Download Therapeutic effect of ecabet sodium in non

Therapeutic effect of ecabet sodium in non-erosive reflux disease of type A gastritis
Tae Ho Kim, Dae Young Cheung, Hyung Geun Kim, Sung Soo Kim, Jin Il Kim, Soo-Heon Park, Sok Won Han
Division of Gastroenterology, Department of Internal Medicine, The Catholic University of Korea, Seoul, Korea
Background
Helicobacter pylori (H. pylori) infection is closely associated with the occurrence of gastric diseases including gastritis, peptic
ulcers, and gastric cancer. Atrophic gastritis is primarily observed in patients with H. pylori infection, which suggests that H. pylori
plays a critical role in the promotion of this disease. H. pylori is a major risk factor for atrophic gastritis followed by gastric
carcinoma. Progression of atrophic gastritis depends upon both bacterial and host factors. Cag A protein, a well-known major
virulent factor, acts as a molecular mechanism in the pathogenesis of H. pylori infection[6]. Host factors are also considered
important to the promotion of atrophicgastritis, and several have been investigated, including interleukin-1 gene polymorphism,
typing of human leukocyte antigen and antiparietal cell antibody. Type B gastritis as metaplastic atrophic gastritis is associated
with chronic Helicobacter pylori infection. There is preferential spread into the antrum and to a lesser extent, the corpus, often in a
patchy distribution that lends the synonym ‘‘multifocal atrophic gastritis’’. Type A gastritis as autoimmune metaplastic atrophic
gastritis, results from an autoimmune attack on the specialized oxyntic glands of the body and fundus, leading to mucosal
inflammatory infiltrates, metaplasia, andglandular atrophy that are essentially restricted to the oxyntic mucosa and do not involve
the antrum. Furthermore, autoimmune gastritis differs from environmental atrophic gastritis in its characteristic neuroendocrine
[enterochromaffinlike (ECL) cellhyperplasia that is the sequela of the hypergastrinemia resulting from parietal cell destruction and
achlorhydria. Ecabet sodium demonstrated some common features with sucralfate as possible mechanisms for antiulcer action:
antipepsin activity, binding to proteins to form a complex that is resistant to the peptic activity of gastric juice, increasing the
capacity of gastricmucosa to synthesize prostaglandin E2 (PGE2) and/or prostacyclin (PGI2), and enhancement of the gastric
mucosal defensive factors such as mucosal blood flow, mucosal adherent mucus, and mucosal bicarbonate secretion. In addition,
ecabet also showed no significant inhibitory effect on acid secretion [13]. Besides these efficacy related effects, ecabet is a
biologically inert substance, showing no other physiological and toxicological effects. But the therapeutic effect of type A and type
B gastritis of ecabet sodium is not explored. The aim of this study is compare the therapeutic effect of ecabet sodium in the nonerosive reflux disease of type A and type B gastritis patients.
Results
Mean age of the patients was 51.5±14.3 and male gender was 32%. Among the following symptoms - fullness, early satiety,
bloating, nausea, vomiting, heartburn, and acid regurgitation, epigastric pain was the most frequent symptom (83.3% in
ecabet sodium group, 70.9% in lansoprazole group). Lansoprazole was more effective in patients with epigastric pain(p<0.01),
and ecabet sodium was more effective in patients with early satiety(p<0.01).
Table 1. Baseline characteristics of the study population
Ecabet sodium group
Lansoprazole group
48
55
Male
16 (33%)
17(31%)
Female
32(67%)
38(69%)
Age (years, mean ± SD*)
53.7±14.8
49.7±13.7
Positive
8(17%)
16(29%)
Negative
21(43%)
15(27%)
N/A
19(40%)
24(44%)
Number of patients
Sex
H.pylori status
Table 2. Frequency of dyspeptic symptoms at baseline
Materials and Methods
Between September 2008 and march 2009, we screened 453 patient. We enrolled 103 patients with reflux symptoms without
erosive esophagitis in endoscopy. We enrolled all consecutive patients with reflux symptoms without erosive esophagitis who are
come to our CUMC gastroenterology clinic for diagnostic upper gastrointestinal endoscopy. Exclusion criteria included age under
18 years or over 75 years, pregnancy or lactation, regular use of steroids or NSAIDs, an experience in administration of any drug
for treating the subject disease, including gastric acid secretion inhibitors (proton pump inhibitor, H2-blocker, etc.) within 4 week of
enrollment. Patients demonstrating gastric ulcer or duodenal ulcer, malignant disease on upper gastrointestinal endoscopy, were
excluded from this study. Other exclusion criteria included serious hepatic, cardiovascular, renal, and hematological diseases.
Patients with previous gastrectomy and eradication therapy for H. pylori infection are excluded. Type A gastritis is assessed by
anti-parietal cell antibody test. Divided into 2 groups, patients randomly received either 1 g ecabet sodium bid, or lansoprazole 15
mg qd for 4 weeks. Dyspepsia assessment by using a diary card and compliance of the test drug are conducted at every 2 weeks
until 4 weeks. The degree of the dyspeptic symptoms was calculated as composite score (Symptom frequency x severity).
Ecabet sodium group
Lansoprazole group
Heartburn sensation
12.5%
29.1%
Acid regurgitation
29.2%
54.5%
Epigastric pain
83.3%
70.9%
Fullness
50.0%
16.4%
Early satiety
20.8%
3.6%
Bloating
10.4%
16.4%
Nausea
22.9%
7.3%
Vomiting
0%
0%
Conclusions
Ecabet sodium was not sufficiently effective on treatment of non-erosive reflux disease. But ecabet sodium was very useful in
reducing dyspeptic symptom especially early satiety. It can be used as a complementary drug in type A gastritis patients with
gastroesophageal reflux symptoms.