Digestive Diseases and Sciences, Vol. 36, No. 5 (May 199I), pp. 577-582
Effect of Omeprazole on Duodenal Ulcer.Associated Antral Gastritis and
Helicobacter pylori W.M. HUI, MBBS, S.K. LAM, MD, J. HO, MB, C.L. LAI, MBBS, A.S.F. LOK, MBBS, M.M.T. NG, MBBS, W.Y. LAU, MBBS, and F.J. BRANICKI, MBChB
This study set out to investigate the effects of omeprazole or ranitidine on the progression of antral gastritis and Helicobacter pylofi in patients with active duodenal ulcer. A double-blind, double-dummy trial was performed in 270 patients, 241 of whom were studied histologically for the presence of H. pylori. Patients were randomized to receive omeprazole, 10 mg every morning, omeprazole, 20 mg every morning, or ranitidine, 150 mg twice a day, for four weeks. Endoscopy was performed on entry and at weekly intervals during the study; at least two antral biopsies were taken on each occasion to assess the activity and degree of chronic inflammation, as reflected by the degree of polymorphonuclear leukocyte infiltration and mononuclear cell infiltration, respectively. Biopsy specimens also were assessed histologically for H. pylori. The sex, age and maximal acid output were comparable in the three treatment groups. The percentages of patients showing an improvement in the activity of gastritis in the four consecutive weeks of treatment were 9%, 40%, 51%, and 53% for omeprazole, 10 mg (N = 78); 14%, 42%, 49%, and 53% for omeprazole, 20 mg (N = 81); and2%, 23%, 30%, and 33% for ranitidine, 150 mg twice a day (N = 82) (life table analysis gave P < 0.01 for both omeprazole regimens compared with ranitidine). The degree of chronic inflammation showed similar changes. The density of H. pylori decreased significantly after treatment with omeprazole, 10 mg or 20 mg, (both, P < 0.00001) but not with ranitidine. The reduction in bacterial density was significantly higher (P < 0.003) in those who showed improvement of gastritis than in those who did not. We conclude that effective acid inhibition with omeprazole improve s antral gastritis and is accompanied by a reduction in antral bacterial density, suggesting that both acid and H. pylori may be involved in the pathogenesis of antral gastritis. KEY WORDS: antral gastritis; Helicobacter pylori: duodenal ulcer; omeprazole; ranitidine.
Antral gastritis occurs in almost all patients with active duodenal ulcer (1). Gastric acid is important in the etiology of duodenal ulcer (2), but its role in Manuscript received May 3, 1990;revised manuscript received October 1, 1990, accepted January 3, 1991. From the Departments of Medicine, Surgery and Pathology, University of Hong Kong, and Government Surgical Unit. Queen Mary Hospital, Hong Kong. Address for reprint requests: Prof. S.K. Lain, MD. University Department of Medicine, Queen Mary Hospital, Pokfulam Road, Hong Kong.
