Citations 13
ASXL1 and CBL mutations are independently predictive of inferior survival in advanced systemic mastocytosis
Pardanani, Animesh , Finke, Christy M. , Zblewski, Darci, Abdelrahman, Ramy A., Wassie, Emnet A, Gangat, Naseema , Hanson, Curtis A. , Ketterling, Rhett P. , Tefferi, Ayalew , Pardanani, Animesh D, Lasho, Terra L. , Zblewski, Darci L, Ketterling, Rhett P
British Journal of Haematology | December 2, 2015 | Volume: 175 | Issue: 3 | Pages: 534-536
Momelotinib treatment‐emergent neuropathy: prevalence, risk factors and outcome in 100 patients with myelofibrosis
Abdelrahman, Ramy A., Begna, Kebede H. , Al‐Kali, Aref , Litzow, Mark R. , Pardanani, Animesh , Tefferi, Ayalew , Hogan, William J.
British Journal of Haematology | December 16, 2014 | Volume: 169 | Issue: 1 | Pages: 77-80
SummaryMomelotinib (a JAK1 and JAK2 inhibitor) induces both anaemia and spleen responses in myelofibrosis (MF). Momelotinib treatment‐emergent peripheral neuropathy (TE‐PN) was documented in 44 (44%) of 100 MF patients treated at our institution; median time of TE‐PN onset was 32 weeks and duration 11 months. Improvement after drug dose reduction or discontinuation was documented in only two patients. TE‐PN was significantly associated with treatment response (P = 0·02) and longer survival (P = 0·048) but significance was lost during multivariate analysis that included treatment duration. TE‐PN did not correlate with initial or maximum momelotinib dose or previous treatment with JAK inhibitor or thalidomide.
Associations and prognostic interactions between circulating levels of hepcidin, ferritin and inflammatory cytokines in primary myelofibrosis
Pardanani, Animesh , Finke, Christy M. , Abdelrahman, Ramy A., Tefferi, Ayalew , Lasho, Terra L.
American Journal of Hematology | February 6, 2013 | Volume: 88 | Issue: 4 | Pages: 312-316
Iron homeostasis is dysregulated in primary myelofibrosis (PMF), given the high prevalence of anemia, need for red blood cell (RBC) transfusions, and disease‐associated inflammatory state. We measured plasma hepcidin levels in 203 consecutive PMF patients at the time of first referral; hepcidin levels were significantly higher as compared to healthy controls ( P < 0.0001), and were correlated with hemoglobin of <10 g/dL, RBC transfusion requirement, serum ferritin of >500 µg/L, higher dynamic international prognostic scoring system (DIPSS)‐plus risk category, the presence of circulating blasts, age of >65 years, and leukocyte count of <4 × 10 9 /L. Increased hepcidin levels predicted for inferior survival independent of six out of the eight DIPSS‐plus prognostic parameters (hazard ratio [HR] = 1.8; P = 0.02), but not when RBC transfusion requirement, hemoglobin of <10 g/dL, or increased serum ferritin were included in the Cox model. Multivariable analysis that considered the four overlapping prognostic variables revealed that increased hepcidin (HR = 1.9; P = 0.03) and increased ferritin (HR = 2.3; P = 0.04), but not hemoglobin of <10 g/dL or RBC transfusion requirement, independently retained their significance for predicting survival. Accordingly, increased levels of both hepcidin and serum ferritin (seen in 29% of patients) predicted inferior survival independent of DIPSS‐plus or increased inflammatory cytokine levels (HR = 2.4; P = 0.002), and could be considered in future prognostic models for PMF. Am. J. Hematol. 88:312–316, 2013. © 2013 Wiley Periodicals, Inc.