NON-STEROID ANTI-INFLAMMATORY DRUGS. A COMPARA· TIVE STUDY. Edgardo G. Smecuol, Julio C. Bai, Emilia Sugai, Horacio Vazquez, Sonia I. Niveloni, Silvia C. Pedreira, Roberto Mazure, Eduardo Maurino, Jon Meddings, Gastroenterology Hosp, Buenos Aires, Argentina; GI Research Group, Univ of Calgary, Calgary-Alberta, Canada. BACKGROUNDS/AIMS: Non-steroid antiinflammatory drugs (NSAIDs) cause gastrointestinal damage both in the upper and distal GI tact. New drugs were developed in order to improve their GI side-effect profile. Our objective was to compale the effect on GI permeability of acute equief- fective doses of 3 different NSAIDs; two of which were designed to reduce GI mucosal injury. MATERIALS: We evaluated 19 healthy volunteers (10 female; median age: 32 years, range: 22-50) who underwent sugar tests in randomized fashion, IS days apart, at (1) baseline; (2) after 2 days of7S mg of slow-release Indomethacin (Indo) (microspheres); (3) after two days of 7.S mg of oral Meloxicam (Melo), which preferentially inhibits COX-2; and (4) after two days of 7S0 mg of Naproxen (Napro). In each test, subjects ingested a solution containing 100g sucrose, Sg lactulose (Lac) and 2g mannitol (Man) in 4S0 ml of water and 2g sucralose, in order to evaluate gastroduodenal, intestinal and colonic permeability, respectively. The urinary excretion of sugars was measured by HPLC. RESULTS: (medianz SliM) Gastric permeability was significantly affected by Napro (sucrose excretion: 110.7 mg.t 13.1; p<O.OS) but not by slow-release Indo (78.7± 12.S) or Melo (9S.9::!: 18.3) when compared with healthy subjects (78.S::!: 12.8). Intestinal permeability was significantly increased by the three different NSAIDs (LaclMan ratio: 0.032±0.003; 0.041 ::!:0.006; 0.034±0.006; after Napro, Indo and Melo, respectively; p<O.OS) ccom- paled to controls (0.022::!:0.OO2). Increased Lac/Man ratios were observed following treatment in 42% of Melo recipients, in 62% of Indo recipients and in 75% of subjects treated with Napro. Colonic permeability was not significantly impaired by any of the 3 drugs. CONCLUSION: We have demonstrated that acute doses of NSAIDs, developed in order to reduce GI mucosal damage, did not significantly increase either gastric or colonic permeability. However, significant small intestinal mucosal damage was observed after ingestion of the three types of drugs with a trend for a greater prevalence using a conventional NSAID such as Napro. Although, increased gastric safety is a clear benefit of these drugs, this protection does not appeal to extend to the small intestine. 5972 PATIENTS RECALL OF NONSTEROIDAL ANTIINFLAMMA- TORY DRUGS (NSAIDS) INTAKE BEFORE AND AFTER ENDOS- COPY. Jose D. Sollano, Romiro P. Babaran, Univ of Santo Tomas, Manila. Philippines. Background: Most investigators suspect surreptitious NSAID intake in the event of major gastrointestinal catastrophies, especially in the elderly although patients have great difficulty recalling such intake. Thus, we usually rely on clinical events in deducing NSAID toxicity, endoscopic lesions being very common in the absence of other significant risk factors. Objectives: We aim to determine if dyspeptic patients forget or deny NSAID intake by confronting them before and after upper GI endoscopy; to determine the adequacy of recall of NSAID use among patients who have lesions suggestive of NSAID injury. Patients and Methods: All patients who underwent upper GI endoscopy due to dyspepsia were asked regarding NSAID use and their responses were classified as; index recall if patients had an immediate recall of NSAID intake when inquired; assisted recall if an initial denial is reported, however, recalled correctly when assisted by a checklist containing all locally-available NSAIDs; confronted recall when the admission of NSAID intake was made only after patients have been informed of lesions found on endoscopy. During endoscopy, lesions were recorded according to the site; size and severity based on the Modified Lanza Scoring System. Results: A total of 266 patients (M: F=l.13:I, mean age = 48.1S+IS.65yrs) underwent upper GI endoscopy due to dyspeptic symptoms. Overall, 182 patients demonstrated gastrodu- odenal lesions. One hundred four patients found to have gastroduodenal lesions had accurate index recall of drug intake while SI patients responded positively only after the assisted recall (57% vs. 28%, p<O.OS). In 27 patients (1S%) who had gastroduodenal lesions, NSAID intake was denied either before or after endoscopy and even when confronted with the endoscopic findings. The mean Lanza scores for index recall, assisted recall and confronted recall ale 2.S1 +, I.S8, and 0.83, respectively (p=<O.OOI). Of 131 patients found to have lesions and positively recalled
Transcript of A retrospective analysis of the correlation of patients' description of melena with...
