Interleukin-8 is not a predictive biomarker for the development of the acute promyelocytic leukemia differentiation syndrome [post]

Luciana Yamamoto de Almeida, Diego Antonio Pereira-Martins, Ana Sílvia Gouvêa Lima, Márcia Sueli Baggio, Luisa Corrêa de Araujo Koury, Ana Paula Lange, Sarah Cristina Bassi, Priscila Santos Scheucher, Eduardo Rego
2020 unpublished
Background: Differentiation syndrome (DS) is the main life-threatening adverse event that occurs in acute promyelocytic leukemia (APL) patients treated with all-trans retinoic acid (ATRA). Cytokine imbalances have been reported to play role during the developing of acute promyelocytic leukemia differentiation syndrome (APL-DS). However, the relationship between the plasma cytokine levels and their prognostic value for the prediction of DS developing in patients with APL during the treatment
more » ... ATRA and anthracyclines has not been previously reported. Methods: In this study, we followed an APL cohort (n=17) over seven days of ATRA therapy in DS (n=6) and non-DS groups (n=11). Interleukin (IL)-1β, IL-6, IL-8, IL-10, IL-12p70 and TNF-α were measured in the peripheral blood plasma from 17 patients with APL and 11 healthy adult controls by using the cytometric bead array method. Results: In non-DS patients, IL-8 plasma levels were significantly reduced in the seventh day of ATRA treatment (34.16; 6.99 to 147.11 pg mL-1 in D0 vs. 10.9; 0 to 26.81 pg mL-1 in D7; p = 0.02) whereas their levels did not discriminate between DS and non-DS development during the entire induction period (all p > 0.05 in D0, D3, and D7). No significant differences were found in IL-6 levels between groups (p > 0.05 in D0-D7). Other cytokines tested were all undetectable in patients with APL or healthy controls. Conclusions: We demonstrated that the modulation of IL-8 following ATRA treatment may occur regardless of the development of DS and, therefore, does not appear to be a predictive biomarker to monitor the APL-DS.
doi:10.21203/rs.3.rs-35297/v4 fatcat:fdqoqc6svbfsjg5wuxnn7mcfxa