antral gastritis is unclear. By contrast, Helicobacter pylori has been demonstrated to have an important role in antral gastritis (3), but its importance in peptic ulcer disease is less certain. The proton pump inhibitor omeprazole is an effective inhibitor of gastric acid secretion (4-7), but its effect on antral gastritis and the density of H. pylori in the stomach is sparsely documented (81I). This study was undertaken to assess the effects of omeprazole on both antral gastritis and H. pylori
Digestive Diseases and Sciences, Vol. 36, No. 5 (May 1991)
0163-2116/91/0500-0577506.50/09 1991PlenumPublishingCorporation
577
HUI ET AL in patients with duodenal ulcer and to compare these effects with those of ranitidine, an H2receptor antagonist. MATERIALS AND METHODS
Patients. All patients in the study were outpatients or inpatients from Queen Mary Hospital, Hong Kong. To be included in the study, patients had to have an active duodenal ulcer confirmed by endoscopy. Exclusion criteria were concurrent medical problems (in particular, renal disease, cardiovascular disease, diabetes mellitus, chronic obstructive airways disease, pyloric stenosis, or an associated gastric ulcer), previous gastric operation, or pregnancy. Written informed consent was obtained from all patients, and the protocol was approved by the Ethics Committee of the University of Hong Kong. The clinical, personal, physiological, and endoscopic characteristics of the patients were recorded and have been reported in detail previously (12, 13). Gastric secretory tests and meal-stimulated gastrin responses were performed on consecutive days following endoscopy. Study Design. The study was of a double-blind, doubledummy design, 4 weeks in duration. Patients were randomized to one of three treatment regimens: omeprazole (Astra, Sweden), 10 mg every morning; omeprazole, 20 mg every morning; ranitidine, 150 mg twice a day. No antacid was prescribed, and no other medication was to be taken without notification of the Ulcer Cliniq. Patients were discouraged from smoking cigarettes and drinking alcohol. Treatment was started within three days of recruitment into the study. Patients were assessed clinically on entry and at weekly intervals during the study. Endoscopy was performed On entry and at weekly intervals until the ulcer had healed or for a maximum of four weeks. Ulcer healing was considered to have taken place only if the ulcer had disappeared completely, and residual erosions are taken to mean nonhealing. At endoscopy, at least two biopsies were taken from the antrum, along the greater curvature (usually 5 cm from the pylorus). The biopsy specimens were sent for histology to assess antral gastritis and H. pylori. This study was carried out concurrently with a study on the efficacy of omeprazole versus ranitidine in the healing of duodenal ulcer. The results relating to efficacy of ulcer healing have been reported previously (14). Assessment of Gastritis. Gastritis was assessed in terms of activity and degree of chronic inflammation, as reflected by the amount of polymorphonuclear leukocyte (polymorph) infiltration, and the degree of infiltration with chronic inflammatory ceils, including mononuclear cells and plasma cells (1, 15). The assessment was made independently by two pathologists, who had no prior knowledge of the clinical findings, and graded as follows: activity--grade 0, no polymorphs; grade 1, occasional polymorphs scattered on entire section; grade 2, moderate polymorph infiltration (between grades 1 and 3); grade 3, numerous polymorphs throughout entire section; and chronic inflammationmgrade 0, no chronic inflammatory cells; grade 1, occasional chronic inflammatory cells scattered in the section; grade 2, moderate chronic in-
578
flammatory cell infiltration (between grades 1 and 3); grade 3, numerous chronic inflammatory cells throughout entire section. Both parameters were assessed independently, and improvement of gastritis was considered to have occurred if specimens indicated transition to a better grade when compared with the initial specimens. Assessment of H. pylori. Biopsy sections were stained for H. pylori using Warthin-Starry stain (16). The method of bacterial staining has been validated previously by culture and smear of the biopsy (17). In that study, 92% of the histologically identified cases were positive on culture, and 98% of the cases with positive culture were identified histologically. Briefly, the numbers of bacteria were graded as follows: grade 0, no characteristic bacteria; grade 1, occasional spiral organisms found after meticulous search; grade 2, scattered bacteria in most high-power fields or scattered groups of numerous bacteria; grade 3, numerous bacteria in most high power fields. The biopsies were assessed for H. pytori and gastritis independently by two experienced pathologists who had no knowledge of the clinical findings. Their results concurred in over 90% of assessments. The pathologists differed by one grade in all the discordant cases, and the higher grade was used for comparison. Statistical Analysis. Groups were compared using the • test with Yates' correction. Life-table analysis was used to compare the improvement between the groups (18-20). Values were expressed as mean and standard error of the mean, and a P value below 0.05 was considered statistically significant.
