**4. Chronic HBV and HCV infections**

The frequency of *H. pylori* infection among patients with chronic hepatitis B is around 30–80% [17]. *H. pylori* infection is confirmed in 79% of patients with postinflammatory liver cirrhosis connected with HBV infection [18]. Favorable effect of *H. pylori* eradication on the course of the disease, including increased platelet count, has been demonstrated in the studies on patients chronically infected with HBV, with compensated liver cirrhosis and thrombocytopenia [19].

Among people chronically infected with HBV with primary liver cancer, *H. pylori* infection is found in 69% of patients. In the group of patients with primary liver cancer, but without HBV infection, *H. pylori* infection is much less frequent, as it is found in 33% of patients. These observations consistently point to unfavorable effect of *H. pylori* infection among HBV-infected patients with liver cirrhosis onto the risk of occurrence of primary liver cancer. Frequency of *H. pylori* infection among patients with chronic hepatitis B correlates with the incidence of hepatocellular cancer, both in men and women [20]. Among this type of patients, fast progression of inflammatory changes in the liver is observed, as well as intensified fibrosis, which promotes occurrence of primary neoplastic lesions [17, 21].

Among patients infected with *H. pylori* and HBV, liver function is impaired (prothrombin time is extended, and AST activity and bilirubin concentration increased), and esophageal varices, ascites and hyperammonemia with hepatic encephalopathy occur much more frequently [18].

Evaluation of *H. pylori* infection among patients with chronic HCV infection is difficult. Some authors state that the frequency of *H. pylori* infection among the patients in this group is about 38%. Around 45% of those result from CagA-synthesizing bacteria. No significant differences are found in the morphological picture of HCV-infected liver, between patients with or without *H. pylori* infection. There is also no correlation between *H. pylori* infection and IL 28B polymorphism [22]. However, many other authors present other observations. *H. pylori* infection may be present in even 70% of patients chronically infected with HCV [23]. Meta-analysis of 20 studies demonstrated higher incidence of *H. pylori* infection among HCV-positive patients, compared to persons without viral infection [17, 24]. Much higher fibrosis, loss of cellular proteins, and glycogen was found in morphological studies of the liver from HCV-positive patients, if those were coinfected with *H. pylori*, compared to those without coinfection [25]**.**

in the stomach, which in turn worsens liver function. This is especially dangerous among patients with advanced liver injury. Studies performed on this group of patients point to high significance of cytopathic effect of *H. pylori* onto hepatocytes [16, 35]. *H. pylori* infection affects increase of portal tension, which is one of the main etiologies of development of esophageal varices [6, 36]. In effect, correlation between the frequency of *H. pylori* infection and advance-

The Importance of *H. pylori* Infection in Liver Diseases http://dx.doi.org/10.5772/intechopen.79969

Although in some studies more frequent *H. pylori* infection among patients with liver cirrhosis cannot be confirmed [38]; however, meta-analysis was performed that included mainly patients with alcoholic liver cirrhosis, which argues for much more frequent occurrence of these bacteria among such patients. *H. pylori* infection is much more frequent among patients with postinflammatory liver cirrhosis (connected with HBV or HCV infection) [37]. Incidence of *H. pylori* infection among patients with liver cirrhosis and concomitant HCV infection increases proportionally to progressing liver failure [39]. Moreover, it has been demonstrated that the highest percentage of people infected with *H. pylori* among those with HCV infection is observed in the case of patients in whom HCC developed [17, 24]. Many pieces of information argue that concomitant infection with *H. pylori* and HCV increases the incidence of HCC. Eradication of these bacteria in patients with cirrhotic liver leads to the increase of platelet count and improves efficacy of antiviral therapy [23, 40]. In the current setting, when direct-acting antivirals are commonly used, this is probably not so important; however, such

*H. pylori* catalyzes the reaction of urea decomposition to ammonia and carbon dioxide; however, among patients with subclinical hepatic encephalopathy, infection with these bacteria does not change the concentration of ammonia in the blood [41]. These observations are inconsistent, because among patients with liver cirrhosis, especially postinflammatory cirrhosis, more frequent occurrence of symptomatic hepatic encephalopathy with hyperammonemia is observed in the case of patients infected with *H. pylori*, compared to patients without this infection [37, 42]. In the studies performed in patients with liver cirrhosis, a correlation between increasing ammonia blood concentration and *H. pylori* infection has been demonstrated. Moreover, ammonia blood concentration was higher among patients with liver cirrhosis infected with *H. pylori*, compared to patients not infected with these bacteria [37].

In experimental studies performed on dogs, an association between *H. pylori* infection and occurrence of hepatocellular carcinoma (HCC) has been evidenced [43]. Evaluation of the effect of *H. pylori* infection on liver carcinogenesis in humans shows that in 58% of patients with HCC and in 62% of patients with CCC in the liver tissue surrounding focal lesion, DNA of these bacteria can be detected [44]. *H. pylori* may disturb the balance between hepatocyte proliferation and activity of apoptosis in the liver. In effect, there is a higher risk of occurrence

In the pathogenesis of biliary duct carcinoma, *H. pylori* infection affects proliferation of biliary duct epithelium and development of inflammatory reaction in these cells. Activation of reactive oxygen species (oxidative stress) and reactive nitrogen species, mainly 8-nitroguanine, in the cells is detected. These reactions damage DNA of stem cells, playing a key role in carcinogenesis [46]. A special role in the development of bile duct carcinoma is attributed to

ment of esophageal varices is observed [37].

studies have not been performed.

of neoplastic cells in the liver [45].

*H. pylori* producing CagA toxin [47].
