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Helicobacter pylori resistance to antibiotics in an hospital area in Seville, Spain
A1300 AGA ABSTRACTS
5933 GASTRIC ELECTRICAL ACTIVITY IN ALCOHOL·INDUCED STOMACH DAMAGE IN HEALTHY VOLUNTEERS. PROTEC· TIVE EFFECT OF AMTOLMETIN GUACYL. Giuseppe Riezzo, Marisa Chiloiro, I R C C S S De Bellis, Castellana G., Italy; I R C C S S De Bellis, Castellana G, Italy. Treatment with NSAIDs is usually accompanied by gastric side effects attributed to prostaglandin inhibition. It was demonstrated that gastric dysmotility may play an important role in the pathogenic mechanism of gastric lesions. Motility is controlled by the gastric electrical activity that can be recorded by means of cutaneous Electrogastrography (EGG). Aim: Electrogastrography and gastric emptying time were performed to evaluate the mechanisms of putative protection from alcohol-induced stomach damage of Amtolmetin Guacyl (AMG) respect to a standard NSAID, a protective drug, and placebo. Patients and Methods: 24 healthy volunteers entered a double blind, randomized, placebo-controlled, crossover study. 12 subjects assumed 400 ml of orange juice with alcohol (12%, v/v) after four days of placebo, AMG (1200 mg/die) or diclofenac (100 mg/die), and other 12 subjects after four days of placebo, AMG or misoprostol (400 J,Lg/die). During each session, gastrointestinal symptom score ranging from o (absent) to 3 (severe) was recorded. EGG was recorded before and for 180 minutes after the test meal. The mean gastric frequency, the instability coefficient of the gastric frequency and power, the percentage of normal slow waves, bradygastria and tachygastria, and power ratio were calculated. Subjects were sonographically studied during the gastric emptying (GE). The final emptying time, the half time and gastric emptying curve were assessed. The area under the curve (AUC) of EGG and GE parameters were calculated and MANOVA was performed. Results: No differences were found in symptom score and AUC of the gastric emptying time among pre-treatments. The AUC of normal slow wave was significantly higher in AMG group (p
5934 IN GERD PATIENTS TAKING A MORNING DOSE OF OMEPRA· ZOLE, BEDTIME LOW·DOSE RANITIDINE IS EQUIVALENT TO BEDTIME OMEPRAZOLE FOR INHIBITION OF NOCTURNAL GASTRIC ACIDITY. Malcolm G. Robinson, Sheila Rodriguez-Stanley, Jerry D. Gardner, Arthur A. Ciociola, Jonathan Filinto, Sattar Zubaidi, Philip B. Miner, Oklahoma Fdn for Digest Research, Oklahoma City, OK; Sci for Organizations, Chatham, NJ; Warner-Lambert Consumer Healthcare, Morris Plains, NJ. Introduction. Subjects treated with a single morning dose of omeprazole experience appreciable nocturnal periods with intragastric pH:54. A 2nd nocturnal dose of omeprazole can reduce this nocturnal acidity. Aim. In patients with GERD who were taking a morning dose of 20mg omeprazole, we compared effects of bedtime dosing with 75mg ranitidine to those with 20mg omeprazole on nocturnal gastric acidity. Methods. Intragastric pH profiles were measured in 15 patients with heartburn ~3 times/week for at least 6 months. Gastric pH was measured for 24 hours after 6 days of treatment with 20mg omeprazole given before breakfast and placebo, 75mg ranitidine or 20mg omeprazole given at 10-11 pm in a randomized, single-blind fashion. Values for pH were converted to acid concentration (mM) and integrated acidity was calculated from the cumulative, timeweighted means of the acid concentrations for every second of the 24-hour recording period. Integrated acidity (mmol.hrlL) was assessed over I-hour intervals. Results. In patients taking a single morning dose of orneprazole, cumulative nocturnal integrated gastric acidity (from lOpm until 8am the following morning) was 151±34 mmol.hrlL. The mean acid concentration over this period was 15.1±3.4 mM (or pH 1.8). Nocturnal ranitidine decreased nocturnal integrated gastric acidity to 53± 10 (p=O.OI), and this decrease persisted for 14 hours, until noon the following day. Nocturnal omeprazole decreased nocturnal integrated gastric acidity to 31 ± IS (p=O.OI), and this decrease with omeprazole was not significantly different from that accomplished with 75mg ranitidine hs (p=O.13). Conclusion. The present results indicate that, in GERD patients who are taking a single morning dose of omeprazole, a bedtime dose of 75mg ranitidine produces substantial inhibition of nocturnal gastric acidity that persists for 14 hours. Moreover, bedtime ranitidine is as effective as a second bedtime dose of 20mg omeprazole for decreasing gastric acidity in this setting.