RESULTS A total of 270 patients were recruited into the study on drug efficacy in duodenal ulcer healing. Twelve, nine, and eight patients were excluded from the omeprazole 10 mg, omeprazole 20 mg, and ranitidine groups, respectively, giving totals of 78, 81, and 82 patients in each of these groups. These exclusions were made for noncompliance with the entry criteria, default, or no biopsy taken during endoscopy. Histological assessment of gastritis was thus performed on 241 patients. The three groups were comparable in their clinical, personal, endoscopic, and physiological characteristics before treatment (Table 1). Duodenal Ulcer Healing. The duodenal ulcer healing rates were 77%, 86%, and 63% at two weeks, and 95%, 96%, and 93% at four weeks, for the omeprazole 10 mg, omeprazole 20 mg, and ranitidine groups, respectively (14). The difference between the group receiving omeprazole 20 mg every morning, and the group receiving ranitidine, 150 mg twice a day, was statistically significant at two weeks (P < 0.001). Digestive Diseases and Sciences, Vol. 36, No. 5 (May 1991)
EFFECTS OF OMEPRAZOLE TABLE 1. PREENTRY CHARACTERISTICS OF PATIENTS WITH ANTRAL GASTRITIS TREATED WITH OMEPRAZOLE OR RANITIDINE
Omeprazole 10 mg every morning
20 mg every morning
78
N Sex (M:F) Age (yr) Age of onset (yr) Duration of symptoms (yr) Pain score (0-3) Blood group O (%) Cigarette smoker (%) Alcohol user (%) Analgesic user (%) Index ulcer Diameter (ram) Depth (mm) Inflammation (0-3) Deformity (0-3) BAO* (mmol/hr)? MAO~: (mmol/hr)? Dsocw(ng/kg/hr)? Fasting gastrin (nmol/liter)? 2-hr-postprandial gastrin (nmol/min/liter)?
81
6.0:1 39.4 • 14 30.40 • 1.5 7.10 • 0.9 1.50 • 0.2 64.0 35.0 5.0 6.0
9.5 2,1 1,2 0.8 3.5 34.2 150.2 4.2 1.2
9 • ---• 9
P value
82
2.5:1 40.80 • 14.0 31.1 --- 1.6 8.8 • 1.0 1.2 ~ 0.1 60.0 34.0 10.0 10.0
11.90 • 2.0 2.0 --- 0.1 1.4 • 0.1 0.8 m 0.1 4.1 - 0.3 35.2 • 2.0 165.5 -- 19.8 3.60 -- 0.3 1.0 -- 0.1
Ranitidine (150 mg twice a day)
1.2 0.13 0.1 0.1 0.2 1.7 18.5 0.4 0.2
2.7: 1 38.20 • 14.5 29.2 • 1.4 7.8 • 0.9 1.6 • 0.2 52.0 25.0 8.0 4.0
0.07 0.7 0.6 0.9 0.1 0.05 0.40 0.59 0.21
9.6 --- 1.2 2.1 • 0.11 1.20 - 0.1 0.80 • 0.1 3.6 • 0.2 34.2 -+ 1.6 151.60 -+ 16.3 3.8 -+ 0.2 1.0 -- 0.1
0.5 0.9 0.5 0.9 0.7 0.9 0.8 0.3 0.9
*BAO, basal acid output. tValues were log transformed before statistical analysis. +MAO, maximal acid output. w dose of pentagastrin for half M A O after correction for BAO.
