Publications by authors named "Sara Gentili"
Objectives: Acquired hemophilia A (AHA) is a rare, but potentially life-threatening, bleeding disorder caused by an autoantibody against factor VIII that interferes with its coagulant function.
Methods: We performed a narrative review focusing on the diagnostic aspects of AHA and on the current treatment strategies with particular regard to new data and therapeutic developments.
Results: The management of this severe hemorrhagic disorder is based on the control of bleeding with the use of bypassing agents and on the utilization of a variety of immunosuppressant agents with the goal of eliminating the autoantibody permanently.
Article Synopsis
- - The study examined the safety and effectiveness of low-dose thalidomide in patients with advanced myelofibrosis, starting treatment at 50 mg and potentially increasing to 400 mg based on tolerance.
- - Out of 63 patients, about half managed to take over 100 mg daily, but the dropout rate at 6 months was 51%, with lower dropouts in those reporting higher fatigue levels.
- - Results showed benefits like improved anemia (22%), reduced need for transfusions (39%), increased platelet counts in 22% of certain patients, and significant reductions in disease severity and fatigue in 31% of participants.
Emergence of additional cytogenetic clones in chronic myelocytic leukemia (CML) patients who become Philadelphia chromosome-negative (Ph-) after alpha-interferon therapy (or more recently with imatinib mesylate) have been described. We report here a case of a novel t(6;7)(p21;q23) that developed in a CML patient in complete cytogenetic remission during imatinib therapy. In this case, fluorescence in situ hybridization and reverse transcriptase polymerase chain reaction showed a normal pattern for BCR and ABL genes, suggesting that a different and unrelated clone developed after the disappearance of the Ph chromosome.
View Article and Find Full Text PDFBackground And Objectives: Overexpression of P-glycoprotein (PGP), a multidrug-related (MDR) protein, is one of the most important factors responsible for reduced drug sensitivity in acute myeloid leukemia (AML). Recently, we demonstrated that the presence of CD56 antigen, an isoform of the neural adhesion molecule, in AML cells is a negative independent prognostic factor for the achievement of complete remission (CR) and correlates with shorter survival. Since in our previous report we observed a more frequent PGP expression in CD56+ patients, we hypothesized that the reduced response to chemotherapy in this group of patients was due to increased PGP-mediated drug efflux.
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