Volume 134, Issue 6 pp. 645-646
Free Access

Treatment options in relapsed or refractory Hodgkin disease patients: the mini-BEAM regimen does exist too

Miguel A. Canales

Miguel A. Canales

Servicio de Hematologia, Universidad Autonoma de Madrid, Hospital Universitario La Paz, Madrid

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Alejandro Martin

Alejandro Martin

Servicio de Hematologia, Hospital Virgen de la Concha, Zamora

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Dolores Caballero

Dolores Caballero

Servicio de Hematologia, Hospital Universitario de Salamanca, Salamanca, Spain. E-mail: [email protected]

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Fernando Hernandez-Navarro

Fernando Hernandez-Navarro

Servicio de Hematologia, Universidad Autonoma de Madrid, Hospital Universitario La Paz, Madrid

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First published: 18 August 2006
Citations: 1

We have read the excellent review on salvage treatment options in several relapsing lymphoma subtypes by Seyfarth et al (2006). In the paragraph related to salvage regimens for relapsed Hodgkin disease (HD), the reader is referred to Table III to see the more frequently used salvage regimens. We were disappointed that our studies regarding the use of mini-BEAM (low-dose carmustine, etoposide, cytarabine, melphalan) in the salvage setting were not cited. But it is more surprising that the mini-BEAM regimen was not included amongst therapeutic options in the flow sheet.

We agree that the mini-BEAM regimen was first employed by investigators from University of Toronto in 1990, and this experience was actualised by Colwill et al (1995). The first series of relapsed or refractory HD patients exclusively treated with mini-BEAM as salvage regimen was reported by Chopra et al (1992). We reported a series of relapsed or refractory patients with HD treated with this regimen in University Hospital La Paz (Madrid), showing a similar response rate to that previously reported (Fernandez-Jimenez et al, 1999). Two years later, we reported a larger series of patients treated with mini-BEAM at the University Hospital La Paz and the University Hospital of Salamanca (Martin et al, 2001). In this study, the overall response rate to mini-BEAM was 84%, which compared favourably with other salvage regimens. In addition, the regimen also proved to be useful for patients with primary refractory disease, with a response rate higher than 70% in this subgroup of patients. The response to mini-BEAM was the most important prognostic factor for overall survival, progression-free or event-free survival. We also presented data regarding the overall survival, with a follow-up much longer than previously reported by Colwill et al (1995) (68 vs. 13 months). Indeed, this report has one of the longest follow-ups of all recently reported papers regarding salvage therapy in HD. As pointed out by several authors, relapses are still frequent, even after 6 years of follow-up in patients with refractory or relapsed HD, making it necessary to have term follow-up in order to reach firm conclusions on the value of these salvage regimens. In this setting, a recent report has retrospectively compared the GDP regimen (Gemcitabine, Dexamethasone and Cisplatin) with the mini-BEAM regimen. Although response rates were similar in both groups (62% vs. 68% respectively), progression-free survival was significantly better for patients who received GDP compared with patients who received mini-BEAM, but the follow-up was too short (median of 1·8 years) (Kuruvilla et al, 2006).

Obviously, prospective studies with larger numbers of patients and longer follow-up comparing different strategies are necessary, but, with the lack of randomised studies, our two studies have demonstrated that mini-BEAM is an effective regimen for treating relapsed HD patients before autologous transplant and, in addition, it has also proved to be useful for patients with primary refractory disease. These conclusions are supported by very long-term follow-up results. For these reasons, we think that Seyfarth et al (2006) should have cited our studies in their review.

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