Activity of Gastritis. The grading of the gastritis had decreased significantly in both the omeprazole 10 mg group (X2 = 24.6, P < 0.001), and the omeprazole 20 mg group (X2 = 25.0, P < 0.001) but not in the ranitidine group (X2 = 5.4, P > 0.05) after treatment (Table 2). The findings were similar when only healed ulcer was considered. The percentage of patients with improvement in gastritis was significantly higher in the omeprazole I0 mg and omeprazole 20 mg groups than in the ranitidine group over four weeks using life-table analysis (both P < 0.01, Figure 1). There was no significant difference between the omeprazole 10 mg and the omeprazole 20 mg groups over the four
weeks. The results were similar when only healed ulcer was considered. Degree of Chronic Inflammation. The grade of gastritis had decreased significantly in both the omeprazole 10 mg group (• = 12.8, P < 0.001), and the omeprazole 20 mg group (X2 = 4.9, P < 0.05) but not in the ranitidine group (• = 0.45, P > 0.1) after two weeks of treatment (Table 3). The findings were similar at the end of four weeks or when only healed ulcer was considered. The percentage of patients with improvement in the degree of chronic inflammation is shown in Figure 2. A significantly higher percentage of patients on omeprazole 20 mg or omeprazole 10 mg had
TABLE 2. ACTIVITY OF GASTRITIS BEFORE AND AFTER 2 WEEKS OF TREATMENT WITH OMEPRAZOLE AND RANITIDINE*
Omeprazole, 10 mg every morning
N Grade Grade Grade Grade
0 (%) 1 (%) 2 (%) 3 (%)
Omeprazole, 20 mg every morning
Ranitidine, 150 mg twice a day
Before
2 weeks
Before
2 weeks
Before
2 weeks
78 10 (12.8) 44 (56.4) 24 (30.8) 0 (0)
77 36 (46.8) 32 (41.6) 8 (10.3) 1 (1.3)
81 13 (16.0) 40 (49.4) 28 (34.6) 0 (0)
76 41 (54.0) 21 (27.6) 14 (18.4) 0 (0)
82 6 (7:3) 36 (43.9) 39 (47.6) 1 (1.2)
79 9 (11.4) 46 (58.2) 24 (30.4) 0 (0)
*X" test, before vs after treatment: omeprazole, 10 mg: • = 24.6. P < 0.001; omeprazole, 20 mg: • = 25.0, P < 0.001; ranitidine, 150 mg: • = 5.4. P > 0.05.
Digestive Diseases and Sciences, Vol. 36, No. 5 (May 1991)
579
HUI ET AL
~
60
r~ 50
4O
///
"- 20
,o
"7.
50--
"s 40--
RAN (n=82]
o
oM~,o ~ ~o
~:o.~
OME20 vs RAN
p ~ O 01
OME10 vs 20
p:0.33
OMEI0 vs RAN
p
Effect of Omeprazole on Duodenal Ulcer.Associated Antral Gastritis and
Helicobacter pylori W.M. HUI, MBBS, S.K. LAM, MD, J. HO, MB, C.L. LAI, MBBS, A.S.F. LOK, MBBS, M.M.T. NG, MBBS, W.Y. LAU, MBBS, and F.J. BRANICKI, MBChB
This study set out to investigate the effects of omeprazole or ranitidine on the progression of antral gastritis and Helicobacter pylofi in patients with active duodenal ulcer. A double-blind, double-dummy trial was performed in 270 patients, 241 of whom were studied histologically for the presence of H. pylori. Patients were randomized to receive omeprazole, 10 mg every morning, omeprazole, 20 mg every morning, or ranitidine, 150 mg twice a day, for four weeks. Endoscopy was performed on entry and at weekly intervals during the study; at least two antral biopsies were taken on each occasion to assess the activity and degree of chronic inflammation, as reflected by the degree of polymorphonuclear leukocyte infiltration and mononuclear cell infiltration, respectively. Biopsy specimens also were assessed histologically for H. pylori. The sex, age and maximal acid output were comparable in the three treatment groups. The percentages of patients showing an improvement in the activity of gastritis in the four consecutive weeks of treatment were 9%, 40%, 51%, and 53% for omeprazole, 10 mg (N = 78); 14%, 42%, 49%, and 53% for omeprazole, 20 mg (N = 81); and2%, 23%, 30%, and 33% for ranitidine, 150 mg twice a day (N = 82) (life table analysis gave P < 0.01 for both omeprazole regimens compared with ranitidine). The degree of chronic inflammation showed similar changes. The density of H. pylori decreased significantly after treatment with omeprazole, 10 mg or 20 mg, (both, P < 0.00001) but not with ranitidine. The reduction in bacterial density was significantly higher (P < 0.003) in those who showed improvement of gastritis than in those who did not. We conclude that effective acid inhibition with omeprazole improve s antral gastritis and is accompanied by a reduction in antral bacterial density, suggesting that both acid and H. pylori may be involved in the pathogenesis of antral gastritis. KEY WORDS: antral gastritis; Helicobacter pylori: duodenal ulcer; omeprazole; ranitidine.
