Liver elastography for risk-assessment of liver toxicity and risk factors for Sinusoidal obstruction syndrome in patients with acute lymphoblastic leukemia receiving inotuzumab ozogamicin - Scorecard - MDSpire
Advertisement
Liver elastography for risk-assessment of liver toxicity and risk factors for Sinusoidal obstruction syndrome in patients with acute lymphoblastic leukemia receiving inotuzumab ozogamicin
Clinical Scorecard: Assessment of Liver Elasticity for Evaluating Hepatic Toxicity Risks and Sinusoidal Obstruction Syndrome Factors in Acute Lymphoblastic Leukemia Patients Treated with Inotuzumab Ozogamicin
At a Glance
Category
Detail
Condition
B-cell acute lymphoblastic leukemia (B-cell ALL) treated with inotuzumab ozogamicin
Key Mechanisms
Inotuzumab ozogamicin-induced hepatic toxicity, particularly sinusoidal obstruction syndrome (SOS), assessed via liver stiffness measurement (LSM) using liver elastography
Target Population
Adult and pediatric patients with relapsed/refractory or newly diagnosed B-cell ALL receiving inotuzumab ozogamicin
Care Setting
Oncology treatment centers including hematopoietic stem cell transplantation (HSCT) units
Key Highlights
Inotuzumab ozogamicin (InO) improves outcomes in B-cell ALL but is associated with increased risk of hepatic toxicity, especially SOS.
Liver elastography is a non-invasive tool that measures liver stiffness and can detect early liver toxicity and portal hypertension related to InO treatment.
Dose reduction and fractionation of InO, along with addition of blinatumomab, reduced SOS incidence from 13% to 2% in relapsed/refractory patients.
Guideline-Based Recommendations
Diagnosis
Use liver elastography to measure shear wave velocity (SWV) for early detection of liver fibrosis and SOS risk in patients receiving InO.
Interpret SWV values: <1.3 m/s normal, 1.3–1.7 m/s excludes compensated advanced chronic liver disease (cACLD), 1.7–2.1 m/s suggests elastographic cACLD, >2.1 m/s indicates clinically significant portal hypertension (CSPH).
Management
Consider dose reduction and fractionation of InO to minimize hepatic toxicity.
Incorporate blinatumomab in consolidation and maintenance phases to reduce SOS risk.
Monitor patients closely who proceed to allogeneic HSCT, as this increases SOS risk.
Monitoring & Follow-up
Perform baseline and serial liver elastography assessments during InO therapy.
Monitor liver function tests including ALT, bilirubin, and albumin levels regularly.
Assess for clinical signs of SOS, especially in patients with elevated liver stiffness or undergoing HSCT.
Risks
Higher risk of SOS with InO exposure, especially post-HSCT (up to 20%).
Additional risk factors include older age, prior liver disease, cumulative InO dose, prior HSCT, active disease at HSCT, and dual-alkylator conditioning regimens.
Patient & Prescribing Data
Adults with newly diagnosed or relapsed/refractory B-cell ALL treated with Mini-HyperCVD-InO-blinatumomab regimen
Post-protocol amendment with reduced and fractionated InO dosing plus blinatumomab resulted in low SOS incidence (2%) despite 50% undergoing HSCT; baseline liver stiffness did not predict grade ≥3 liver toxicity.
Clinical Best Practices
Incorporate baseline liver elastography to stratify hepatic toxicity risk before initiating InO therapy.
Apply dose modifications and fractionation of InO to reduce SOS incidence.
Use combination therapy including blinatumomab to improve safety and efficacy.
Closely monitor liver function and elastography findings throughout treatment, especially prior to HSCT.
Recognize and manage SOS risk factors proactively in patients receiving InO.
by Jayastu Senapati, Elias Jabbour, Nicholas J. Short, Nitin Jain, Fadi Haddad, Tharakeswara Bathala, Iuliia Kovalenko, Aram Bidikian, Farhad Ravandi, Issa Khouri, Tapan M. Kadia, Rebecca Garris, Guillermo Montalban Bravo, Kelly Chien, Elizabeth Shpall, Partow Kebriaei, Hagop M. Kantarjian
