Active Peptic Ulcer Disease in Patients with Hepatitis C Virus-Related Cirrhosis: The Role of<i>Helicobacter pylori</i>Infection and Portal Hypertensive Gastropathy

Dore, Maria Pina; Mura, D.; Deledda, S.G.; Maragkoudakis, Emmanouil; Pironti, A.; Realdi, Giuseppe

doi:10.1155/2004/150674

Cited by 22 publications

(16 citation statements)

References 18 publications

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“…Nonetheless, 22% of these patients with worsening PHG had a documented episode of upper gastrointestinal bleeding. These observations are consistent with prior reports of a greater short-term risk of upper gastrointestinal bleeding in patients with severe versus mild PHG (23, 24). In addition, subjects with worsening PHG were also at much higher risk of experiencing a clinical complication from their liver disease compared to those with stable or improved PHG.…”

Section: Discussionsupporting

confidence: 93%

Development and Progression of Portal Hypertensive Gastropathy in Patients With Chronic Hepatitis C

Fontana

Sanyal

Ghany

et al. 2011

American Journal of Gastroenterology

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OBJECTIVES To determine the incidence and risk factors associated with new onset and worsening portal hypertensive gastropathy (PHG) in patients with chronic hepatitis C (CHC). METHODS 831 CHC patients with bridging fibrosis or cirrhosis at entry were prospectively monitored for clinical and histological liver disease progression while receiving either low dose peginterferonα2a or no antiviral therapy in the HALT-C Trial. Upper endoscopy with grading of PHG was performed at baseline and year 4 of the study. The presence and severity of PHG were determined using the NIEC criteria and worsening PHG was defined as a score increase of > 1 point. RESULTS During a median follow-up of 3.85 years, 50% of the 514 subjects without PHG developed new onset PHG while 26% of the 317 patients with baseline PHG had worsening PHG. Independent predictors of new onset PHG included higher alkaline phosphatase and being diabetic, while predictors of worsening PHG were Caucasian race, lower albumin, and higher serum AST/ ALT ratio and HOMA levels. New onset and worsening PHG were significantly associated with clinical as well as histological progression. New onset and worsening PHG were also associated with new onset and worsening of gastroesophageal varices. CONCLUSIONS New onset and worsening PHG develops at a rate of 12.9% per year and 6.7% per year, respectively, in non-responder CHC patients with advanced fibrosis. If confirmed in other studies, endoscopic surveillance for PHG may need to be tailored to individual patient risk factors.

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Section: Discussionsupporting

confidence: 93%

Development and Progression of Portal Hypertensive Gastropathy in Patients With Chronic Hepatitis C

Fontana

Sanyal

Ghany

et al. 2011

American Journal of Gastroenterology

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“…In this study, peptic ulcer and oesophageal varices were high in group III and group IV (68.75% and 75% P > 0.001) vs other groups, and this was associated with high prevalence of H. pylori IgG antibodies in these two groups. Several studies have evidenced a high seroprevalence of H. pylori among cirrhotic patients, and this may explain the frequent occurrence of peptic ulcer disease in these patients [8,10,17,21,22,25].…”

Section: Discussionmentioning

confidence: 99%

“…Two‐hundred litres of buffer AE was added to the QIAamp spin column and incubated at room temperature for 5 min before centrifuging at 8000 rpm for 1 min once again. The eluate was collected in a sterile tube and stored at −20 °C until used [7,17].…”

Section: Methodsmentioning

confidence: 99%

Role of Helicobacter pylori in patients with HCV‐related chronic hepatitis and cirrhosis with or without hepatocellular carcinoma: possible association with disease progression

Esmat

El-Bendary

Zakarya

et al. 2011

Journal of Viral Hepatitis

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The discovery of Helicobacter hepaticus as a causal agent of hepatitis and hepatocellular carcinoma (HCC) in mice has stimulated interest in looking for Helicobacter species in human liver samples. In this study, we searched for association between H. pylori and HCV-related liver disease. Liver specimens were collected from eighty-five patients; they were divided into five different groups according to liver pathology (METAVIR system). Group I (the 1st control group) consisted of 16 patients with chronic hepatitis C without histological activity. Group II consisted of 25 patients with chronic active hepatitis C, Group III, 17 patients with HCV-related cirrhosis and Group IV, 16 patients with HCV-related cirrhosis and HCC. Group V (2nd control group) consisted of 11 patients suffering from gastro duodenal and gall bladder diseases but negative for HCV. All cases were tested by polymerase chain reaction on liver samples for the presence of H. pylori DNA Cag A gene. Routine biochemical, radiological and RT-PCR for HCV RNA were also performed for all cases. The positivity of H. pylori PCR CagA gene in liver tissue was directly proportional to the severity of liver pathology, this being 75%, 52.9% and 32% in groups IV, III and II, respectively, which was more significant than the 1st and 2nd control groups (P < 0.001). There was a significant difference between H. pylori PCR values when compared to METAVIR staging (F) in different groups (P = 0.001). Helicobacter pylori PCR (Cag A gene) was positive in about 28.2% cases of late fibrosis (F3 + F4) while positivity was (5.9%) in early fibrosis (F1 + F2) (P = 0.0001). There was significant difference between H. pylori PCR (Cag A gene) in liver tissue and METAVIR activity in different groups (P = 0.002) as most of H. pylori PCR-positive cases were METAVIR activity A1 and A2 (15.3% and 12.9%, respectively). There was no association between H. pylori PCR and quantitative HCV RNA (P = 0.531). Also there was no significant difference of Child-Pugh staging in the H. pylori PCR-positive group when compared to the negative group (P = 0.996). There may be an association between the presence of H. pylori (Cag A gene) in the liver and disease progression in HCV-related chronic hepatitis and cirrhosis with and without HCC.

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“…For example, cirrhotic patients are known to have a higher risk of DU independent of H. pylori infection, mainly in the presence of oesophageal varices or congestive gastropathy, which means that the prevalence of H. pylori in patients with cirrhosis and with peptic ulcer disease generally falls below 60% 176–180 . These results suggest that the pathogenesis of ulcer disease in a substantial proportion of patients with cirrhosis may not be related to H. pylori infection 181–184 .…”

Section: Explanations For Helicobacter Pylori‐negative Ulcersmentioning

confidence: 99%

Review article: Helicobacter pylori‐negative duodenal ulcer disease

Gisbert

2009

Aliment Pharmacol Ther

113

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Active Peptic Ulcer Disease in Patients with Hepatitis C Virus-Related Cirrhosis: The Role ofHelicobacter pyloriInfection and Portal Hypertensive Gastropathy

Cited by 22 publications

References 18 publications

Development and Progression of Portal Hypertensive Gastropathy in Patients With Chronic Hepatitis C

Development and Progression of Portal Hypertensive Gastropathy in Patients With Chronic Hepatitis C

Role of Helicobacter pylori in patients with HCV‐related chronic hepatitis and cirrhosis with or without hepatocellular carcinoma: possible association with disease progression

Review article: Helicobacter pylori‐negative duodenal ulcer disease

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