Antral gastritis occurs in almost all patients with active duodenal ulcer (1). Gastric acid is important in the etiology of duodenal ulcer (2), but its role in Manuscript received May 3, 1990;revised manuscript received October 1, 1990, accepted January 3, 1991. From the Departments of Medicine, Surgery and Pathology, University of Hong Kong, and Government Surgical Unit. Queen Mary Hospital, Hong Kong. Address for reprint requests: Prof. S.K. Lain, MD. University Department of Medicine, Queen Mary Hospital, Pokfulam Road, Hong Kong.
antral gastritis is unclear. By contrast, Helicobacter pylori has been demonstrated to have an important role in antral gastritis (3), but its importance in peptic ulcer disease is less certain. The proton pump inhibitor omeprazole is an effective inhibitor of gastric acid secretion (4-7), but its effect on antral gastritis and the density of H. pylori in the stomach is sparsely documented (81I). This study was undertaken to assess the effects of omeprazole on both antral gastritis and H. pylori
Digestive Diseases and Sciences, Vol. 36, No. 5 (May 1991)
0163-2116/91/0500-0577506.50/09 1991PlenumPublishingCorporation
577
HUI ET AL in patients with duodenal ulcer and to compare these effects with those of ranitidine, an H2receptor antagonist. MATERIALS AND METHODS
Patients. All patients in the study were outpatients or inpatients from Queen Mary Hospital, Hong Kong. To be included in the study, patients had to have an active duodenal ulcer confirmed by endoscopy. Exclusion criteria were concurrent medical problems (in particular, renal disease, cardiovascular disease, diabetes mellitus, chronic obstructive airways disease, pyloric stenosis, or an associated gastric ulcer), previous gastric operation, or pregnancy. Written informed consent was obtained from all patients, and the protocol was approved by the Ethics Committee of the University of Hong Kong. The clinical, personal, physiological, and endoscopic characteristics of the patients were recorded and have been reported in detail previously (12, 13). Gastric secretory tests and meal-stimulated gastrin responses were performed on consecutive days following endoscopy. Study Design. The study was of a double-blind, doubledummy design, 4 weeks in duration. Patients were randomized to one of three treatment regimens: omeprazole (Astra, Sweden), 10 mg every morning; omeprazole, 20 mg every morning; ranitidine, 150 mg twice a day. No antacid was prescribed, and no other medication was to be taken without notification of the Ulcer Cliniq. Patients were discouraged from smoking cigarettes and drinking alcohol. Treatment was started within three days of recruitment into the study. Patients were assessed clinically on entry and at weekly intervals during the study. Endoscopy was performed On entry and at weekly intervals until the ulcer had healed or for a maximum of four weeks. Ulcer healing was considered to have taken place only if the ulcer had disappeared completely, and residual erosions are taken to mean nonhealing. At endoscopy, at least two biopsies were taken from the antrum, along the greater curvature (usually 5 cm from the pylorus). The biopsy specimens were sent for histology to assess antral gastritis and H. pylori. This study was carried out concurrently with a study on the efficacy of omeprazole versus ranitidine in the healing of duodenal ulcer. The results relating to efficacy of ulcer healing have been reported previously (14). Assessment of Gastritis. Gastritis was assessed in terms of activity and degree of chronic inflammation, as reflected by the amount of polymorphonuclear leukocyte (polymorph) infiltration, and the degree of infiltration with chronic inflammatory ceils, including mononuclear cells and plasma cells (1, 15). The assessment was made independently by two pathologists, who had no prior knowledge of the clinical findings, and graded as follows: activity--grade 0, no polymorphs; grade 1, occasional polymorphs scattered on entire section; grade 2, moderate polymorph infiltration (between grades 1 and 3); grade 3, numerous polymorphs throughout entire section; and chronic inflammationmgrade 0, no chronic inflammatory cells; grade 1, occasional chronic inflammatory cells scattered in the section; grade 2, moderate chronic in-