A1308 AGA ABSTRACTS
5968H.PYLORI ERADICATION IS NOT ABLE TO PREVENT THEATHEROSCLEROSIS ASSOCIATED WITH HOMOCYSTEINE.Daisuke Shirasaka, Nobuo Aoyama, Toshiyuki Sakai, Takahiro Ikemura,Masanori Sakashita, Kohei Kuroda, Shuji Maekawa, Casmir Wambura,Shigeyuki Ebara, Takashi Inoue, Masaki Miyamoto, Masato Kasuga, KobeUniv Sch of Med, Kobe, Japan.
Background: In an environment of increased gastric juice pH which areassociated with Helicobacter pylori infection, the folate absorption may bereduced and this result in increase the blood concentration of homocysteine(Hey) which is known to be a risk factor for atherosclerosis. H.pylorieradication decreases gastric juice pH, however, it is not clear that thefolate absorption and the blood concentration of Hcy are changed afterH.pylori eradication and this result in the prevention of atherosclerosis.Materials and Methods: Thirty patients, who had received H.pylori eradication and found to be H.pylori negative after eradication, participated inthis study. In the morning before breakfast, gastric juice samples aspiratedthrough the suction channel of the endoscope and blood samples wereobtained, before and after H.pylori eradication. Gastric juice pH, the bloodconcentration of folic acid (FA), vitamin BI2 (BI2), and Hey were measured. Results: Gastric juice pH decreased after eradication (mean pH3.89::!:2.79 and 1.92::!: 1.69, p<0.05). FA and BI2 had no change (mean FA[ng/ml] 6.6::!:3.4 and 6.8::!:2.9, mean BI2 [pg/m!] 49±230 and 454::!:212).However, Hey increased after H.pylori eradication (mean Hcy [umol/L]1O.8±S.3 and II.7::!:6.0, p<0.05). Conclusions: H.pylori eradication increased the blood concentration of Hey and is not able to reduce the riskfactor for atherosclerosis associated with homocysteine.
5969A RETROSPECTIVE ANALYSIS OF THE CORRELATION OFPATIENTS' DESCRIPTION OF MELENA WITH GASTROENTER·OLOGISTS' INTERPRETATION AND THE PRESENCE OF UPPER GASTROINTESTINAL TRACT LESIONS.Archana K. Shyamsunder, Atenodoro Ruiz, Ramprasad Dandillaya, MarieL. Borum, George Washington Univ, Washington, DC.