5935 ONE·WEEK THERAPY WITH OMEPRAZOLE OR RANITIDINE BISMUTH CITRATE PLUS CLARITHROMYCIN AND AMOXI· CILLIN FOR TREATMENT OF HELICOBACTER PYLORI IN· FECTION. Maria Rojas, Pedro Hergueta, Rafael Romero, BIas 1. Gomez, Francisco J. Pellicer, Juan M. Herrerias, Hosp Univ Virgen Macarena, Seville, Spain. Objective: To compare the efficacy of omeprazole, clarithroycin and amoxicillin versus ranitidine bismuth citrate, clarithromycin and arnoxicil-
GASTROENTEROLOGY Vol. 118, No.4
lin twice daily for 7 days treatment of Helicobacter pylori infection. Methods: 115 patients with H. pylori infection confirmed by histology and rapid urease test were recruited (M=52, F=53, mean age 46.4±13). 103 had endoscopy-proven peptic ulcer disease, 5 dyspepsia ulcer-like and 6 rosacea. None of them had undergone previous anti-helicobacter pylori therapy. Patients were randomized to receive either regimen OCA 7 (orneprazole 20 mg b.i.d., clarithromycin 500 mg b.i.d, and amoxicillin 1000 mg b.i.d.) or RBC-C-A 7 (ranitidine bismuth citrate 400 mg b.i.d., clarithromycin 500 mg b.i.d, and amoxicillin 1000 mg b.i.d.) all for 7 days. Eradication was confirmed with histology (2 biopsies from both gastric antrum and body) or l3C-urea breath test at least two months after completing therapy. Statistical analysis were performed by means of the X2 test. Results: According to intention to treat analysis, eradication rates were 82% (44/55) for OCA 7 and 90% (54/60) for RBC-C-A 7 (p>0.05). Conclusions: Both treatments were well tolerated and effective in Helicobacter pylori eradication. No statistical differences were found between the two different treatments.
5936 HELICOBACTER PYLORI RESISTANCE TO ANTIBIOTICS IN AN HOSPITAL AREA IN SEVILLE, SPAIN. Rafael Romero, Maria Rojas, Anabel Suarez, Carmen Conejo, Pedro Hergueta, Juan M. Martin, Enrique Linares, Manuel Rodriguez, Francisco J. Pellicer, Juan M. Herrerias, Hosp Univ Virgen Macarena, Sevilla, Spain. Objective:To evaluate the prevalence of metronidazole, clarithrornycin, amoxicilline and tetracycline resistant Helicobacter pyloristrains among patients refered for an upper gastrointestinal endoscopy at an Universitary Hospital in Seville, Spain. Patients and methods: Between March 1998 and November 1999 we included 173 patients (M:109; F:64; mean age 44±) with suspected peptic ulcer disease. The diagnostic of H. pylori was made by means of a rapid urease test, histology, Gram stain and culture of antrum and corpus gastric biopsies obtained by endoscopy. Antimicrobial sensitivity was determined by the methods of diffusion with E-test. Results:We demonstrated H. pylori infection in 122 patients and culture was possible in 90 cases, 62 in patients without prior treatment of eradication and 28 among which one previous treatment failed. In the first group, resistance to metronidazole was 42% (26/62), to clarithromycin 13% (8/62) and resistance to both drugs was 10% (6/62). In the second group, the rate of resistance was 50% (14128), 61% (17/28) and 36% (10128), including a strain resistant to metronidazole, clarithromycine and tetracycline. We did not find resistance to amoxicillin. Conclusions:There was a significantly higher clarithromycin resistance rate among H. pylori isolates from previously treated patients than no treated subjects. Culture of gastric mucosa biopsies illustrates moreover the resistance to antibiotics and allows to adjust a specific treatment at a determined geographical area.