578
flammatory cell infiltration (between grades 1 and 3); grade 3, numerous chronic inflammatory cells throughout entire section. Both parameters were assessed independently, and improvement of gastritis was considered to have occurred if specimens indicated transition to a better grade when compared with the initial specimens. Assessment of H. pylori. Biopsy sections were stained for H. pylori using Warthin-Starry stain (16). The method of bacterial staining has been validated previously by culture and smear of the biopsy (17). In that study, 92% of the histologically identified cases were positive on culture, and 98% of the cases with positive culture were identified histologically. Briefly, the numbers of bacteria were graded as follows: grade 0, no characteristic bacteria; grade 1, occasional spiral organisms found after meticulous search; grade 2, scattered bacteria in most high-power fields or scattered groups of numerous bacteria; grade 3, numerous bacteria in most high power fields. The biopsies were assessed for H. pytori and gastritis independently by two experienced pathologists who had no knowledge of the clinical findings. Their results concurred in over 90% of assessments. The pathologists differed by one grade in all the discordant cases, and the higher grade was used for comparison. Statistical Analysis. Groups were compared using the • test with Yates' correction. Life-table analysis was used to compare the improvement between the groups (18-20). Values were expressed as mean and standard error of the mean, and a P value below 0.05 was considered statistically significant.
RESULTS A total of 270 patients were recruited into the study on drug efficacy in duodenal ulcer healing. Twelve, nine, and eight patients were excluded from the omeprazole 10 mg, omeprazole 20 mg, and ranitidine groups, respectively, giving totals of 78, 81, and 82 patients in each of these groups. These exclusions were made for noncompliance with the entry criteria, default, or no biopsy taken during endoscopy. Histological assessment of gastritis was thus performed on 241 patients. The three groups were comparable in their clinical, personal, endoscopic, and physiological characteristics before treatment (Table 1). Duodenal Ulcer Healing. The duodenal ulcer healing rates were 77%, 86%, and 63% at two weeks, and 95%, 96%, and 93% at four weeks, for the omeprazole 10 mg, omeprazole 20 mg, and ranitidine groups, respectively (14). The difference between the group receiving omeprazole 20 mg every morning, and the group receiving ranitidine, 150 mg twice a day, was statistically significant at two weeks (P < 0.001). Digestive Diseases and Sciences, Vol. 36, No. 5 (May 1991)
EFFECTS OF OMEPRAZOLE TABLE 1. PREENTRY CHARACTERISTICS OF PATIENTS WITH ANTRAL GASTRITIS TREATED WITH OMEPRAZOLE OR RANITIDINE
Omeprazole 10 mg every morning
20 mg every morning
78
N Sex (M:F) Age (yr) Age of onset (yr) Duration of symptoms (yr) Pain score (0-3) Blood group O (%) Cigarette smoker (%) Alcohol user (%) Analgesic user (%) Index ulcer Diameter (ram) Depth (mm) Inflammation (0-3) Deformity (0-3) BAO* (mmol/hr)? MAO~: (mmol/hr)? Dsocw(ng/kg/hr)? Fasting gastrin (nmol/liter)? 2-hr-postprandial gastrin (nmol/min/liter)?
