Imatinib mesylate therapy induces reduction in neutrophil gelatinase-associated lipocalin serum levels and increase in leptin concentrations in chronic myeloid leukemia patients in molecular remission

• Published in: Acta haematologica Vol. 127; no. 1; p. 1
• Main Authors: Alonci, Andrea, Allegra, Alessandro, Russo, Sabina, Penna, Giuseppa, Bellomo, Giacomo, D'Angelo, Arianna, Campo, Salvatore, Cannavò, Antonino, Centorrino, Raffaella, Musolino, Caterina
• Format: Journal Article
• Language: English
• Published: Switzerland 01.01.2012
• Subjects: Acute-Phase Proteins; Adult; Aged; Antineoplastic Agents - administration & dosage; Benzamides; Female; Follow-Up Studies; Humans; Imatinib Mesylate; Leptin - blood; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - blood; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy; Lipocalin-2; Lipocalins - blood; Male; Middle Aged; Piperazines - administration & dosage; Proto-Oncogene Proteins - blood; Pyrimidines - administration & dosage; Remission Induction
• ISSN: 1421-9662
• DOI: 10.1159/000330948

The aim of the present study was to determine serum levels of neutrophil gelatinase-associated lipocalin (NGAL) and leptin in patients with chronic myeloid leukemia (CML) at diagnosis and after imatinib therapy when patients achieved a complete molecular remission. The study was conducted on 22 patients with CML in the chronic phase and 10 healthy subjects. The median serum NGAL levels in CML patients at diagnosis were significantly higher compared to age-matched controls. After imatinib therapy, all patients achieved complete molecular remission and NGAL levels decreased and were found significantly lower with respect to the baseline. No significant correlations were found between NGAL levels and other disease parameters. Before imatinib therapy, the median blood leptin levels were not significantly different from those of controls. After therapy with imatinib, all patients in molecular remission presented an increase in leptin levels. Future research is eagerly awaited as it may demonstrate the real role of NGAL and leptin in the onset and progression of CML.