5937 IN VITRO EVIDENCE OF THE PROTECTIVE EFFECT OF PHOSPHA TIDYLCHOLINE (PC) AGAINST BILE SALT CYTOTOXICITY. Suzan H. Rooijakkers, Rebecca L. Darling, Lenard M. Lichtenberger, Katholieke Univ Nijrnegen, Nijmegen, Netherlands; Univ of Texas Med Sch, Houston, TX.
Background: The mechanism which protects the epithelium of the gall bladder and intestinal mucosa from the detergent properties of bile salts is not fully understood. We have previously obtained in vivo evidence, that biliary PC protects the ileal mucosa from the injurious effects of the bile salt, sodium deoxycholate (SDC). Methods: In the present study we employed a culture line of polarized human intestinal Caco-2 cells and freshly isolated human red blood cells (rbcs) to investigate whether unsaturated PC (purified from soy lecithin) protects human cells from bile salt injury under controlled in vitro conditions. Caco-2 cells were cultured on Transwell porous membranes in enriched growth medium. The electrical resistance (R) across the membranes was measured daily to assess when cellular confluence was reached (R>200 Ohrnecrrr'). At this time, the medium bathing the luminal face of the cells was replaced with a chemically defined medium containing SDC (O-lmM) alone or in the presence of PC (0.4-4 mM) and the R measured for the subsequent 120 min. Rbcs were isolated from freshly collected plasma, washed in Hepes buffer and incubated in varying cones, of SDC alone or in the presence of PC over a 10 min period, followed by centrifugation and spectrophotometric analysis of the supernatant to estimate hemolytic activity. Results: Exposure of Caco-2 cells to SDC cones of > 0.4 mM induced a maximal decrease in R, which could be dose-dependently reversed by the addition of PC to the medium, with 0.8 mM PC inducing a complete recovery of R. We also demonstrated that the hemolytic activity of SDC (which was observed at cone. > 2 mM) could be completely blocked if PC was added to the incubation buffer at equimolar cone or greater. Conclusion: PC in the unsaturated state, to mimic the properties of biliary PC, has the capacity to protect human intestinal cells and rbcs from bile salt injury. These findings suggest that one of the major roles of biliary PC is to protect gall bladder and intestinal epithelial cells from the cytotoxic activity of bile salts, perhaps by promoting the formation of mixed micelles. (Supported by NIH grant DK 53195).
5933 GASTRIC ELECTRICAL ACTIVITY IN ALCOHOL·INDUCED STOMACH DAMAGE IN HEALTHY VOLUNTEERS. PROTEC· TIVE EFFECT OF AMTOLMETIN GUACYL. Giuseppe Riezzo, Marisa Chiloiro, I R C C S S De Bellis, Castellana G., Italy; I R C C S S De Bellis, Castellana G, Italy. Treatment with NSAIDs is usually accompanied by gastric side effects attributed to prostaglandin inhibition. It was demonstrated that gastric dysmotility may play an important role in the pathogenic mechanism of gastric lesions. Motility is controlled by the gastric electrical activity that can be recorded by means of cutaneous Electrogastrography (EGG). Aim: Electrogastrography and gastric emptying time were performed to evaluate the mechanisms of putative protection from alcohol-induced stomach damage of Amtolmetin Guacyl (AMG) respect to a standard NSAID, a protective drug, and placebo. Patients and Methods: 24 healthy volunteers entered a double blind, randomized, placebo-controlled, crossover study. 12 subjects assumed 400 ml of orange juice with alcohol (12%, v/v) after four days of placebo, AMG (1200 mg/die) or diclofenac (100 mg/die), and other 12 subjects after four days of placebo, AMG or misoprostol (400 J,Lg/die). During each session, gastrointestinal symptom score ranging from o (absent) to 3 (severe) was recorded. EGG was recorded before and for 180 minutes after the test meal. The mean gastric frequency, the instability coefficient of the gastric frequency and power, the percentage of normal slow waves, bradygastria and tachygastria, and power ratio were calculated. Subjects were sonographically studied during the gastric emptying (GE). The final emptying time, the half time and gastric emptying curve were assessed. The area under the curve (AUC) of EGG and GE parameters were calculated and MANOVA was performed. Results: No differences were found in symptom score and AUC of the gastric emptying time among pre-treatments. The AUC of normal slow wave was significantly higher in AMG group (p