81
6.0:1 39.4 • 14 30.40 • 1.5 7.10 • 0.9 1.50 • 0.2 64.0 35.0 5.0 6.0
9.5 2,1 1,2 0.8 3.5 34.2 150.2 4.2 1.2
9 • ---• 9
P value
82
2.5:1 40.80 • 14.0 31.1 --- 1.6 8.8 • 1.0 1.2 ~ 0.1 60.0 34.0 10.0 10.0
11.90 • 2.0 2.0 --- 0.1 1.4 • 0.1 0.8 m 0.1 4.1 - 0.3 35.2 • 2.0 165.5 -- 19.8 3.60 -- 0.3 1.0 -- 0.1
Ranitidine (150 mg twice a day)
1.2 0.13 0.1 0.1 0.2 1.7 18.5 0.4 0.2
2.7: 1 38.20 • 14.5 29.2 • 1.4 7.8 • 0.9 1.6 • 0.2 52.0 25.0 8.0 4.0
0.07 0.7 0.6 0.9 0.1 0.05 0.40 0.59 0.21
9.6 --- 1.2 2.1 • 0.11 1.20 - 0.1 0.80 • 0.1 3.6 • 0.2 34.2 -+ 1.6 151.60 -+ 16.3 3.8 -+ 0.2 1.0 -- 0.1
0.5 0.9 0.5 0.9 0.7 0.9 0.8 0.3 0.9
*BAO, basal acid output. tValues were log transformed before statistical analysis. +MAO, maximal acid output. w dose of pentagastrin for half M A O after correction for BAO.
Activity of Gastritis. The grading of the gastritis had decreased significantly in both the omeprazole 10 mg group (X2 = 24.6, P < 0.001), and the omeprazole 20 mg group (X2 = 25.0, P < 0.001) but not in the ranitidine group (X2 = 5.4, P > 0.05) after treatment (Table 2). The findings were similar when only healed ulcer was considered. The percentage of patients with improvement in gastritis was significantly higher in the omeprazole I0 mg and omeprazole 20 mg groups than in the ranitidine group over four weeks using life-table analysis (both P < 0.01, Figure 1). There was no significant difference between the omeprazole 10 mg and the omeprazole 20 mg groups over the four
weeks. The results were similar when only healed ulcer was considered. Degree of Chronic Inflammation. The grade of gastritis had decreased significantly in both the omeprazole 10 mg group (• = 12.8, P < 0.001), and the omeprazole 20 mg group (X2 = 4.9, P < 0.05) but not in the ranitidine group (• = 0.45, P > 0.1) after two weeks of treatment (Table 3). The findings were similar at the end of four weeks or when only healed ulcer was considered. The percentage of patients with improvement in the degree of chronic inflammation is shown in Figure 2. A significantly higher percentage of patients on omeprazole 20 mg or omeprazole 10 mg had
TABLE 2. ACTIVITY OF GASTRITIS BEFORE AND AFTER 2 WEEKS OF TREATMENT WITH OMEPRAZOLE AND RANITIDINE*
Omeprazole, 10 mg every morning
N Grade Grade Grade Grade
0 (%) 1 (%) 2 (%) 3 (%)
Omeprazole, 20 mg every morning
Ranitidine, 150 mg twice a day
Before
2 weeks
Before
2 weeks
Before
2 weeks
78 10 (12.8) 44 (56.4) 24 (30.8) 0 (0)
77 36 (46.8) 32 (41.6) 8 (10.3) 1 (1.3)
81 13 (16.0) 40 (49.4) 28 (34.6) 0 (0)
76 41 (54.0) 21 (27.6) 14 (18.4) 0 (0)
82 6 (7:3) 36 (43.9) 39 (47.6) 1 (1.2)
79 9 (11.4) 46 (58.2) 24 (30.4) 0 (0)
*X" test, before vs after treatment: omeprazole, 10 mg: • = 24.6. P < 0.001; omeprazole, 20 mg: • = 25.0, P < 0.001; ranitidine, 150 mg: • = 5.4. P > 0.05.
Digestive Diseases and Sciences, Vol. 36, No. 5 (May 1991)
579
HUI ET AL
~
60
r~ 50
4O
///
"- 20
,o
"7.
50--
"s 40--
RAN (n=82]
o
oM~,o ~ ~o
~:o.~
OME20 vs RAN
p ~ O 01
OME10 vs 20
p:0.33
OMEI0 vs RAN
p