INTRODUCTION Melena usually correlates with an upper gastrointestinal(GI) source of bleeding. Since stool is not always available for directobservation by a physician, reliance upon a patient's stool description maybe necessary. This is a retrospective analysis of the correlation of patients'description of black and/or taITY stool with (1) gastroenterologists' interpretation, and (2) presence of an upper GI source of blood loss. METHODS A retrospective chart review of consecutive consults between January1998 and June 1999 performed by the university gastroenterology servicewas conducted. All consults for the evaluation of melena were selected foranalysis. Consults with incomplete or unclear stool description were excluded. Patients' and gastroenterologists' description of the stool wererecorded. Results of the GI evaluation were also recorded. Data wereanalyzed to correlate patients' description of black and/or tarry stool with(1) gastroenterologists' interpretation, and (2) upper GI lesions. RESULTSOf 519 consults, 77 were obtained for evaluation of melena, 9 wereexcluded due to incomplete data, leaving 68 for study inclusion. The meanage of the population was 5S years (range 23-94). In 44 (6S%) a gastroenterologist identified the stool as melena. In 7 (1O%)agastroenterologistdid not identify the stool as melena. In the remaining 17 (2S%), there wasno clear description of the stool by a gastroenterologist. Of the SI cases inwhich a gastroenterologist's description of stool was available, 44(86%)correlated with the patient's description. Review of esophagogastroduodenoscopy (EGO) results revealed that 49 (72%) had demonstrable upper GIlesions. Nine (13%) EGOs did not identify a lesion. In 2 cases, an EGO wasnot performed because the stool color was attributed to the consumption ofPeptobismol and in I case an EGO was not completed due to clinicalinstability. In the remaining 7 (10%), results of the EGO were unavailable.In 8 of the 9 cases in which there was a negative EGO, a colonoscopy wasperformed and lower GI lesions were identified in 7. CONCLUSIONS Inthe majority of cases, patients' description of black and/or taITY stools isreliable and correlates with a gastroenterologist's interpretation and thepresence of an upper GI source of blood loss. Decisions regarding diagnostic evaluation can be based upon patients' description of melena.
5970GASTRIC SECRETORY FUNCTION IN CATS WITH HELICOBACTER PYLORI ASSOCIATED GASTRITIS.Kenneth W. Simpson, Dalit Strauss-Ayali, Reinhard K. Straubinger, Eugenio Scanziani, Patrick L. McDonough, Alix F. Straubinger, Yung-FUChang, Maria I. Esteves, Fox G. James, Cyntia Domeneghini, Naila Arebi,John Calam, Cornell Univ, Ithaca, NY; Univ of Milan, Milan, Italy; MIT,Boston, MA; Imperial Coli, London, United Kingdom.
Background & Aims: The pathogenesis of gastric secretory abnormalitiesin people with H. pylori infection is unclear. This study evaluated gastricsecretory function and the mucosal inflammatory response in cats withnaturally acquired H. pylori infection. Methods: Twenty H. pylori infectedand 19 Helicobacter-itee cats were evaluated. Gastric secretory functionwas assessed by measuring pentagastrin stimulated acid secretion, fastingplasma gastrin, and antral mucosal gastrin and somatostatin immunoreactivity. The mucosal inflammatory response was evaluated by light microscopy, and by RT-PCR of the proinflammatory cytokines IL-I a, IL-l {3, IL-8and TNF-ain gastric mucosa. Results: Gastric secretory function was
GASTROENTEROLOGY Vol. 118, No.4
similar in both infected and uninfected cats. Mononuclear inflammation,lymphoid follicle hyperplasia, atrophy, and fibrosis were observed primalily in H. pylori infected cats, with the pylorus most severely affected.Neutrophilic and eosinophilic infiltrates, epithelial dysplasia, and up-regulation of mucosal IL-l {3and IL-8 were observed solely in infected cats.There was no relationship of bacterial colonization density or gastricinflammation to gastric acid output or plasma gastrin concentrations. Conclusions:H. pylori infection in cats is associated with pylorus dominantgastritis, up-regulation of mucosal IL-I {3and IL-8 and marked lymphoidfollicle hyperplasia, but normal gastric secretory function. Our findingsargue against a direct effect of urease or other H. pylori associated factorson the gastric secretory-axis in the cat.
5971GASTROINTESTINAL PERMEABILITY TO ACUTE DOSES OFNON-STEROID ANTI-INFLAMMATORY DRUGS. A COMPARA·TIVE STUDY.Edgardo G. Smecuol, Julio C. Bai, Emilia Sugai, Horacio Vazquez, SoniaI. Niveloni, Silvia C. Pedreira, Roberto Mazure, Eduardo Maurino, JonMeddings, Gastroenterology Hosp, Buenos Aires, Argentina; GI ResearchGroup, Univ of Calgary, Calgary-Alberta, Canada.
