Meta-analysis of the role of Helicobacter pylori in non-steroidal anti-inflammatory drug (NSAID)—associated gastropathy

Meta-analysis of the role of Helicobacter pylori in non-steroidal anti-inflammatory drug (NSAID)—associated gastropathy

AJG – September, 2000 Abstracts the distal stomach, GE expressed as percent retention was calculated by dividing the counts in the distal stomach {[...

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AJG – September, 2000

Abstracts

the distal stomach, GE expressed as percent retention was calculated by dividing the counts in the distal stomach {[T(t)]⫺[P(t)]} by the total amount that had entered the distal stomach {[T(0)]⫺[P(t)]}. Results: (see table, % retention expressed as mean⫾SEM; *p⬍0.05, **p⬍0.01 vs normal control). At 30 min and 1 hr, total, proximal, and distal GE in GERD, NUD, and GERD⫹NUD were similar to C. For GERD, total and proximal GE were delayed compared to C at 3 hr. For NUD, total and distal GE were delayed at 2 and 3 hr but proximal GE was delayed only at 2 hr. For GERD⫹NUD, total, proximal, and distal GE were delayed at 2 and 3 hr. Conclusions: Selective abnormalities of proximal and distal GE were observed in GERD and NUD: proximal gastric retention in GERD; whereas distal gastric retention in NUD. These results suggest that delayed proximal GE and delayed distal GE may be important factors in the pathogenesis of GERD and NUD, respectively. Group GERD NUD GERD⫹ NUD Control

1 hr TGE

1 hr PGE

1 hr DGE

2 hr TGE

2 hr PGE

2 hr DGE

3 hr TGE

3 hr PGE

3 hr DGE

66 ⫾ 3 38 ⫾ 3 45 ⫾ 4 36 ⫾ 4 17 ⫾ 3 23 ⫾ 3 18 ⫾ 4* 7 ⫾ 1* 12 ⫾ 3 67 ⫾ 3 36 ⫾ 4 50 ⫾ 3 44 ⫾ 4** 21 ⫾ 4*32 ⫾ 4* 25 ⫾ 4** 9 ⫾ 3 19 ⫾ 3** 69 ⫾ 3 42 ⫾ 3 48 ⫾ 3 42 ⫾ 3** 20 ⫾ 2*29 ⫾ 2* 20 ⫾ 2** 7 ⫾ 1** 14 ⫾ 2** 64 ⫾ 3 36 ⫾ 4 44 ⫾ 3 30 ⫾ 3

11 ⫾ 2 21 ⫾ 3

9⫾2

3⫾1

6⫾1

144 Intestinal metaplasia of the gastric cardia: A prospective study with enhanced magnification endoscopy Moises Guelrud, MD, FACG, Idamys Herrera, MD, Harold Essenfeld, MD, Julio Castro, MD. Policlı´nica Metropolitana, Caracas, Venezuela, and Donald Antonioli, MD. Beth Israel Deaconess Hospital, Boston, Massachusetts The purpose of the study is to evaluate the usefulness of Enhanced magnification endoscopy (EME), a technique that combines the use of magnification endoscopy (ME) and acetic acid (AA) instillation for the detection of specialized intestinal metaplasia (SIM) at the gastric cardia. Methods: 251 patients undergoing elective gastroscopy underwent EME with an Olympus GIF-200Z (zoom 35⫻) and 1.5% AA instillation. Patients were included if the squamocolumnar junction and the esophagogastric junction were judged to be at the same level. AA surface patterns were characterized prior to AA-directed biopsy of suspected areas and correlated with histology. Two pathologists blinded to the biopsy method read each biopsy. Logistic regression was performed to determine if targeted biopsies of surface patterns could predict IMC. Results: 4 patients were excluded due to unclear definition of the surface pattern after EME. EME detected 4 different endoscopic patterns. Pattern I: round pits, II: reticular, III: villous, and IV: ridged. Overall, EME identified IMC in 86 of the 247 patients, a prevalence of 34.2%. Table shows the yield of detecting SIM according to endoscopic patterns: Type of epithelium SIM

