Clinical Articles Open Access
Copyright ©The Author(s) 1996. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 25, 1996; 2(2): 104-105
Published online Jun 25, 1996. doi: 10.3748/wjg.v2.i2.104
Prevalence of Helicobacter pylori in cirrhotic patients with portal hypertensive gastropathy
Hai-Hang Zhu
Hai-Hang Zhu, Associated Professor of Internal Medicine, having 5 papers published, Director of the Department of Gastroenterology, North Jiangsu Hospital, Yangzhou Medical College, Yangzhou 225001, Jiangsu Province, China.
Author contributions: Zhu HH solely contributed to this work.
Correspondence to: Dr. Hai-Hang Zhu, Associated Professor, Director of the Department of Gastroenterology, North Jiangsu Hospital, Yangzhou Medical College, Yangzhou 225001, Jiangsu Province, China
Telephone: +86-514-7312935
Received: April 7, 1996
Revised: May 25, 1996
Accepted: June 8, 1996
Published online: June 25, 1996

Abstract

AIM: To determine the relation between Helicobacter pylori infection and portal hypertensive gastropathy.

METHODS: Thirty-four patients diagnosed with portal hypertensive gastropathy according to the McCormack criteria were studied, and 136 age- and sex-matched individuals with chronic superficial gastritis served as controls. H. pylori infection was assessed by the rapid urease test.

RESULTS: H. pylori infection was confirmed in 19 of 34 (55.9%) patients and in 74 of 136 (54.4%) controls. There was no significant difference in H. pylori infection rates of the patients and controls (P < 0.05). The findings show that the presence of H. pylori was not closely associated with portal hypertensive gastropathy. In addition, there was no significant difference in H. pylori infection rates in patients sub-grouped by severity of gastropathy, duration of the disease and Child-Pugh classification of liver function (P < 0.05). The results suggest that factors other than H. pylori infection may be important in the pathogenesis of endoscopic changes.

CONCLUSION: The prevalence of H. pylori infection was not higher in portal hypertensive gastropathy patients than in controls with chronic superficial gastritis who were matched by sex and age. H. pylori infection is unrelated to the severity of endoscopic changes, duration of the disease and Child-Pugh classification of liver function. H. pylori infection is not the only essential factor for the development of portal hypertensive gastropathy.

Key Words: Helicobacter pylori, Hypertension, portal, Stomach diseases, Helicobacter infections



INTRODUCTION

Congestive gastropathy is a frequent endoscopic finding in patients with portal hypertension and is believed to be responsible for approximately 20% of episodes of bleeding in these patients. The pathogenesis of the disorder is, however, controversial. It has been reported that there is a high prevalence of Helicobacter pylori colonization in cases of portal hypertension, particularly in patients with gastric erosions[1]. In contrast, some other reports have shown no relation between H. pylori infection and portal hypertensive gastropathy[2]. The purpose of this study was to determine whether H. pylori infection is a necessary factor for the development of portal hypertensive gastropathy in Chinese patients and to further investigate the relationship between H. pylori infection and the severity of endoscopic changes, the disease duration and the Child-Pugh classification of cirrhosis.

MATERIALS AND METHODS
Patients

Thirty-four patients with portal hypertensive gastropathy were included in this study. These patients were represented by 31 males and 3 females, and their mean age was 47.0 ± 6.7 years-old (range: 25-67 years-old). The diagnosis was confirmed by endoscopy, according to the McCormack criteria. Liver function was graded according to the Child-Pugh criteria[3], and 12 patients were grade A, 11 were grade B, and 10 were grade C. The duration of the cirrhosis was < 4 years for 22 patients and > 4 years for 12 patients. The severity of endoscopic changes was graded according to the McCormack criteria, with 15 patients graded as mild (mosaic or snake skin appearance), 10 as moderate (erythema), and 9 as severe (erosion or hemorrhagic lesion).

Controls

Since, most epidemiological studies to date have shown an increasing prevalence of H. pylori with age, to eliminate the influence of age, we used case-control methods to choose patients with chronic superficial gastritis as controls. All controls were matched by age and sex.

Detection of H. pylori

All patients and controls underwent upper gastrointestinal endoscopy. Two antral biopsied specimens were taken for each case and assessed via the rapid urease test (CLO test; Shanghai Institute of Digestive Diseases). H. pylori infection was diagnosed if two specimens tested positive for H. pylori.

Data analysis and statistical methods

The prevalence of H. pylori infection was compared between patients and controls. The difference in the severity of endoscopic changes, disease duration and the Child-Pugh classification of cirrhosis was statistically analyzed between the H. pylori-positive and -negative patients by using the χ2 test. Significance was set at P < 0.05.

