Annals of medicine and surgery (2012) · 2026
Occult hepatitis B: the masked driver of portal hypertension and life-threatening variceal hemorrhage.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Kaphle Prabhat, Koirala Raj Kumar, Upadhyaya Maya, Karna Supriya, Giri Dhanlaxmi, Gupta Pukar, Pahari Nabin, Ojha Liladhar, Bhatta Suman, Bhatt Rohit
Аннотация
INTRODUCTION AND IMPORTANCE: Occult hepatitis B infection (OBI), characterized by undetectable hepatitis B surface antigen (HBsAg) but detectable HBV DNA, is an underrecognized contributor to chronic liver injury and portal hypertension. Portal hypertension (PHT) commonly complicates chronic liver disease, often in the setting of cirrhosis, and can lead to life-threatening variceal hemorrhage without typical biochemical or imaging abnormalities.
CASE PRESENTATION: We report a case of a 30-year-old Bangladeshi male with acute upper gastrointestinal bleeding and esophageal varices in the setting of occult HBV infection. The patient lacked classical risk factors for hepatitis B, and initial viral serology was negative for HBsAg and anti-HBc. However, HBV DNA testing later confirmed occult infection. Liver ultrasound was unremarkable, showing no signs of cirrhosis or focal lesions. The patient was managed successfully with supportive care, propranolol, and multiple sessions of EVL. Acute bleeding was controlled by blood transfusion and intravenous fluid resuscitation. Endoscopic variceal ligation sessions were performed to prevent rebleeding. During follow-up, varices remained stable without further bleeding. The patient is under ongoing surveillance for portal hypertension complications.
CONCLUSION: OBI is a hidden cause of portal hypertension and variceal bleeding. HBV DNA testing is essential in patients with portal hypertension and negative serology. Prompt EVL and vigilant follow-up are critical to preventing fatal outcomes.
CASE PRESENTATION: We report a case of a 30-year-old Bangladeshi male with acute upper gastrointestinal bleeding and esophageal varices in the setting of occult HBV infection. The patient lacked classical risk factors for hepatitis B, and initial viral serology was negative for HBsAg and anti-HBc. However, HBV DNA testing later confirmed occult infection. Liver ultrasound was unremarkable, showing no signs of cirrhosis or focal lesions. The patient was managed successfully with supportive care, propranolol, and multiple sessions of EVL. Acute bleeding was controlled by blood transfusion and intravenous fluid resuscitation. Endoscopic variceal ligation sessions were performed to prevent rebleeding. During follow-up, varices remained stable without further bleeding. The patient is under ongoing surveillance for portal hypertension complications.
CONCLUSION: OBI is a hidden cause of portal hypertension and variceal bleeding. HBV DNA testing is essential in patients with portal hypertension and negative serology. Prompt EVL and vigilant follow-up are critical to preventing fatal outcomes.