Pattern I

Pattern II

Pattern III

Pattern IV

0%

4.09 (%)

57.7 (%)

100 (%)

Odds ratio: Pattern II: 0.064 (p⬍0.000); Pattern III: 5.5 (p⬍0.000); Pattern IV: 2.68 (p⬍0.045). Endoscopy vs histology (Pearson’s correlation coefficient 0.61). Conclusions: EME is an accurate method to detect intestinal metaplasia in the gastric cardia. EME is useful to target biopsies and thus avoid sampling error. IMC is a more frequent lesion than previously reported. Its clinical significance is uncertain and has to be established. 145 Efficacy of gastric brushing in the diagnosis of Helicobacter pylori infection Purpose: Gastric biopsies performed during gastroscopy are the gold standard to diagnose Helicobacter Pylori infection. Patients who are on

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anticoagulant therapy have an increased risk of bleeding from the biopsy. Brushing during gastroscopy and Giemsa stain might offer an alternate method to diagnose active infection with Helicobacter Pylori and may have a reduced risk of bleeding in patients on anticoagulation. Gastric cytology has been previously evaluated for the diagnosis of H. Pylori infection: Edmonds PR. Diagnostic Cytopathology. 8(6):563, 1992, and Huang MS. Acta Cytologica. 40(4):714, 1996. In this pilot project 23 patients with duodenal ulcer or gastroduodenitis diagnosed by endoscopy underwent gastric antral brushing cytology and gastric antral biopsies during gastroendoscopic examination to assess the value of gastric brushing cytology in the diagnosis of Helicobacter Pylori infection. Methods: The brushing cytology materials were obtained from the antrum of the stomach in all patients and stained with Diff-Quick® Giemsa stain for immediate interpretation. The biopsy specimen was stained with Hematoxylin-eosin in each patient. We then compared the results of brushing cytology with those of histology. The brushing cytology slides were blindly interpreted by a different pathologist than the one interpreting the histology slides. Results: Four of the twenty-three patients (17%) were diagnosed as positive for H. Pylori organisms using brushing cytology, compared to five using histology (21%). Using positive or negative results from the histology test as the gold standard, a true positive result was found in all four cases. A true negative in eighteen patients, a false negative in one patient, there were no false positive results. The specificity and sensitivity of brushing cytology were 100% and 80% respectively. Conclusion: 1. Gastric brushing cytology provides an accurate, inexpensive and easy technique in the rapid detection of H. pylori infection. 2. The gastric cytology can be prepared and interpreted immediately upon completion of the procedure; thus the results are available before the biopsy report. 146 Meta-analysis of the role of Helicobacter pylori in non-steroidal antiinflammatory drug (NSAID)—associated gastropathy Huang J-Q, Lad R, Hunt RH. Division of Gastroenterology, McMaster University Medical Center, Hamilton, Ontario, Canada. H. pylori infection and NSAID use are well established independent risk factors for peptic ulcers (PU). However, it is not clear if any interaction exists between these two factors in the formation of PU. Aims: To evaluate 1) the prevalence of PU in H. pylori-infected NSAID takers compared to non-infected NSAID users; 2) any interactions between the two factors and the magnitude of any effect. Methods: A fully recursive literature search for full papers was performed to February 2000 with the key words of “NSAID, pylori and ulcer”. Studies meeting the following criteria were included: a) studies assessing the relationship between PU, H. pylori infection and NSAID use; b) ulcer documented by endoscopy. Excluded: patients with recent use of antiulcer drugs or antibiotics or with a history of gastric surgery; duplicate publications or non-English articles; studies without raw data for retrieval. Results: 328 potentially relevant Medline citations were retrieved with 16 studies, consisting of 1694 subjects, meeting the predefined inclusion criteria. Ulcer rates are shown in the table: Groups (n. arms) Case-control studies PUs in NSAID users (5) PUs in controls (5) Overall PU in NSAID users (16)

