Adefovir-Induced Pancreatitis: A Rare but Serious Side Effect 1268

Adefovir is a nucleotide analog which is FDA approved for the management of chronic hepatitis B virus infection. It interferes with HBV viral RNA-dependent DNA polymerase resulting in inhibition of viral replication. We present a rare case of acute pancreatitis in a patient with long term use of Hep...

Full description

Saved in:
Bibliographic Details
Published inThe American journal of gastroenterology Vol. 113; no. Supplement; p. S728
Main Authors Makar, Ranjit, Elmofti, Yousif, Sheraz, Faizan, Houston, Trevor, Wahid, Shahid
Format Journal Article
LanguageEnglish
Published New York Wolters Kluwer Health Medical Research, Lippincott Williams & Wilkins 01.10.2018
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Adefovir is a nucleotide analog which is FDA approved for the management of chronic hepatitis B virus infection. It interferes with HBV viral RNA-dependent DNA polymerase resulting in inhibition of viral replication. We present a rare case of acute pancreatitis in a patient with long term use of Hepsera (Adefovir) for the management of chronic hepatitis B virus infection. 58-year-old lady with past history of chronic hepatitis B viral infection presented to the emergency room with acute onset of mid-epigastric abdominal pain, radiating to the back. Past surgical history was significant for gastric bypass and cholecystectomy in 2004. History of chronic hepatitis B viral infection due to an unprotected sexual encounter. She had been regularly following with a hepatologist and had been in remission while on long term Adefovir (Hepsera) for the past 10 years. She denied any recent alcohol or drug use. Denied any other medication or recent ingestion of any toxins or herbal supplements. Examination was significant for tenderness on light palpation in the epigastric region without any significant rigidity or guarding. Initial workup revealed hematocrit at 55, ALP: 100, ALT:247, AST: 141, TBil: 0.4, lipase: 2400, triglyceride at 137 and calcium 10.1. Ultrasound abdomen noted an absent gallbladder, common bile duct diameter at 7 mm. MRCP did not reveal and biliary or pancreatic ductal dilatation with no filling defects (Image1). Autoimmune workup was negative for autoimmune pancreatitis. Hepsera was held on day 1. In the absence of an identifiable cause for her acute pancreatitis, we attributed adefovir as the likely etiology for her pancreatitis. Pancreatitis as a potential adverse reaction to adefovir was not included in the initial package insert but was later added based on post marketing experience. To our knowledge there has been only one prior case report in a liver transplant recipient patient who developed acute pancreatitis upon initiation of adefovir for hepatitis B virus suppression. Interestingly our patient developed pancreatitis after long term use which has previously not been reported. The likely hypothesis is the depletion of mitochondrial DNA which has been noted as the mechanism with other anti retroviral drugs implicated in causing pancreatitis. Even though pancreatitis is not a common side effect associated with adefovir use, clinicians should discuss pancreatitis as a rare but serious adverse reaction associated with adefovir use.
ISSN:0002-9270
1572-0241
DOI:10.14309/00000434-201810001-01268