Role of h. pylori in congestive gastropathy

ROLE OF THE PRESENCE AND TREATMENT OF H.
PYLORI AND OTHER TREATMENT MODALITIES ON
THE COURSE OF CONGESTIVE GASTROPATHY
Shindy Mohammed Shendy
Tropical medicine department, Theodor Bilharz Research Institute
Gastric mucosal lesions that were described with liver cirrhosis and portal hypertension include
acute gastric lesions, hemorrhagic gastritis, erosive gastritis or acute gastric erosions (Franco et al.,
1977). McCormick and his colleagues postulated congestive gastropathy rather than gastritis in 1985.
These lesions were classified into mild gastropathy when mosaic pattern of multiple erythematous
areas outlined by a white reticular network or a scarlatina- like pattern of fine pink speckling was
detected and severe gastropathy of cherry red spots on a finely granular mucosa (D’Amico et al.,
1990). In these studies, the prevalence of mild gastropathy ranged from 20% – to- 94% and of severe
gastropathy from 7% – to – 41% in patients with cirrhosis and portal hypertension.
The pathogenesis of PHG is still unclear. Elevated portal pressure can induce changes of local
hemodynamics, thus causing congestion in the upper stomach and gastric tissue damage. These
changes may then activate cytokines and growth factors, such as tumor necrosis factor alpha, which
are substances that activate endothelial constitutive nitric oxide synthase and endothelin 1 in the portal
hypertensive gastric mucosa. Overexpressed nitric oxide synthase produces an excess of nitric oxide,
which induces hyperdynamic circulation and peroxynitrite overproduction. The overproduction of
peroxynitrite, together with endothelin overproduction may cause an increased susceptibility of gastric
mucosa to damage. When combined with impaired mucosal defense and healing, these factors may
together produce PHG in patients with portal hypertension (Ohta et al., 2002).
Reduced gastric mucosal defense caused by H pylori may account for the pathogenesis of GI
lesions in liver cirrhosis. H. pylori is strongly associated with peptic ulcer disease and chronic gastritis,
however, several studies showed no relationship between H. pylori infection and congestive
gastropathy in liver cirrhosis (Fujiwara et al., 1998).
After oesophageal and fundal varices, portal hypertensive gastropathy (PHG) is the second most
frequent cause for bleeding in cirrhotic patients. It accounts for 1 to 8% of primary upper
gastrointestinal hemorrhage. Also, it accounts for 30 to 60% of secondary acute or chronic bleeding,
mainly after sclerosing therapy of varices. Endoscopy is diagnostic either by showing a typical
'mosaic-pattern' in mild, and a single or confluent 'cherry red spots' in severe forms. Helicobacter
pylori or NSAID-induced gastropathy are to be distinguished by biopsies. Secondary prophylaxis with
propranolol especially after sclerosing therapy is recommended, primary prophylaxis not (Hermann R,
1997). Evidence in the literature suggests that hypertensive gastropathy might not represent a
favorable environment for Helicobacter pylori thus making the diagnostic sensitivity of the biopsy
lower than expected (Farinati F et al, 1998).
The aim of this work is to investigate the role and the eradication of H. pylori in the treatment of
portal hypertensive gastropathy in comparison with other suggested treatments such as Daflon,
sucralfait, propranolol and verapamil. Our intimate aim is to find a simple treatment; if possible; for
such common gastro-intestinal disease.

Materials and methods:
This study includes 64 patients who have liver cirrhosis and portal hypertensive gastropathy with
or without H. pylori infection. Patients were admitted to Theodor Bilharz Research Institute and were
subjected to history taking and clinical examination. Urine, stool, sigmoidoscopy, upper endoscopy
and gastric biopsies for histopathology and H. pylori staining before and after treatment were done in
all patients. Abdominal ultrasound examination was performed to evaluate the liver disease and its
manifestations. CBC, liver function tests, kidney function tests and blood sugar were done routinely in
all patients. Most of the patients were diagnosed by previous liver biopsy during the course of their
disease. H. pylori serology using ELISA was done in all patients. Patients in this study were divided
into the following groups:
Group I: included 21 patients with congestive gastropathy and H. pylori infection and were treated
with eradication therapy for H. pylori (PPI, amoxicillin and clarithromythin in the standard
doses) followed by PPI for 2 weeks.
Group II: included 20 patients without H. pylori infection and without history of injection
sclerotherapy are treated with sucralfait 2gm twice daily and Daflon 500 mg three times
daily for three months (Daflon is a purified flavinoid fraction corresponding to diosomin90%
and hesperidin flavinoid 10% tablets; Les laboratories, Servier, France).
Group III: 23 patients without H. pylori infection and with history of injection sclerotherapy are
treated with propranolol 40 mg three times daily and verapamil 80 mg three times daily for
three months.
Statistical Analysis
Statistical analysis was performed using the SPSS 12 for window statistical Package Results are
expressed as absolute values and mean ± SD. Statistical analysis of the data was carried out using the
ANOVA test. For correlation studies, the Pearson correlation coefficient was used. A p -value of <
0.05 was considered significant.
RESULTS:
Table 1: Some clinical features of patients in the three groups:
Group No. of patients Age
Sex H pylori positivity Bleeding status
Male Female Serology biopsy present absent
Group I 21 48.9±13.6 13 8 21 21 0 21
Group II 20 44.85±12.8 11 9 2 0 0 20
Group III 23 44.86±14.5 14 9 5 0 23 0
Table 2: Symptomatic improvement of dyspeptic symptoms in all groups:
Group Number of patients suffering
from dyspeptic manifestations
No
improvement
Mild
improvement
Marked
improvement
Group I 20/21 0 5 15
Group II 14/20 4 7 3
Group III 17/23 3 8 6