5934 IN GERD PATIENTS TAKING A MORNING DOSE OF OMEPRA· ZOLE, BEDTIME LOW·DOSE RANITIDINE IS EQUIVALENT TO BEDTIME OMEPRAZOLE FOR INHIBITION OF NOCTURNAL GASTRIC ACIDITY. Malcolm G. Robinson, Sheila Rodriguez-Stanley, Jerry D. Gardner, Arthur A. Ciociola, Jonathan Filinto, Sattar Zubaidi, Philip B. Miner, Oklahoma Fdn for Digest Research, Oklahoma City, OK; Sci for Organizations, Chatham, NJ; Warner-Lambert Consumer Healthcare, Morris Plains, NJ. Introduction. Subjects treated with a single morning dose of omeprazole experience appreciable nocturnal periods with intragastric pH:54. A 2nd nocturnal dose of omeprazole can reduce this nocturnal acidity. Aim. In patients with GERD who were taking a morning dose of 20mg omeprazole, we compared effects of bedtime dosing with 75mg ranitidine to those with 20mg omeprazole on nocturnal gastric acidity. Methods. Intragastric pH profiles were measured in 15 patients with heartburn ~3 times/week for at least 6 months. Gastric pH was measured for 24 hours after 6 days of treatment with 20mg omeprazole given before breakfast and placebo, 75mg ranitidine or 20mg omeprazole given at 10-11 pm in a randomized, single-blind fashion. Values for pH were converted to acid concentration (mM) and integrated acidity was calculated from the cumulative, timeweighted means of the acid concentrations for every second of the 24-hour recording period. Integrated acidity (mmol.hrlL) was assessed over I-hour intervals. Results. In patients taking a single morning dose of orneprazole, cumulative nocturnal integrated gastric acidity (from lOpm until 8am the following morning) was 151±34 mmol.hrlL. The mean acid concentration over this period was 15.1±3.4 mM (or pH 1.8). Nocturnal ranitidine decreased nocturnal integrated gastric acidity to 53± 10 (p=O.OI), and this decrease persisted for 14 hours, until noon the following day. Nocturnal omeprazole decreased nocturnal integrated gastric acidity to 31 ± IS (p=O.OI), and this decrease with omeprazole was not significantly different from that accomplished with 75mg ranitidine hs (p=O.13). Conclusion. The present results indicate that, in GERD patients who are taking a single morning dose of omeprazole, a bedtime dose of 75mg ranitidine produces substantial inhibition of nocturnal gastric acidity that persists for 14 hours. Moreover, bedtime ranitidine is as effective as a second bedtime dose of 20mg omeprazole for decreasing gastric acidity in this setting.
5935 ONE·WEEK THERAPY WITH OMEPRAZOLE OR RANITIDINE BISMUTH CITRATE PLUS CLARITHROMYCIN AND AMOXI· CILLIN FOR TREATMENT OF HELICOBACTER PYLORI IN· FECTION. Maria Rojas, Pedro Hergueta, Rafael Romero, BIas 1. Gomez, Francisco J. Pellicer, Juan M. Herrerias, Hosp Univ Virgen Macarena, Seville, Spain. Objective: To compare the efficacy of omeprazole, clarithroycin and amoxicillin versus ranitidine bismuth citrate, clarithromycin and arnoxicil-
GASTROENTEROLOGY Vol. 118, No.4
lin twice daily for 7 days treatment of Helicobacter pylori infection. Methods: 115 patients with H. pylori infection confirmed by histology and rapid urease test were recruited (M=52, F=53, mean age 46.4±13). 103 had endoscopy-proven peptic ulcer disease, 5 dyspepsia ulcer-like and 6 rosacea. None of them had undergone previous anti-helicobacter pylori therapy. Patients were randomized to receive either regimen OCA 7 (orneprazole 20 mg b.i.d., clarithromycin 500 mg b.i.d, and amoxicillin 1000 mg b.i.d.) or RBC-C-A 7 (ranitidine bismuth citrate 400 mg b.i.d., clarithromycin 500 mg b.i.d, and amoxicillin 1000 mg b.i.d.) all for 7 days. Eradication was confirmed with histology (2 biopsies from both gastric antrum and body) or l3C-urea breath test at least two months after completing therapy. Statistical analysis were performed by means of the X2 test. Results: According to intention to treat analysis, eradication rates were 82% (44/55) for OCA 7 and 90% (54/60) for RBC-C-A 7 (p>0.05). Conclusions: Both treatments were well tolerated and effective in Helicobacter pylori eradication. No statistical differences were found between the two different treatments.
