Background： The ^13C urea breath test （^13C-UBT） is the gold standard for detecting Helicobacterpylori infection. H. pylori pathogenesis in patients with hepatitis B virus （HBV） and related diseases remains obscu...Background： The ^13C urea breath test （^13C-UBT） is the gold standard for detecting Helicobacterpylori infection. H. pylori pathogenesis in patients with hepatitis B virus （HBV） and related diseases remains obscure. We used ^13C-UBT to detect H. p.vlori 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 ^13C-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 ）. 11. 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 ^13C-UBT-positive group were significantly higher than in the ^13C-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 ^13C-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 ^13C-UBT-positive group were significantly higher than in the ^13C-UBT-negative group （P 〈 0.05）. Conclusions： It is possible that H. pylori infection could increase liver damage caused by HBV. 1t. pylori eradication should be performed in patients with complicating H. pylori infection to delay hepatic disease progression.展开更多
文摘Background： The ^13C urea breath test （^13C-UBT） is the gold standard for detecting Helicobacterpylori infection. H. pylori pathogenesis in patients with hepatitis B virus （HBV） and related diseases remains obscure. We used ^13C-UBT to detect H. p.vlori 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 ^13C-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 ）. 11. 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 ^13C-UBT-positive group were significantly higher than in the ^13C-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 ^13C-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 ^13C-UBT-positive group were significantly higher than in the ^13C-UBT-negative group （P 〈 0.05）. Conclusions： It is possible that H. pylori infection could increase liver damage caused by HBV. 1t. pylori eradication should be performed in patients with complicating H. pylori infection to delay hepatic disease progression.