H. pylori (ⴙ) n/T.n (%)

H. pylori (ⴚ) n/T.n (%)

OR (95% CI)

119/242 (49.2)a 86/344 (25)b 344/831 (41.4)

80/308 (26)c 17/307 (5.5)d 201/809 (24.8)

2.8 (1.9–3.9) 5.7 (3.3–9.8) 2.1 (1.7–2.6)

n/T.n⫽number with PU/total number of subjects. a vs. b, OR⫽2.9 (95% CI 2.0 – 4.1); a vs. d, OR⫽16.5 (95% CI 9.5–28.6); c vs. d, OR⫽5.99 (95% CI 3.5–10.4). All ORs and 95% CIs were calculated with the Mantel-Haenszel method.

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Abstracts

Conclusions: Both H. pylori infection and NSAID use independently and significantly increase the relative risk of peptic ulcer. H. pylori infection further increases the risk of ulcer over that seen with NSAIDs alone. Thus, there is a synergism between these two risk factors on peptic ulceration. 147 Helicobacter pylori eradication with tetracycline, furazolidone and bismuth (TFB), and rate of reinfection one year after successful treatment D de Idiaquez, MD, C Seminario, MD, J Huerta Mercado, MD, J Cabello, MD, J Cok, MD, A Bussalleu, MD, FACG. Peruvian University Cayetano Heredia, Lima, Peru. H. pylori (HP) is a prevalent infection in Peru. High rates of resistance against some antibiotics as well as elevated costs affect the effectiveness of some therapies. Aim: To assess the effectiveness of the combination of tetracycline, furazolidone and bismuth in eradicating HP; changes in histologic pattern; and the reinfection rate one year after HP eradication. Methods: Patients with HP infection, found in antral biopsies with HE staining, were included. They received for ten days tetracycline 500 mg qid, furazolidone 100 mg qid, and colloidal bismuth subcitrate 120 mg qid. Patients were instructed to come back 8 weeks after starting therapy, where four antral biopsies were taken. Biopsies done before and after treatment were evaluated for: presence and density of HP; depth and grade of chronic gastritis, presence and grade of inflammatory activity, glandular atrophy, grade and extent of mucinous damage, presence of intestinal metaplasia, and presence of lymphoid follicles. Patients with HP negative control were evaluated one year later with biopsies to determine reinfection. Results: 59 patients (30 men and 29 women) completed per protocol, age range 14 –73, HP eradication was achieved in 54 (91.5%). Control biopsies of these 54 patients showed improvement in all the histologic parameters (p⬍0.001) except in glandular atrophy and intestinal metaplasia. Thirty of 54 patients negative for HP were evaluated a year later for reinfection. Three (10%) were again positive for HP. Conclusions: TFB scheme is effective in HP eradication. This is followed by an improvement in several histologic parameters. Although 10% become reinfected we consider this scheme is cost-effective for HP infection in low income populations with high HP infection prevalence. 148 Hp eradication rates and symptoms in patients with proven peptic ulcers Chin Hur, MD, Pierre F. Michetti, MD, Ciavan Kelly, MD. Beth Israel Deaconess Medical Center/Harvard Medical School, Boston, MA, USA. Purpose: A large amount of published data unequivocally supports the practice of Helicobacter pylori (Hp) eradication in patients with peptic ulcer disease (PUD). The aim of this study was to determine what percentage of patients with endoscopically diagnosed PUD were treated and eradicated and its effect on symptoms. Methods: Patients with PUD were identified from a review of our institution’s endoscopy records from 1995 to 1998. Out of the patients identified, those who had documented Hp infection by either pathology or serology were eligible for our study. Study participation involved completing a questionnaire and then providing a stool sample. We used the Meridian Diagnostics Hp stool antigen test (EIA) to check for current infection. Out of 174 patients contacted, 53 completed the study (30.5%). Results: ●

