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Evaluation of Helicobacter pylori Infection in Patients with Chronic Hepatic Disease

BACKGROUND: The (13)C urea breath test ((13)C-UBT) is the gold standard for detecting Helicobacter pylori infection. H. pylori pathogenesis in patients with hepatitis B virus (HBV) and related diseases remains obscure. We used (13)C-UBT to detect H. pylori infection in patients with chronic HBV infe...

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Detalles Bibliográficos
Autores principales: Huang, Ju, Cui, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5282670/
https://www.ncbi.nlm.nih.gov/pubmed/28091405
http://dx.doi.org/10.4103/0366-6999.197980
Descripción
Sumario:BACKGROUND: The (13)C urea breath test ((13)C-UBT) is the gold standard for detecting Helicobacter pylori infection. H. pylori pathogenesis in patients with hepatitis B virus (HBV) and related diseases remains obscure. We used (13)C-UBT to detect H. pylori infection in patients with chronic HBV infection, HBV-related cirrhosis, HBV-related hepatic carcinoma, and other chronic hepatic diseases. METHODS: A total of 131 patients with chronic hepatitis B (HB), 179 with HBV-related cirrhosis, 103 with HBV-related hepatic carcinoma, 45 with HBV-negative hepatic carcinoma, and 150 controls were tested for H. pylori infection using (13)C-UBT. We compared H. pylori infection rate, liver function, complications of chronic hepatic disease, serum HBV-DNA, serum alpha-fetoprotein (AFP), and portal hypertensive gastropathy (PHG) incidence among groups. RESULTS: HBV-related cirrhosis was associated with the highest H. pylori infection rate (79.3%). H. pylori infection rate in chronic HB was significantly higher than in the HBV-negative hepatic carcinoma and control groups (P < 0.001). H. pylori infection rate in patients with HBV-DNA ≥10(3) copies/ml was significantly higher than in those with HBV-DNA <103 copies/ml (76.8% vs. 52.4%, P < 0.001). Prothrombin time (21.3 ± 3.5 s vs. 18.8 ± 4.3 s), total bilirubin (47.3±12.3 μmol/L vs. 26.6 ±7.9 μmol/L), aspartate aminotransferase (184.5 ± 37.6 U/L vs. 98.4 ± 23.5 U/L), blood ammonia (93.4 ± 43.6 μmol/L vs. 35.5 ± 11.7 μmol/L), and AFP (203.4 ± 62.6 μg/L vs. 113.2 ± 45.8 μg/L) in the (13)C-UBT-positive group were significantly higher than in the (13)C-UBT-negative group (P < 0.01). The incidence rates of esophageal fundus variceal bleeding (25.4% vs. 16.0%), ascites (28.9% vs. 17.8%), and hepatic encephalopathy (24.8% vs. 13.4%) in the (13)C-UBT-positive group were significantly higher than in the 13C-UBT-negative group (P < 0.01). The percentages of patients with liver function in Child-Pugh Grade C (29.6% vs. 8.1%) and PHG (43.0% vs. 24.3%) in the (13)C-UBT-positive group were significantly higher than in the (13)C-UBT-negative group (P < 0.05). CONCLUSIONS: It is possible that H. pylori infection could increase liver damage caused by HBV. H. pylori eradication should be performed in patients with complicating H. pylori infection to delay hepatic disease progression.