Study of H . Pylori Infection in Patients with Portal Hypertensive Gastropathy

Background and study aim: The association between H. pylori infection and cirrhosis in patients with hepatitis C virus has been documented in different parts of the world. Eradication treatment may prove beneficial in those patients with chronic hepatitis C. The aim of the present study was to study H. pylori infection in patients with portal hypertensive gastropathy. 
Patients and Methods: This study was conducted on Session [CurrentTestPartID] patients; 45 patients with portal hypertensive gastropathy (Group A). In addition to 15 patients with chronic gastritis without portal hypertension (Group B). All patients were subjected to full history tacking and complete physical examination. Routine laboratory investigation including, CBC, PT, PC, INR, SGOT, SGPT, S. Albumin, S. Bilirubin. Radiological examination including abdominal ultrasound, and Doppler study for Portal vein. Upper GIT endoscopy, and biopsies from the antrum. Histopathological examination of the biopsies for assessment of congestive gastropathy and H. pylori infestation if present. 
Results: This study demonstrated that the Session [CurrentTestPartID]% of patients of group A and 66% of patients of group B have H. pylori infection. There was no predilection for H. pylori infections in patients with PHG than those in patients with gastritis. In group A, 53% of patients with varices had H. pylori infection while 47% did not have H. pylori infection. Also, 76% of the non H. pylori patients had esophageal varices while Session [UserIDID]% of patients with non H. pylori subgroup had no varices. Additionally, patients of group A with mild PHG and H pylori constituted 26.5%, those with moderate PHG and H pylori constituted 47% while patients with severe PHG and H pylori constituted 26.5%. 
Conclusion: This study demonstrated that there is no predilection concerning the presence of H pylori infection in patients with PHG and there is no relation between the degree of PHG and the presence of H pylori infection.


INTRODUCTION
PHG while extremely common in patients with portal hypertension, is an uncommon cause of significant bleeding in these patients.When portal hypertensive gastropathy is the sole cause of bleeding, there is diffuse mucosal oozing with no other lesions, such as varices, to account for the GI bleeding and anemia.The mucosa is friable, and bleeding presumably occurs when the ectatic vessels rupture.The severity of gastropathy is related to the level of portal pressure, the level of hepatic vascular resistance, and the degree of reduction in hepatic blood flow [1].
PHG may correlate with the severity of liver disease.Gastric mucosal blood flow is increased in patients with cirrhosis and PHG compared with those without gastropathy, suggesting that the pathogenesis of this disorder may be related to both congestion and hyperemia in the stomach [2].
H. pylori is recognized as a pathogen of upper gastrointestinal diseases, such as acute and chronic gastritis, duodenal and gastric ulcers and mucosa-associated lymphoid tissue (MALT) lymphoma.H. pylori has also been closely associated with development of gastric adenocarcinoma.

Aim of the work
The aim of the present work was to study H. pylori infection in patients with portal hypertensive gastropathy.

PATIENTS AND METHODS
This study has been conducted on 60 patients attending endoscopy unit of National Hepatology Institute and Tropical Medicine Department classified into two groups :Group (A)includes 45 patients with portal hypertensive gastropathy (PHG), they were 32 males and 13 females, their ages ranged from 19 to 63 years and group (B) included 15 patients with chronic gastritis without portal hypertension, they were 10 males and 5 females, their ages ranged from 24 to 55 years.All patients were subjected to full history tacking and complete physical examination, laboratory investigation (CBC, INR, SGOT, SGPT, S. albumin, S. bilirubin), abdominal ultrasound with Doppler study, upper GIT endoscopy, and biopsies from gastric antrum and body for histopathological examination and detection of H. pylori infection.PHG were classified endoscopically into three grades based on Tanoue et al classification: G I (mild mucosal reddening), G II (severe redness and a fine reticular pattern separating the areas of raised edematous mucosa "mosaic"), G III (hemorrhagic spots plus G II). Histopathological features of PHG include dilatation of the capillaries & collecting venules in submucosa and in severe cases these vessels become markedly dilated and extend to mucosa which become severely congested and edematous.

RESULTS
The results of the present study showed that there were no statistical significant differences between the two groups concerning gender distribution and age.The clinical examination showed that patients of group A demonstrate that 11% had pallor, 20% had tinge of jaundice, 17% showed lower limb edema, 71% had hepatomegaly and 40% had splenomegaly.Patients of group B were clinically free according to the inclusion criteria.As regard liver functions, there was a statistically significant deterioration of some liver function tests in patients of group A than those of group B. Coming to CBC, there were statistically significant decrease in RBCs, hemoglobin, and platelets count, while no significant differences in WBCs and eosinophils.
Table (1) shows that there was statistically significant difference between the two groups regarding haemoglobin and platelets.There was no statistically significant difference between the two groups regarding WBCs and eosinophils (Fig. 1).
Concerning abdominal ultrasound, the results showed that patients of group A, 45% of them showed chronic liver disease while 55% showed manifestation of cirrhosis.Also 71% had splenomegaly, More than 95% had dilated PV and more than 33% showed collateral vessels of portosystemic circulation.Table (2) shows that the direction of blood flow is hepatopedal in all patients of gastritis while in patients with PHG only 58% was hepatopedal while 31% was hepatofugal and 11% was bidirectional.It also shows that although the flow was faster in gastritis group than the PGH group, yet there was no statistical significant difference as regards the PV velocity among the studied groups.
Coming to the endoscopic findings, this study demonstrated that among patients in group A, 31% had esophageal varices, 44% had mild PHG, 36% showed moderate and 20% had severe PHG.While patients of group B showed no manifestation of PHG, but peptic erosions; mild and moderate in some of them (Figs.2).Table (3) shows that there was statistically significant difference between the two groups regarding the presence of esophageal varices and PHG and no statistically significant difference between the two groups regarding inflammation.

Table (4) represents the distribution of H. pylori
in histopathological study of gastric biopsy specimen among studied groups.There was no significant difference between studied groups as regard presence of H. pylori infection.66.67% of PHG group had H. pylori infection versus 60% of gastritis group meaning that there is no specific predilection for H. pylori infections in patients with PHG than those in patients with gastritis.
Moreover, there was no significant difference between severity of PHG and the presence of H. pylori infection (table 5) Table (6) shows that there was statistically significant difference between the two groups regarding pathological finding concerning the presence of lymphoid aggregates and the presence of mucosal cell atrophy which show a highly significant increase in PHG group.There was no statistical significant difference regarding the immunological activity and the presence of metaplasia or dysplasia.

Figure ( 1
Figure (1) :Child classification of the studied group H. pylori has been reported to induce hepatotoxicity in vitro.Furthermore, several investigators have reported a high prevalence of H. pylori infection in patients with chronic liver diseases [3].Although H. pylori is generally believed to be sensitive to bile, several studies have shown that H. pylori is detectable in the liver and biliary tract and that H. pylori can survive in bile-rich environment.These findings indicate that bile-resistant H. pylori may survive in the liver and biliary tract.The association between H. pylori infection and cirrhosis in patients with hepatitis C virus has been documented in different parts of the world.

Table ( 1
): Main elements of the blood picture of the studied groups

Table ( 3
): Endoscopic finding of the studied groups