BACKGROUNDS/AIMS: Non-steroid antiinflammatory drugs (NSAIDs)cause gastrointestinal damage both in the upper and distal GI tact. Newdrugs were developed in order to improve their GI side-effect profile. Ourobjective was to compale the effect on GI permeability of acute equieffective doses of 3 different NSAIDs; two of which were designed to reduceGI mucosal injury. MATERIALS: We evaluated 19 healthy volunteers (10female; median age: 32 years, range: 22-50) who underwent sugar tests inrandomized fashion, IS days apart, at (1) baseline; (2) after 2 days of7S mgof slow-release Indomethacin (Indo) (microspheres); (3) after two days of7.S mg of oral Meloxicam (Melo), which preferentially inhibits COX-2;and (4) after two days of 7S0 mg of Naproxen (Napro). In each test,subjects ingested a solution containing 100g sucrose, Sg lactulose (Lac)and 2g mannitol (Man) in 4S0 ml of water and 2g sucralose, in order toevaluate gastroduodenal, intestinal and colonic permeability, respectively.The urinary excretion of sugars was measured by HPLC. RESULTS:(medianzSliM) Gastric permeability was significantly affected by Napro(sucrose excretion: 110.7 mg.t 13.1; p<O.OS)but not by slow-release Indo(78.7± 12.S) or Melo (9S.9::!: 18.3) when compared with healthy subjects(78.S::!: 12.8). Intestinal permeability was significantly increased by thethree different NSAIDs (LaclMan ratio: 0.032±0.003; 0.041 ::!:0.006;0.034±0.006; after Napro, Indo and Melo, respectively; p<O.OS) ccompaled to controls (0.022::!:0.OO2). Increased Lac/Man ratios were observedfollowing treatment in 42% of Melo recipients, in 62% of Indo recipientsand in 75% of subjects treated with Napro. Colonic permeability was notsignificantly impaired by any of the 3 drugs. CONCLUSION: We havedemonstrated that acute doses of NSAIDs, developed in order to reduce GImucosal damage, did not significantly increase either gastric or colonicpermeability. However, significant small intestinal mucosal damage wasobserved after ingestion of the three types of drugs with a trend for agreater prevalence using a conventional NSAID such as Napro. Although,increased gastric safety is a clear benefit of these drugs, this protection doesnot appeal to extend to the small intestine.
5972PATIENTS RECALL OF NONSTEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDS) INTAKE BEFORE AND AFTER ENDOSCOPY.Jose D. Sollano, Romiro P. Babaran, Univ of Santo Tomas, Manila.Philippines.
Background: Most investigators suspect surreptitious NSAID intake in theevent of major gastrointestinal catastrophies, especially in the elderlyalthough patients have great difficulty recalling such intake. Thus, weusually rely on clinical events in deducing NSAID toxicity, endoscopiclesions being very common in the absence of other significant risk factors.Objectives: We aim to determine if dyspeptic patients forget or denyNSAID intake by confronting them before and after upper GI endoscopy;to determine the adequacy of recall of NSAID use among patients whohave lesions suggestive of NSAID injury. Patients and Methods: Allpatients who underwent upper GI endoscopy due to dyspepsia were askedregarding NSAID use and their responses were classified as; index recall ifpatients had an immediate recall of NSAID intake when inquired; assistedrecall if an initial denial is reported, however, recalled correctly whenassisted by a checklist containing all locally-available NSAIDs; confrontedrecall when the admission of NSAID intake was made only after patientshave been informed of lesions found on endoscopy. During endoscopy,lesions were recorded according to the site; size and severity based on theModified Lanza Scoring System. Results: A total of 266 patients (M:F=l.13:I, mean age = 48.1S+IS.65yrs) underwent upper GI endoscopydue to dyspeptic symptoms. Overall, 182 patients demonstrated gastroduodenal lesions. One hundred four patients found to have gastroduodenallesions had accurate index recall of drug intake while SI patients respondedpositively only after the assisted recall (57% vs. 28%, p<O.OS). In 27patients (1S%) who had gastroduodenal lesions, NSAID intake was deniedeither before or after endoscopy and even when confronted with theendoscopic findings. The mean Lanza scores for index recall, assistedrecall and confronted recall ale 2.S1 +, I.S8, and 0.83, respectively(p=<O.OOI). Of 131 patients found to have lesions and positively recalled
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