Effect of therapy on OV and PHG in the three groups (Tables 3, 4 & 5):
Table 3: Oesophageal varices and portal hypertensive gastropathy in patients with H pylori infection
(group I):
OV PHG PHG, in biopsy
Grade Before ttt After ttt Degree Before ttt After ttt Degree Before ttt After ttt
Grade I : 5 5 Absent 00 3 Absent 0 6
Grade II : 6 6 Mild 10 15 Mild 10 11
Grade III: 9 10 Severe 11 3 Severe 11 4
Grade IV : 1 0
Signif: P=0.7 NS P= 0.001 sign. P=0.000 sig
Table 4: Oesophageal varices and portal hypertensive gastropathy in patients treated with Daflon and
sucralfait (group II):
Grade I : 6 6 Absent 0 6 Absent 0 6
Grade IV : 2 2
Signif: P=0.8 NS. P= 0.005 : sig. P=0.001 : sig
Table 5: Oesophageal varices and portal hypertensive gastropathy in patients with history of
injection sclerotherapy, treated with propranolol and verapamil (group III):
Grade 0: 15 14 Grade I : 6 7 Absent 0 5 Absent 0 6
Grade IV : 0 0
Signif: P= 0.6 NS P= 0.006 : Sig P= 0.003 : Sig
Comparison of the response of oesophageal varices, and gastropathy to therapy between the three
groups using Levene's Test for Equality of Variances for independent samples test found that only
oesophageal varices improved significantly in group I in comparison to group II. No differences in
the response of PHG in the three groups.
Oesophageal varices were found the only predictive variable among all studied variables for the
presence and severity of PHG.
Most of these patients are suffering from dyspeptic symptoms in the form of epigastric
discomfort and pain after meals, flatulence and distension. This was more marked in patients with H
pylori infection. There is substantial improvement after treatment in all patients that was most
marked in patients of group I after eradication of H pylori.

Discussion
In this study, portal hypertensive gastropathy (PHG) and H pylori infection were found a common
asssociation in Egyptian patients with liver cirrhosis. H pylori infection may be another factor that
helps in the development of PHG. This is proved in this study by the significant improvement in such
condition after eradication therapy. Such improvement was noticed mainly in the severe cases which
become mild after treatment in group I. However, there is no significant change in the mild cases of
gastropathy. Thus, H pylori may only add to the severity of the condition but not the initiative factor.
Increased expression of inducible nitric oxide synthase (iNOS) has been reported in gastric mucosa of
patients with Helicobacter pylori infection or portal hypertensive gastropathy (PHG) but probably
there is no additive or synergistic impact between H. pylori and PHG on iNOS expression.
Furthermore, It was found that expression of iNOS was significantly higher in patients with severe
PHG than in those with mild PHG and without PHG (Arafa UA et al; 2003).
Sucralfait and the venotonic medication; Daflon; also produced significant improvement in PHG,
even in mild cases. Sucralfait being a cytoprotective agent to the gastric mucosa added to daflon
produced such effect in these patients despite no effect on the large vessels; esophageal varices. These
simple and safe medications can be added to the management of these patients particularly those with
dyspeptic symptoms from PHG.
After injection sclerotherapy and band ligation, the development of PHG increases (Primignant M
et al 2000 and Dong L et al 2003). The use of propranolol and calcium channel blocker; verapamil as
secondary prophylaxis for both esophageal varices and PHG seems effective. In this study they
produced significant improvement in PHG with changing of most severe cases to mild and complete
disappearance of 6 mild lesions. In spite of this marked improved; some cases still have milder grades
of varices on treatment (recurrent or not completely eradicated by previous endoscopic therapy).
In this study, esophageal varices were found the only predictive variable for the presence and
severity of PHG. This finding is similar to the finding of Dong L. et al. (2003) who found that
gastroesophageal varicosity was closely related to PHG, but their degrees are not related.
In some studies, H. pylori was found less frequently in congestive gastropathy patients than in the
control group and presence and severity of congestive gastropathy is independent of the H. pylori
status (Dai L and Wu X; 1999, Dong L et al 2003, and Batmanabane et al 2004). These researchers
suggested that there might be no need for its routine eradication in patients with PHG and it was
concluded that portal hypertensive gastropathy does not provide a favorable environment for the
colonization of H. pylori.
The prevalence of gastropathy in different studies (and this study) was correlated with the duration
of disease, presence and size of esophagogastric varices, and a previous history of endoscopic variceal
sclerotherapy (Primignant M et al 2000).
In this study, there is substantial improvement in all patients that was most marked in patients
having additional H pylori infection (group I), after eradication therapy. Thus, gastritis due to H pylori
adds more loads on the symptomatology of these patients and it is advised to eradicate this infection in
patients with cirrhosis.
It is concluded from this study that H pylori may aggravate this disease process and its eradication
may be beneficial in patients with liver cirrhosis and portal hypertension. Also, other treatment
modalities were effective in decreasing the severity of this disease, which means that this disease
process may be aggravated by other factors than H pylori i.e. multifactorial. Such treatment can be

used in combination with or after eradication therapy. More prolonged studies are recommended to
prove that such effect is long lasting and is not due to other factors.
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