[Backgrounds]The gastric mucosa of patients with portal hypertension was found to be different with that of patients with common gastritis in the pathological changes, treatment and prognosis by Sarfeh et al in 1984, so he named it portal hypertensive gastritis in order to differentiate it from common gastritis. In 1985, McCormack et al set up a pathological investigation of the biopsy specimens, operative specimens and postmortem specimens from the patients with portal hypertension. They found that blood vessels in the mucosa and submucosa become dilated and twisted, and the vessel wall become thickened, with less inflammatory cells around it, so they advocated that congestive gastropathy was the name much more suitable. Portal hypertensive gastropathy was put forward by Sarfeh et al in 1986, which was continued to use up to now.PHG is defined as a condition in which macroscopic alterations occur in the gastric mucosa, and usually be found in patients with liver cirrhosis and portal hypertension. The main histological change is that blood vessels in the mucosa and submucosa become dilated and twisted, and the vessel wall become thickened. The clinical significance of this condition lies in its potential to lead to transfusion-dependent anemia as well as acute life-threatening bleeding episodes in patients with cirrhosis and portal hypertension, further aggravating hepatocellular function in these patients. PHG has been reported to be the cause of as many as 0%-35% of gastrointestinal hemorrhages in patients with portal hypertension. Therefore, in order to prevent such tragedies various studies have been carried out to clarify the physiopathology of portal hypertensive gastropathy, resulting in a wide diversity of hypotheses. The majority of them suggested that increased pressure of the portal venous system, increased splanchnic blood flow and changes in the regulatory mechanism of the local vascular tonus were involved in this disease. However the role of H. pylori in the development of these alterations is still controversial.H. pylori is a microaerophilic, Gram-negative, spiral bacterium, which was first isolated by Australian researchers Warren and Marshall from the gastric mucosa of a patient with gastritis in 1983.Then, a great number of researches have shown the close relationship between H.pylori and the occurrence of diseases in gastrointestinal tract such as dyspepsia, chronic gastritis, peptic ulcer, gastric lymphoma and gastric cancer. It was known that H.pylori is a chief risk factor of chronic gastritis and peptic ulcer, and also one of the causative factors of gastric lymphoma as well as gastric cancer. It was reported that the infection rate of H.pylori in adults of developed countries and developing countries was 30% to 50% and 40% to 80% respectively. For China the infection rate was a little higher, showing 40% to 90%. Therefore, the infection of H.pylori is drawing more and more attention among people. As PHG is also a kind of disease occurring in gastric mucosa, what's more, portal hypertension is not the only cause involved in the course of PHG, we took HP in consideration in order to find out the correlations of H. pylori infection with portal hypertensive gastropathy and its complicated upper gastrointestinal hemorrhage in patients with liver cirrhosis and to evaluate if it is necessary to eradicate H. pylori in these patients.Up to now, several investigators have evaluated the effect of H. pylori on liver cirrhosis and PHG with controversial results. Some reports have shown a higher seroprevalence and suggested a synergistic effect of H. pylori on liver cirrhosis and PHG. However, this increased prevalence was associated with a piece of negative histological evidence. In contrast, most studies have not found any correlation between H. pylori and PHG. Some of them even have reported a marked lower prevalence of H. pylori in cirrhotic patients with PHG compared to controls.Studies on the relationship between H.pylori and PHG not only focused on the infection rate, but also on the influence of H. pylori infection on serum ammonia levels as well as the expression of inducible nitric oxide synthase (iNOS), for the reason that serum ammonia level and iNOS play an important role in the course of PHG. [Objective]The current study was conducted to ascertain the prevalence of H. pylori in patients with PHG and determine whether it contribute to the presence and/or the severity of the disease as well as the complicated upper gastrointestinal hemorrhage. [Methods]A total of 115 consecutive patients presented with portal hypertensive gastropathy were included in the study, of which 55 patients were complicated with upper gastrointestinal bleeding and 60 patients without it. Liver cirrhosis was diagnosed by a combination of clinical, laboratory and imaging examinations (abdominal US, CT, and/or MRI). PHG was diagnosed endoscopically by its characteristic features by at least two experienced endoscopists independently and was classified into two types in accordance with the McCormack classification:mild PHG, snakeskin pattern and/or fine pink speckling; severe PHG, cherry-red spots and/or bleeding PHG. In all patients, diagnostic upper endoscopy was performed using an Olympus (Olympus Optical Co, Tokyo, Japan) videoendoscope system.H. pylori status was determined by means of a rapid urease test and also by the C14 urea breath test or the anti-H. pylori IgG levels in serum. A gastric antral biopsy specimen from each patient was taken within 5 cm of the pylorus. Then it can give a rough level of H pylori infection using the rapid urease test. The urea breath test with C14 was performed according to an established protocol (the agentia and H. pylori survey meter were supplied by Shenzhen yanghe Tech Co., Ltd). An enzyme linked immunosorbent assay with high sensitivity and specificity was used to detect serum anti-H pylori IgG antibodies. The presence of at least two positive tests was considered as a positive H. pylori state and three negative items indicated H. pylori negative.The subjects were asked about their drinking and NSAID taking history. Daily alcohol intake in grams per day was recorded. More than 20 grams per day for women or more than 80 grams per day for men with the duration for more than a year would be seen as a risk factor. Patients who had a history of overdose treatment with NSAID in the previous two weeks also got a risk factor.[Results]The rate of H. pylori infection was lower in patients with PHG (30.4%) than that in patients with chronic gastritis (47.7%) (P<0.05). H. pylori positive rate was higher in mild PHG (38.2%) than that in severe PHG (25.9%), although this did not reach statistical significance. No correlation was found between H. pylori infection and the incidence and severity of bleeding in patients with PHG. The differences of Child-Push classification grading among the three groups (patients with PHG and upper gastrointestinal hemorrhage, patients with PHG but without upper gastrointestinal hemorrhage and cirrhotic patients without PHG) were statistically significant (P<0.05). The alcohol consumption was much higher in patients with PHG and bleeding than that in patients with PHG but without bleeding (P<0.05).[Conclusions]PHG does not provide a favorable environment for the colonization of H. pylori. The H. pylori infection is not related to the pathogenesis and severity of PHG in cirrhotic patients. Furthermore, H. pylori are unlikely to contribute to the presence and severity of upper gastrointestinal hemorrhage in patients with PHG. Therefore, there might be no need for its routine eradication in patients with PHG who are or aren't complicated with upper gastrointestinal hemorrhage. But the remarkable correlation of liver function with PHG and bleeding suggests that factors doing harm to liver function should be taken in consideration and analyzed statistically and purposefully. In addition to using pharmacological agents (such asβ-blockers, somatostatin, vasopressin, gastric mucosal protective agents and so on) and surgical methods, elimination of known risk factors for gastric injury such as alcohol is also critical to reduce the frequency of bleeding episodes in patients with PHG. |