RESULTS

H. pylori infection was confirmed by the rapid urease test for 19 of the 34 (55.9%) patients and for 74 of the 136 (54.4%) controls. There was no significant difference in H. pylori infection rate between patients and controls (P > 0.05), indicating that the presence of H. pylori was not closely associated with portal hypertension.

The relationship between H. pylori infection and the severity of endoscopic changes, duration of the disease and Child-Pugh liver function classification of cirrhosis is shown in Table 1. Similarly, there was no significant difference in the rate of H. pylori infection between the different grades of severity of gastropathy, duration of the disease and Child-Pugh liver function classification (P > 0.05). The findings further suggest that factors other than H. pylori may be important in the pathogenesis of the endoscopic changes.

Table 1 Factors associated with H. pylori infection in portal hypertensive gastropathy n (%).
FactornH. pylori infection
Severity of endoscopic changes
Mild159 (60.0)
Moderate106 (60.0)
Severe94 (44.4)
Duration of the disease (a)
≤ 42212 (54.5)
> 4127 (58.3)
Child-Pugh classification
A126 (50.0)
B117 (63.6)
C106 (60.0)
DISCUSSION

There is a strong correlation between H. pylori infection and histologically-confirmed gastritis, duodenitis and duodenal ulceration; infection with the organism may also contribute to an increased risk of gastric carcinoma. Although the endoscopic appearance of portal hypertensive gastropathy is usually more noticeable in the fundus of the stomach[4], we choose antral biopsy specimens for this study so as to avoid bleeding and increase the detection rate of H. pylori colonization. We initially suspected that the colonization of H. pylori might be related to the endoscopic change. Our results do not, however, support this hypothesis, as we found no relation between H. pylori infection and portal hypertensive gastropathy. Our findings are similar to McCormack′s[2]. The question of whether H. pylori infection should be treated when identified in patients with portal hypertensive gastropathy has not been evaluated. Since the presence of H. pylori is unrelated to the endoscopic appearance, we only treat the patients to improve their dyspeptic symptoms.

We feel that the most likely explanation for the pathogenesis of the endoscopic change in portal hypertensive gastropathy is that mucosal congestion may render the mucosa more prone to injury or reduce its capacity to repair injury. Animal experiments showed an increased susceptibility of the portal hypertensive mucosa to injury induced by agents such as bile acid, aspirin, alcohol, or H. pylori[5]. However, whether the results from this animal model can be generalized to explain human portal hypertensive gastropathy awaits further studies.

In summary, this study shows that the prevalence of H. pylori infection is not higher in portal hypertensive gastropathy patients than that in chronic superficial gastritis patients who were matched by age and that the H. pylori infection is unrelated to the severity of endoscopic changes, the duration of the disease and the Child-Pugh classification of liver function. H. pylori infection is not the only necessary factor for the development of portal hypertensive gastropathy.

Footnotes

Original title: China National Journal of New Gastroenterology (1995-1997) renamed World Journal of Gastroenterology (1998-).

S- Editor: Filipodia L- Editor: Jennifer E- Editor: Zhang FF

References
1.  Paoluzi P, Piatroisuti A, Marchagiano . Prevalence of Campylobacter pylori in cirrhotic patients with gastric erosions. Gastroenterology. 1988;94:A342 (abstract).  [PubMed]  [DOI]  [Cited in This Article: ]
2.  McCormick PA, Sankey EA, Cardin F, Dhillon AP, McIntyre N, Burroughs AK. Congestive gastropathy and Helicobacter pylori: an endoscopic and morphometric study. Gut. 1991;32:351-354.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 46]  [Cited by in F6Publishing: 48]  [Article Influence: 1.5]  [Reference Citation Analysis (0)]
3.  McCormack TT, Sims J, Eyre-Brook I, Kennedy H, Goepel J, Johnson AG, Triger DR. Gastric lesions in portal hypertension: inflammatory gastritis or congestive gastropathy? Gut. 1985;26:1226-1232.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 372]  [Cited by in F6Publishing: 331]  [Article Influence: 10.6]  [Reference Citation Analysis (0)]
4.  Hardo PG, Tugnait A, Hassan F, Lynoch DAF, West AP, Mapstone NP. Helicobacter pylori infection and dental care. Gut. 1995;37:44-46.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 54]  [Cited by in F6Publishing: 52]  [Article Influence: 2.1]  [Reference Citation Analysis (0)]
5.  Sarfeh IJ, Soliman H, Waxman K, Coccia M, Rypins EB, Bui HX, Tarnawski A. Impaired oxygenation of gastric mucosa in portal hypertension. The basis for increased susceptibility to injury. Dig Dis Sci. 1989;34:225-228.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 67]  [Cited by in F6Publishing: 17]  [Article Influence: 2.1]  [Reference Citation Analysis (0)]