Successful Treatment of Tenofovir Alafenamide-Induced Lactic Acidosis: A Case Report.
Publication/Presentation Date
10-1-2023
Abstract
Nucleoside or nucleotide analogues (NAs) have the potential to cause lactic acidosis by inhibiting DNA polymerase-γ of human mitochondria and impairing aerobic metabolism. Patients may be asymptomatic, have mild non-specific symptoms, or present in multisystem organ failure. There is a paucity of data to guide management of life-threatening lactic acidosis due to NA therapy. Here we describe a case of a 60-year old critically ill male with decompensated cirrhosis secondary to hepatitis B virus (HBV) infection who developed severe lactic acidosis (13.8 mmol/L) 2 days after initiation of tenofovir alafenamide (TAF). All other possible etiologies for the elevated lactate were ruled out. Lactic acidosis resolved rapidly with TAF discontinuation and supplementation with cofactors supporting mitochondrial oxidative phosphorylation, including coenzyme Q10, levocarnitine, riboflavin, and thiamine. This case highlights the ability of TAF to cause lactic acidosis early after therapy initiation, especially in susceptible hosts, and reviews the potential role for cofactor supplementation for drug-induced mitochondrial injury.
Volume
36
Issue
5
First Page
1260
Last Page
1263
ISSN
1531-1937
Published In/Presented At
Arnouk, S., Whitsett, M., Papadopoulos, J., Stewart Lewis, Z., Dagher, N. N., Feldman, D. M., & Park, J. S. (2023). Successful Treatment of Tenofovir Alafenamide-Induced Lactic Acidosis: A Case Report. Journal of pharmacy practice, 36(5), 1260–1263. https://doi.org/10.1177/08971900221105042
Disciplines
Medicine and Health Sciences
PubMedID
35635046
Department(s)
Department of Medicine
Document Type
Article