Successful treatment of anemia in idiopathic myelofibrosis with recombinant human erythropoietin

Hasselbalch, Hans Carl; Clausen, Nielsaage Tøffner; Jensen, Bente

doi:10.1002/ajh.10076

Cited by 26 publications

(29 citation statements)

References 16 publications

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“…In this sense, it must be pointed out that most patients with IM have serum erythropoietin levels appropriate to the degree of anaemia (Barosi et al, 1993a). The experience with erythropoietin therapy in IM is limited, with only a few small series having been reported (Aloe-Spiriti et al, 1993;Tefferi & Silverstein, 1994;Bourantas et al, 1996;Rodríguez et al, 1998;Hasselbalch et al, 2002). Response rates range from 33 to 100%, although the criteria of response employed are not uniform.…”

Section: Erythropoietinmentioning

confidence: 99%

“…There have been many reports on this therapy in IM, although many refer to individual patients or small series. In some studies, interferon had no effect on the anaemia or splenomegaly and, although it often decreased the leucocytes and the platelets, this was sometimes an undesirable effect (Hasselbalch, 1988;List & Doll, 1992). This, and the frequent side effects, led to treatment discontinuation in most patients.…”

Section: Interferonmentioning

confidence: 99%

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Modern management of myelofibrosis

Cervantes

2005

Br J Haematol

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SummaryThe conventional treatment of myelofibrosis involves a wait‐and‐see approach for asymptomatic patients, oral chemotherapy for the hyperproliferative forms of the disease, androgens or erythropoietin for the anaemia, and splenectomy in selected patients. Low‐dose thalidomide plus prednisone is a well‐tolerated therapy for the anaemia and the thrombocytopenia of myelofibrosis, whereas imatinib has shown little efficacy. Allogeneic stem cell transplantation (allo‐SCT) is the only curative therapy for myelofibrosis. Its standard modality has an associated mortality of about 30% and can be applied to younger patients with high‐risk disease or resistant to conventional treatment. Reduced‐intensity conditioning allo‐SCT involves a low mortality and is a promising therapy for patients aged 45–70 years old with the above characteristics. Autologous SCT is a palliative therapy for patients resistant to conventional treatment who lack a suitable donor. The next candidates for the treatment of myelofibrosis are the thalidomide derivatives, the proteasome inhibitors, and vascular endothelial growth factor neutralizing antibodies.

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Section: Erythropoietinmentioning

confidence: 99%

Section: Interferonmentioning

confidence: 99%

Modern management of myelofibrosis

Cervantes

2005

Br J Haematol

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“…43 subgroup of patients with MMM (52,53). Sometimes EPO by itself may be able to improve the anemia in these patients (54). Due to its pleotropic effects on cytokine production and its inhibitory effects on angiogenesis, thalidomide has received considerable attention as a therapeutic agent for MMM (55) as has been the case with multiple myeloma (56,57).…”

Section: Treatment For Anemiamentioning

confidence: 99%

“…Therapy with these cytoreductive agents often leads to worsening cytopenias. Therefore, these agents are often combined with EPO in an attempt to limit drug-induced anemia and there is some evidence that such combinations may enhance the therapeutic effect of the regimen (54).…”

Section: Treatment For Splenomegalymentioning

confidence: 99%

Myelofibrosis with Myeloid Metaplasia: New Developments in Pathogenesis and Treatment

2004

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Myeloid metaplasia with myelofibrosis (MMM) is a chronic myeloproliferative disorder (CMPD) characterized by progressive anemia, massive splenomegaly, both hepatosplenic and non-hepatosplenic extramedullary hematopoiesis (EMH), a leukoerythroblastic blood smear, circulating progenitor cells, and marked bone marrow stromal reaction including collagen fibrosis, osteosclerosis and angiogenesis. The overall median survival is 5 years although it might range from 2 to 15 years depending on the presence or absence of clinically defined prognostic factors. Death is often due to leukemic transformation, portal hypertension or infection. In addition to shortened survival, quality of life is often affected by frequent red blood cell transfusions, profound constitutional symptoms, and cachexia. Drug therapy and autologous hematopoietic stem cell transplantation (HSCT) are of only palliative value and have not been shown to improve survival. The role of allogeneic HSCT, both myeloablative and non-myeloablative, is actively being investigated. Both splenectomy and radiation therapy have defined therapeutic roles to control EMH-associated symptoms. Analysis of the molecular biology of the disease is underway with the aid of animal models leading to the identification of novel therapeutic targets. Among the novel agents tested, thalidomide seems the most promising although newer agents are on the horizon.

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“…Over the last 20 years, therapies that attempt to lessen the degree of anemia (recombinant erythropoietin, danazol, thalidomide, lenalidomide, and pomalidomide), myeloproliferation and splenomegaly (melphalan, hydroxyurea, interferon, cladribine), and marrow fibrosis (pirfenidone, monoclonal antibodies to transforming growth factor b) have each been evaluated in clinical trials with modest efficacy. [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18] The use of none these agents has been associated with a clear survival benefit for MF patients. In fact, only recently have randomized phase 3 trials been completed in patients with MF that provide the foundation for evidence-based therapeutic decisions.…”

Section: Introductionmentioning

confidence: 99%

A comprehensive review and analysis of the effect of ruxolitinib therapy on the survival of patients with myelofibrosis

Mascarenhas

Hoffman

2013

Blood

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Myelofibrosis is a hematological malignancy with a median survival of approximately 5 to 7 years. Allogeneic stem cell transplantation is the only therapeutic modality that provides a cure for myelofibrosis patients. Recently, ruxolitinib has been shown in 2 phase 3 studies to be effective in reducing splenomegaly and improving symptoms in myelofibrosis patients. Although conventional markers of disease burden (marrow histopathological features, cytogenetic and molecular markers, and reversal of cytopenias) were not uniformly improved, a survival advantage in favor of ruxolitinib therapy was demonstrated. The use of historical control cohorts to compare survival was implemented in 2 different analyses of patients enrolled in the phase 1/2 studies and has further added fuel to the controversy surrounding the significance of this survival advantage. Ruxolitinib therapy results in a dramatic reduction in circulating proinflammatory cytokine levels, which has been associated with improvement in symptoms and performance status and may provide a link to improved survival. We analyze the various data published and place in perspective the significance of the prolongation of survival associated with ruxolitinib therapy. This critical review of these data may allow physicians to more rationally assess the benefits that can be anticipated with the appropriate use of this therapy.

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Successful treatment of anemia in idiopathic myelofibrosis with recombinant human erythropoietin

Cited by 26 publications

References 16 publications

Modern management of myelofibrosis

Modern management of myelofibrosis

Myelofibrosis with Myeloid Metaplasia: New Developments in Pathogenesis and Treatment

A comprehensive review and analysis of the effect of ruxolitinib therapy on the survival of patients with myelofibrosis

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