19 research outputs found

    Tapentadol prolonged release for patients with multiple myeloma suffering from moderate-to-severe cancer pain due to bone disease

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    CONTEXT: Myeloma bone disease (MBD) is a devastating complication of multiple myeloma that leads to severe pain. OBJECTIVES: The aim of this study was to evaluate the efficacy and tolerability of tapentadol prolonged release (PR) in the management of patients with MBD suffering from moderate-to-severe cancer pain. METHODS: A 12-week prospective study was carried out in 25 opioid-naïve MBD patients. Patients initially received twice-daily doses of tapentadol PR 50 mg. Doses were then managed to maintain adequate relief or dose-limiting toxicity. The following parameters were recorded at weekly intervals for 4 weeks, and then at weeks 8 and 12: pain, opioid-related adverse effects, use of other analgesics, DN4 (Douleur Neuropathique 4) score. Quality of life (SF-36 [36-item short-form health survey]) was measured at baseline and at final evaluation. RESULTS: Of 25 patients, 22 completed the study. Pain intensity significantly decreased from baseline to all the week intervals (P<0.01). Quality of life significantly improved with respect to all SF-36 subscale parameters (P<0.01), and so did both the physical and mental status (P<0.01). Tapentadol PR significantly reduced DN4 mean value (P<0.01) and the number of patients with neuropathic component (DN4 ≥4) (P<0.01). After 8 weeks of treatment, all patients were negative for the DN4 score. Tapentadol PR was well tolerated, and the use of other analgesics was reduced during the study period. CONCLUSION: Tapentadol PR started in doses of 100 mg/day was effective and well tolerated in opioid-naïve MBD patients with moderate-to-severe pain. Tapentadol PR can be considered a first-choice opioid in cancer patients suffering from mixed pain with a neuropathic component

    Azacitidine to consolidate and deepen the therapeutic response achieved by intensive induction treatment in a young patient affected by NPM1mut-AML who has become ineligible for high-dose consolidation

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    Acute myeloid leukemia (AML) is the most common leukemia in adults. In spite of the most recent discoveries about the molecular landscape of this disease, the treatment of elderly and unfit young patients continues to be a great challenge. The hypomethylating agents (HMA) still represent an effective therapeutic option for these categories, especially for the low-risk subgroups. We report the case of a young patient with NPM1mut-AML who underwent a first cycle of intensive induction treatment, achieving a complete remission, but suffered from a serious life-threatening neurologic toxicity. Due to the ineligibility to further lines of intensive chemotherapy, we decided to consolidate the response with azacitidine, administered according to the regular schedule. The minimal residual disease (MRD), monitored through the NPM1 mutation at diagnosis, progressively decreased and became undetectable after 36 cycles of hypomethylating therapy. After 1 year from discontinuation of azacitidine, MRD remains undetectable. Therefore, HMA might still represent a feasible and effective option for patients with low-risk AML, especially when the standard chemotherapy is not indicated, or as maintenance therapy in nontransplantable patients

    The therapeutic response and clinical outcome of adults with ALL1(MLL)/AF4 fusion positive acute lymphoblastic leukemia according to the GIMEMA experience

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    The clinical outcome of 21 adults with ALL1(MLL)/AF4 positive acute lymphoblastic leukemia enrolled in the GIMEMA LAL 2000 trial and of 25 patients entered into the previous 0496 study is reported. LAL 2000 included more intensive consolidation and transplants. Complete remission rates were 90% and 88% in the LAL 2000 and 0496 trials, respectively. Fifteen patients were transplanted (5 autologous, 10 allogeneic). At 36 months, overall and disease free survivals were 32.9%, 31.8%, 28% and 27.3%, in LAL 2000 and 0496 trials, respectively. Relapses remained the main reason of failure occurring in 10 and 16 of the 19 and 22 responding patients. In the LAL 2000 study, 4 relapses were observed before transplant. Thus, ALL1(MLL)/AF4 abnormality characterized a subset of patients with adverse prognosis in which the overall strategy adopted in the LAL 2000 study, rather than transplants per se, failed to improve the patient clinical outcome

    Antiviral treatment including entecavir plus tenofovir disoproxil fumarate for HBV reactivation following a rituximab-based regimen

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    Entecavir and tenofovir disoproxil fumarate are potent and effective antiviral drugs that now represent recommended treatment options for chronic HBV infection. However, no or very limited clinical evidence is currently available on these drugs for the management of HBV reactivation in patients with haematological malignancies. Herein, we report a case of HBV reactivation in a patient with non-Hodgkin's lymphoma following a rituximab-based regimen, and who was successfully treated with a combination antiviral treatment including entecavir and tenofovir disoproxil fumarate

    A complete remission induced by valproic acid in a patient with essential thrombocytemia JAKV617F- positive

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    INTRODUCTION: Polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF) are myeloproliferative neoplasms characterized by excessive proliferation of myeloid/erythroid lineage cells and JAK2V617F somatic mutation. Since current treatments of MPNs are unlikely to cure or offer remission to patients, there is a clear necessity of new therapies. Histone Deacetylase inhibitors (HDACi) are a new class of drugs with a potential activity in this group of disease. Among these, valproic acid (VPA) is a well tolerated and long since used drug for the treatment of epilepsy and bipolar disorders. At concentration equivalent to those used by neuro-psychiatrists (> 50 μg/ml), VPA acts as a powerful HDACi, that has been shown to be promising in the treatment of both solid and hematological tumors. Therefore herein we present a 52 years-old woman with JAK2V617F ET who received VPA for a bipolar disorder. METHODS: Diagnosis of ET, was done 2 years before our observation, at the time of an episode of angina pectoris treated with four coronary by-passes. Patient started treatment with antiplatelet drugs and hydrossiurea (HU). However, due to a severe intolerance, HU was intermittently assumed never reaching therapeutic concentration and disease control. During this period, the patient developed heightened mood (either euphoric or irritable), decreased need for sleep and hyperactivity. A psychiatric evaluation allowed to made the diagnosis of bipolar disorder type II. Thus the patient definitively stopped HU and started VPA at increasing doses, reaching a therapeutic serum level of 76 μg/ml after four months with a dosage of 1500 mg/day and achieving the complete remission of her manic phase of the bipolar disorder. RESULTS: As for the clinical course of ET, her hemochromocytometric values before VPA were: Hb 14.3 gr/dl, WBC count 11.3 x 109/L and platelets 793 x 109/L. Two months after reaching the VPA therapeutic level we observed a significant decrease in the values of Hb, WBC and Platelet that resulted 12.9 gr/dl, 6.3 x 109/l and 403 x 109/L, respectively. Since, these values are remained stable after more than one-year of VPA treatment, the patient has been classified in complete remission (CR) of disease (figure 1). Molecular monitoring of disease during VPA treatment was performed by evaluating JAK2 gene dosage and JAK2WT and JAK2V617F transcript levels at diagnosis and after 4, 8 and 12 month from the start of VPA. Although, the JAK2 gene dosage remained constant upon treatment,, JAK2WT and JAK2V617F transcript levels significantly increased at each time points. CONCLUSION: Data herein reported demonstrated, for the first time, the achievement of CR induced by the HDACi VPA in a ET patient intolerant to HU. The findings that JAK2WT and JAK2V617F transcript levels increased, despite the achievement of therapeutic response, support that JAK2 is not fully implicated in the pathogenesis of Ph(-) MPN
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