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Response to 5‐azacytidine in a patient with relapsed Hodgkin Lymphoma and a therapy‐related myelodysplastic syndrome

Treatment with hypomethylating agents, such as 5-azacytidine (Vidaza; Celgene Corporation, Summit, NJ, USA), has shown efficacy in patients with high-risk myelodysplastic syndromes (MDS) (Kantarjian et al, 2007; Fenaux et al, 2009; Voso et al, 2009) and is becoming the standard of care in this setting. 5-azacytidine has been shown to prolong the time to leukaemic transformation and improve overall survival in higher risk MDS (Fenaux et al, 2009). Chromosome 7 deletions, which are frequent in therapy-related myeloid neoplasms and are associated with poor prognosis, are associated with a favourable response to 5-azacytidine (Raj et al, 2007). To our knowledge, there are no clinical data on the role of hypomethylating drugs in Hodgkin lymphoma (HL), and there is only limited experience with other ‘epigenetic’ drugs, such as inhibitors of histone deacetylases (HDAC) (Dickinson et al, 2009). We report a patient with a therapy-related MDS and a concomitant relapse of HL who was treated with 5-azacytidine. A 46-year-old man was diagnosed in 1996 with classical nodular sclerosis HL, stage IIB with supradiaphragmatic nodal involvement, and was treated with eight cycles of ABVD chemotherapy (doxorubicin, bleomycin, vinblastine, dacarbazine), achieving complete remission (CR). The first relapse occurred in 2000 and treatment consisted of the Stanford V regimen, consisting of weekly administration of cytotoxic drugs (mechlorethamine, doxorubicin, vinblastine, vincristine, bleomycin, etoposide, prednisone) for 12 weeks, followed by 36-Gy involved-field radiotherapy on cervical node residue. The second relapse occurred in 2002, and was treated with DHAP (dexamethasone, cytarabine, cisplatin)-like chemotherapy, followed by autologous stem cell transplantation using BEAM (carmustine, etoposide, cytarabine, melphalan) as conditioning regimen, obtaining CR. Two years later the patient had a new, histologicallydocumented, relapse of HL with B-symptoms, and was treated with involved-field radiotherapy (total dose 4500 cGy), and four cycles of MOPP chemotherapy (mechlorethamine, vincristine, procarbazine, prednisone), achieving CR. At this time the patient had an impaired haematological reserve, which required reduction of chemotherapy dose, packed red blood cell and platelet transfusions, antibiotics and granulocyte colony-stimulating factor administration, and had relapsing episodes of paroxysmal atrial fibrillation. In 2006, due to persistent macrocytosis, mild neutropenia and thrombocytopenia, he was diagnosed with therapy-related MDS (t-MDS), with 4% bone marrow blasts, monosomy 7 and del(12)(p11) in 14 of 20 metaphases, resulting in an Intermediate-1 score in the International Prognostic Scoring System (IPSS). The t-MDS did not show any signs of progression until 2009, when platelet and absolute neutrophil counts significantly decreased, with no evidence of lymphoma involvement at the trephine biopsy. A computerized tomography (CT) scan revealed multiple enlarged subdiaphragmatic lymph nodes, with a high [18F]-2-fluoro-2-deoxy-dglucose–positron emission tomography (F-FDG PET)/CT metabolic activity, and a maximal Standardized Uptake Value (SUV) of 16 (Fig 1A). A CT-guided biopsy of the inguinal lymph node confirmed the fourth relapse of HL. At 59 years of age, the patient had an Eastern Cooperative Oncology Group (ECOG) performance status of 1, with significant comorbidities including pulmonary emphysema, hypertension, recurrent paroxysmal atrial fibrillation, an ascending thoracic aortic aneurysm, and post-surgical