P2920 - The Use of Combination Nucleos(t)ide Analogues to Treat Acute Livery Injury Secondary to Hepatitis B Reactivation

Adalberto Gonzalez, MD¹, Mohammad Alomari, MD¹, Kanwarpreet Tandon, MD², Faris H. Pacha, DO³, Xaralambos Zervos, DO⁴, Nikhil Kapila, MD^4
1Digestive Disease Institute, Cleveland Clinic Foundation, Weston, FL; ²Cleveland Clinic Florida, Weston, FL; ³Larkin Community Hospital, South Miami, FL; ⁴Liver Transplant Institute, Cleveland Clinic Florida, Weston, FL

Introduction: Acute liver injury or failure can occur in up to 25-50% of patients with Hepatitis B virus (HBV) reactivation and may be difficult to manage. We present a unique case of combination antiviral therapy for acute liver injury (ALI) from HBV reactivation.

Case Description/Methods: An 82-year-old Male with follicular lymphoma came to the ED for abnormal liver function tests (LFTs) on outpatient labs. He was asymptomatic. He was receiving weekly Rituximab for follicular lymphoma. He denied recent illness, alcohol use, or drug use. Vital signs were stable. Physical exam showed no jaundice, scleral icterus, hepatomegaly, or asterixis. Labs showed a WBC of 6, Hemoglobin of 13.1, Platelets 129, total bilirubin of 0.6, alkaline phosphatase of 84, ALT 686, AST 354, and INR of 1.2. An ultrasound of the right upper quadrant with Doppler of the portal and hepatic veins was normal. Labs to assess for causes of ALI were normal except for the HBV serology: HBV surface antigen positive, HBV surface antibody negative, HBV core antibody IgM negative, HBV core antibody IgG positive, and HBV e antigen positive. He was diagnosed with HBV reactivation. Rituximab was discontinued, and he was placed on tenofovir alafenamide. At treatment initiation, his HBV DNA was 10,924,632 IU/mL. The patient’s symptoms, LFTs, and HBV DNA were monitored. After 3 weeks, he had developed jaundice, scleral icterus, and his LFTs had worsened: bilirubin of 24, ALT 3114, AST 1538, INR 2.1. His HBV DNA was 1,912,539. A tenofovir resistance test showed no resistance. Due to worsening LFTs, entecavir was added to tenovir. After 6 weeks of dual antiviral therapy, HBV DNA was 1,240 IU/mL, bilirubin 6.1, AST 39, ALT 34, INR 1.4. The patient continues to be monitored.

Discussion: We discontinued Rituximab and began therapy with tenofovir at the first sign of a HBV reactivation. However, patients may progress to fulminant liver failure despite treatment, especially if initiated too late. Despite appropriate treatment, our patient’s ALI worsened and HBV DNA remained elevated. Thus, we added entecavir for added viral suppression, which aided in suppressing the HBV DNA and improving the patient’s LFTs. This case report provides a unique example of the use of combination nucleos(t)ide analogue therapy for the treatment of an acute liver injury from HBV reactivation. To our knowledge, this has not been previously reported in the literature.



Disclosures:


Adalberto Gonzalez, MD¹, Mohammad Alomari, MD¹, Kanwarpreet Tandon, MD², Faris H. Pacha, DO³, Xaralambos Zervos, DO⁴, Nikhil Kapila, MD⁴. P2920 - The Use of Combination Nucleos(t)ide Analogues to Treat Acute Livery Injury Secondary to Hepatitis B Reactivation, ACG 2021 Annual Scientific Meeting Abstracts. Las Vegas, Nevada: American College of Gastroenterology.