Premium
Risk factors for exacerbation of gastroesophageal varices and portosystemic encephalopathy during treatment with nucleos(t)ide analogs for hepatitis B virus‐related cirrhosis
Author(s) -
Nagaoki Yuko,
Aikata Hiroshi,
Daijyo Kana,
Teraoka Yuji,
Honda Fumi,
Nakamura Yuki,
Hatooka Masahiro,
Morio Kei,
Fujino Hatsue,
Nakahara Takashi,
Kawaoka Tomokazu,
Miki Daiki,
Tsuge Masataka,
Hiramatsu Akira,
Imamura Michio,
Kawakami Yoshiiku,
Ochi Hidenori,
Chayama Kazuaki
Publication year - 2018
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/hepr.12996
Subject(s) - medicine , gastroenterology , cirrhosis , portosystemic shunt , hepatic encephalopathy , gastric varices , exacerbation , liver function , portal hypertension , encephalopathy , varices
Aim The aim of this study was to determine the risk factors for worsening of gastroesophageal varices (GEVs) and development of portosystemic encephalopathy in patients with hepatitis B virus (HBV)‐related cirrhosis during nucleos(t)ide analog (NA) treatment. Methods One hundred and thirty‐seven patients with HBV‐related cirrhosis were enrolled in this retrospective cohort study. Findings of portal hemodynamics with computed tomography, liver function, and endoscopic examinations during NA treatment were assessed. Results Among 137 patients, feeding vessels for GEVs (left gastric vein, posterior gastric vein, and short gastric vein) were present in 56 (41%) patients, and extrahepatic portosystemic shunt (paraesophageal vein, paraumbilicul vein, and splenorenal shunt) were present in 36 (26%) patients at the start of NA treatment. Although NA treatment was successful, significant improvements were not observed in portosystemic collateral vessels 3 years after NA treatment and GEVs were exacerbated in 48 (35%) patients. The cumulative 5‐ and 10‐year exacerbation rate of GEVs was 27% and 50%, respectively. By multivariate analysis, the existence of feeding vessels for GEVs at the start of NA treatment was the independent predictive factor for the exacerbation of GEVs ( P < 0.001). Eight patients who had extrahepatic portosystemic shunt at the start of NA treatment developed portosystemic encephalopathy during follow‐up. The 3‐ and 5‐year incidence of that was 5% and 8%, respectively. Conclusions The presence of portosystemic collateral vessels at the start of NA treatment increases the risk of GEVs worsening and development of portosystemic encephalopathy in patients with HBV‐related cirrhosis, despite improvement of liver function and success in reducing viral loads with NA treatment.