● ●

Of the 53 patient stools tested for active Hp infection, 3/53 (5.7%) were positive. All three patients who were positive reported that they had completed eradication therapy. 46 out of 53 (86.8%) recalled having been treated for their Hp infection and 45 out of the 46 (97.8%) reported that they finished their regimen. 38 out of 53 (71.4%) reported digestive symptoms with their original

AJG – Vol. 95, No. 9, 2000

ulcer. 26 out of 38 (68.4%) no longer have symptoms after eradication while 11/37* (29.7%) continued to have symptoms after eradication at the time of survey. *(One of the symptomatic patients was not eradicated.) Conclusions: A substantial percentage of patients who had symptoms with their ulcer and infection continue to have these symptoms even after successful eradication. 149 The intestinal metaplasia of the gastric cardia is associated with Helicobacter pylori infection Seong Gook Jeon, Yi Kyung Chun. Samsung Cheil Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea. Purpose: Whether cardia intestinal metaplasia (IM) is associated with gastroesophageal reflux disease (GERD) or Helicobacter pylori (H. pylori) infection is unknown. The aim of the present study was to investigate the role of GERD and H. pylori infection in the development of cardia IM. Methods: Thirty-seven consecutive patients with reflux esophagitis on EGD were studied. Age and sex matched, 32 asymptomatic subjects were used as a control group. Exclusion criteria included the use of antibiotics within 30 days before EGD, prior gastric or esophageal surgery, current peptic ulcer disease or gastric cancer and previous H. pylori eradication. Two biopsy specimens were obtained from antrum, body, fundus and cardia, respectively. All biopsy specimens were stained with H&E, alcianblue and Giemsa. The severity of gastritis was graded according to the updated Sydney system. Results: Carditis in controls was more severe than that in patients with reflux esophagitis. The prevalence rate of H. pylori increased with greater degree of carditis in each groups (p⬍0.05). The prevalence of cardia IM was not significantly different between patients with reflux esophagitis (24.3%) and controls (46.7%). But H. pylori infection was more common in subjects with cardia IM compared to subjects without cardia IM in each groups (p⬍0.05). Conclusions: Cardia IM is associated with H. pylori infection, but not GERD. 150 Does a Cox-2 inhibitor, rofecoxib have low potential for causing acute gastric lesion: “A double blind, randomized, placebo controlled trial” Kapioroglu1 S, Bafu1 A, Kayrier1 K, Aydun2 F, Ozoran3 Y. Karadeniz (Black Sea) Technical University, School of Medicine, Department of Internal Medicine, Section of Gastroenterology1, Department of Microbiology2, and Pathology3, Trabzon, Turkey. Purpose: In this study it was aimed to examine the effect of rofecoxib, a selective inhibitor of COX-2 enzyme, to the acute gastric mucosal lesion and to correlate its effect with aspirin. Methods: This study was planned as double blind, randomized and placebo controlled. Mean age of voluntary persons (n:26) was 47⫾2.98 divided into three groups. Patients were excluded if they had active duodenal, gastric or oesophageal ulcers or oesophagitis at baseline endoscopy. Volunteers were given randomized placebo (n:10), aspirin (n:10) (500 mg aspirin-Bayer, Germany), and rofecoxib (n:16) (VIOXX 50 mg MSD, USA) with 50 ml of water after 12 hours fasting period at 08.00 a.m. Three hours after each therapy, gastroduodenoscopy was performed to the volunteers. Mucosa of duodenum and stomach was screened by endoscopy. Biopsies were taken to determine the presence of histopathology and H. pylori. Treatment groups were similar at baseline with respect to age, sex, H. pylori status, alcohol or smoking use. Results: Endoscopic scores of groups were: 0.60⫾0.28 in placebo, 3.30⫾0.25 in aspirin, and 0.59⫾0.25 in rofecoxib. Acute gastric lesion score in rofecoxib group was similar with placebo group. Lesion scores were found significantly high in aspirin group when compared with placebo