Antineoplastics

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Reactions 1172 - 6 Oct 2007 S Antineoplastics Myelodysplastic syndrome (first report with interleukin-2) successfully treated with lenalidomide: 2 case reports Two patients developed secondary myelodysplastic syndrome (MDS) after receiving antineoplastics and radiotherapy for gastro-oesophageal adenocarcinoma (patient 1) and follicular non-Hodgkin’s lymphoma (patient 2); both patients responded to lenalidomide. Patient 1, a 74-year-old man, was initially diagnosed in June 1999 and had previously undergone esophagectomy and post- operative radiotherapy. He was treated with chemotherapy comprising mitomycin, interleukin-2, epirubicin, etoposide, fluorouracil, folinic acid [leucovorin] and methotrexate [dosages and duration of treatment to reaction onset not stated]. In 2001 he developed a mild thrombocytopenia. A bone marrow biopsy in March 2003 demonstrated a hypocellular marrow with trilineage dysplasia. He received eyrthropoietin with no improvement, and was dependent on RBC transfusion. Early in 2006 he developed progressive anaemia and thrombocytopenia, and his haemoglobin level was 8.8 g/dL, his WBC was 2400/µL and his platelets were 54 000/L. In June 2006 he was initiated on lenalidomide 10 mg daily for 10 consecutive days. This was interrupted for 7 days due to a pruritic rash, but resumed at 5 mg daily. After 2 months of treatment his haemoglobin level rose and platelet count improved moderately. A repeat bone marrow biopsy showed no residual dysplasia. He remained on lenalidomide 5 mg daily. Patient 2, a 50-year-old man, was treated with chemotherapy comprising cyclophosphamide, doxorubicin, vincristine and prednisone [dosages and duration of treatment to reaction onset not stated], followed by iodine-131 tositumomab [dosage and duration of treatment to reaction onset not stated] in May 2003. After a relapse in November 2004 he received three cycles of rituximab, ifosfamide, carboplatin and etoposide [dosages and duration of treatment to reaction onset not stated]. Plerixafor and granulocyte colony-stimulating factor were used to mobilise peripheral blood stem cells. He underwent a total body irradiation and conditioning regimen with cyclophosphamide, followed by autologous stem cell rescue. Thrombocytopenia persisted on days 100 and 180 post-procedure. In February 2006 a bone marrow evaluation indicated MDS, and 3 months later a repeat evaluation demonstrated dyserythropoiesis, dysmegakaryopoiesis and a complex karyotype with cytogenetic abnormalities. In July 2006 his platelet count began to decline. He was initiated on lenalidomide 10 mg daily for 30 days, after which time his platelet count recovered. Cytogenetic analysis revealed clonal evolution with new abnormalities. He received a donor transplant in September 2006. To date there was no evidence of MDS relapse. Author comment: "Both radiation therapy and traditional DNA-interactive antineoplastics. . .are known genotoxins with the potential to induce MDS or acute myeloid leukaemia (AML) that commonly harbors a chromosome 5q deletion with high frequency of evolution to AML and short overall survival." Melchert M, et al. Remitting activity of lenalidomide in treatment-induced myelodysplastic syndrome. Leukemia 21: 1576-1578, No. 7, Jul 2007 - USA 801091576 » Editorial comment: A search of AdisBase and Medline did not reveal any previous case reports of myelodysplastic syndrome associated with interleukin-2. The WHO Adverse Drug Reactions database did not contain any reports of myeloproliferative disorders associated with interleukin-2. 1 Reactions 6 Oct 2007 No. 1172 0114-9954/10/1172-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved

Transcript of Antineoplastics

Page 1: Antineoplastics

Reactions 1172 - 6 Oct 2007

★ SAntineoplastics

Myelodysplastic syndrome (first report withinterleukin-2) successfully treated withlenalidomide: 2 case reports

Two patients developed secondary myelodysplasticsyndrome (MDS) after receiving antineoplastics andradiotherapy for gastro-oesophageal adenocarcinoma (patient1) and follicular non-Hodgkin’s lymphoma (patient 2); bothpatients responded to lenalidomide.

Patient 1, a 74-year-old man, was initially diagnosed in June1999 and had previously undergone esophagectomy and post-operative radiotherapy. He was treated with chemotherapycomprising mitomycin, interleukin-2, epirubicin, etoposide,fluorouracil, folinic acid [leucovorin] and methotrexate[dosages and duration of treatment to reaction onset notstated]. In 2001 he developed a mild thrombocytopenia. Abone marrow biopsy in March 2003 demonstrated ahypocellular marrow with trilineage dysplasia. He receivedeyrthropoietin with no improvement, and was dependent onRBC transfusion. Early in 2006 he developed progressiveanaemia and thrombocytopenia, and his haemoglobin levelwas 8.8 g/dL, his WBC was 2400/µL and his platelets were54 000/L. In June 2006 he was initiated on lenalidomide 10 mgdaily for 10 consecutive days. This was interrupted for 7 daysdue to a pruritic rash, but resumed at 5 mg daily. After2 months of treatment his haemoglobin level rose and plateletcount improved moderately. A repeat bone marrow biopsyshowed no residual dysplasia. He remained on lenalidomide5 mg daily.

Patient 2, a 50-year-old man, was treated withchemotherapy comprising cyclophosphamide, doxorubicin,vincristine and prednisone [dosages and duration of treatmentto reaction onset not stated], followed by iodine-131tositumomab [dosage and duration of treatment to reactiononset not stated] in May 2003. After a relapse in November2004 he received three cycles of rituximab, ifosfamide,carboplatin and etoposide [dosages and duration of treatmentto reaction onset not stated]. Plerixafor and granulocytecolony-stimulating factor were used to mobilise peripheralblood stem cells. He underwent a total body irradiation andconditioning regimen with cyclophosphamide, followed byautologous stem cell rescue. Thrombocytopenia persisted ondays 100 and 180 post-procedure. In February 2006 a bonemarrow evaluation indicated MDS, and 3 months later a repeatevaluation demonstrated dyserythropoiesis,dysmegakaryopoiesis and a complex karyotype withcytogenetic abnormalities. In July 2006 his platelet countbegan to decline. He was initiated on lenalidomide 10 mg dailyfor 30 days, after which time his platelet count recovered.Cytogenetic analysis revealed clonal evolution with newabnormalities. He received a donor transplant in September2006. To date there was no evidence of MDS relapse.

Author comment: "Both radiation therapy and traditionalDNA-interactive antineoplastics. . .are known genotoxins withthe potential to induce MDS or acute myeloid leukaemia(AML) that commonly harbors a chromosome 5q deletionwith high frequency of evolution to AML and short overallsurvival."Melchert M, et al. Remitting activity of lenalidomide in treatment-inducedmyelodysplastic syndrome. Leukemia 21: 1576-1578, No. 7, Jul 2007 -USA 801091576

» Editorial comment: A search of AdisBase and Medline didnot reveal any previous case reports of myelodysplasticsyndrome associated with interleukin-2. The WHO AdverseDrug Reactions database did not contain any reports ofmyeloproliferative disorders associated with interleukin-2.

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Reactions 6 Oct 2007 No. 11720114-9954/10/1172-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved