Pharmacogenetics may be the key to providing individualized treatment to patients who become anemic after hepatitis C treatment, according to a recent review
Pharmacogenetics may be the key to providing individualized treatment to patients with the hepatitis C virus (HCV), according to a recent review. The review, written by Javier Ampuero, PhD, MD, and Manuel Romero-Gomez, MD, of the University of Seville in Spain, was published in the journal Future Medicine.
“The aim of this review is to discuss the implications of the novel pharmacogenetic data on the RBV-induced anemia in HCV treatment,” say the authors. Pharmacogenetics examines how drugs are metabolized from a genetic standpoint. In HCV treatment, ribavirin (RBV) and peginterferon (pegIFN) had been the standard, until direct acting agents (DAAs) were introduced in the last few years. Even with the use of DAAs, RBV remains important in HCV therapy.
The most common adverse effect of RBV is anemia, though the reviewers note, “RBV-induced anemia characteristically is dose related and reversible,” adding that “the development of anemia is considered a desirable effect since it may be an indirect marker of higher efficacy.” However, in some cases therapy with RBV must be stopped due to anemia.
The authors say, “Understanding the molecular mechanisms by which genes are able to modulate the appearance of RBV-induced anemia would help to the identification of high-risk groups of patients.” They go on to point out that pharmacogenetics could help “distinguish the population of patients that may require more intensive monitoring and aggressive treatment strategies.”
Being able to identify the patients most at risk for developing RBV-induced anemia is particularly important given the fact that RBV is included in most of the current DAA therapies. The authors conclude, “pharmacogenetics could be part of an optimal strategy for the individualized management of RBV-induced anemia in HCV infection.”