5936 HELICOBACTER PYLORI RESISTANCE TO ANTIBIOTICS IN AN HOSPITAL AREA IN SEVILLE, SPAIN. Rafael Romero, Maria Rojas, Anabel Suarez, Carmen Conejo, Pedro Hergueta, Juan M. Martin, Enrique Linares, Manuel Rodriguez, Francisco J. Pellicer, Juan M. Herrerias, Hosp Univ Virgen Macarena, Sevilla, Spain. Objective:To evaluate the prevalence of metronidazole, clarithrornycin, amoxicilline and tetracycline resistant Helicobacter pyloristrains among patients refered for an upper gastrointestinal endoscopy at an Universitary Hospital in Seville, Spain. Patients and methods: Between March 1998 and November 1999 we included 173 patients (M:109; F:64; mean age 44±) with suspected peptic ulcer disease. The diagnostic of H. pylori was made by means of a rapid urease test, histology, Gram stain and culture of antrum and corpus gastric biopsies obtained by endoscopy. Antimicrobial sensitivity was determined by the methods of diffusion with E-test. Results:We demonstrated H. pylori infection in 122 patients and culture was possible in 90 cases, 62 in patients without prior treatment of eradication and 28 among which one previous treatment failed. In the first group, resistance to metronidazole was 42% (26/62), to clarithromycin 13% (8/62) and resistance to both drugs was 10% (6/62). In the second group, the rate of resistance was 50% (14128), 61% (17/28) and 36% (10128), including a strain resistant to metronidazole, clarithromycine and tetracycline. We did not find resistance to amoxicillin. Conclusions:There was a significantly higher clarithromycin resistance rate among H. pylori isolates from previously treated patients than no treated subjects. Culture of gastric mucosa biopsies illustrates moreover the resistance to antibiotics and allows to adjust a specific treatment at a determined geographical area.
5937 IN VITRO EVIDENCE OF THE PROTECTIVE EFFECT OF PHOSPHA TIDYLCHOLINE (PC) AGAINST BILE SALT CYTOTOXICITY. Suzan H. Rooijakkers, Rebecca L. Darling, Lenard M. Lichtenberger, Katholieke Univ Nijrnegen, Nijmegen, Netherlands; Univ of Texas Med Sch, Houston, TX.
Background: The mechanism which protects the epithelium of the gall bladder and intestinal mucosa from the detergent properties of bile salts is not fully understood. We have previously obtained in vivo evidence, that biliary PC protects the ileal mucosa from the injurious effects of the bile salt, sodium deoxycholate (SDC). Methods: In the present study we employed a culture line of polarized human intestinal Caco-2 cells and freshly isolated human red blood cells (rbcs) to investigate whether unsaturated PC (purified from soy lecithin) protects human cells from bile salt injury under controlled in vitro conditions. Caco-2 cells were cultured on Transwell porous membranes in enriched growth medium. The electrical resistance (R) across the membranes was measured daily to assess when cellular confluence was reached (R>200 Ohrnecrrr'). At this time, the medium bathing the luminal face of the cells was replaced with a chemically defined medium containing SDC (O-lmM) alone or in the presence of PC (0.4-4 mM) and the R measured for the subsequent 120 min. Rbcs were isolated from freshly collected plasma, washed in Hepes buffer and incubated in varying cones, of SDC alone or in the presence of PC over a 10 min period, followed by centrifugation and spectrophotometric analysis of the supernatant to estimate hemolytic activity. Results: Exposure of Caco-2 cells to SDC cones of > 0.4 mM induced a maximal decrease in R, which could be dose-dependently reversed by the addition of PC to the medium, with 0.8 mM PC inducing a complete recovery of R. We also demonstrated that the hemolytic activity of SDC (which was observed at cone. > 2 mM) could be completely blocked if PC was added to the incubation buffer at equimolar cone or greater. Conclusion: PC in the unsaturated state, to mimic the properties of biliary PC, has the capacity to protect human intestinal cells and rbcs from bile salt injury. These findings suggest that one of the major roles of biliary PC is to protect gall bladder and intestinal epithelial cells from the cytotoxic activity of bile salts, perhaps by promoting the formation of mixed micelles. (Supported by NIH grant DK 53195).