Antineoplastics/tacrolimus
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Reactions 1213 - 2 Aug 2008 S Antineoplastics/tacrolimus Guillain-Barre syndrome?: 2 case reports Two patients developed Guillain-Barre syndrome after exposure to high-dose antineoplastics and immunosuppressants associated with peripheral blood stem cell (PBSC) transplantation. Patient 1, a 47-year-old man was diagnosed with multiple myeloma in January 2004 and received vincristine, doxorubicin and dexamethasone. After priming with high-dose cyclophosphamide [dosage not stated] and granulocyte colony-stimulating factor, PBSCs were harvested. Six months after diagnosis, he underwent autologous PBSC transplantation preceded by high-dose melphalan 200 mg/m 2 . He started maintenance therapy with thalidomide 3 months later. In April 2005, he experienced weakness and numbness in his feet, which ascended to his thighs and upper limbs. Thalidomide was withdrawn, but his condition continued to deteriorate. Laboratory findings only revealed elevated protein (137 mg/dL) in his CSF. He was transferred to a special institution; at this time he was unable to ambulate. He had a decreased sensitivity to touch and pain below the T12 level, with grade 0/5 muscle strength in distal muscles of the lower extremities. His deep tendon reflexes were absent. Changes consistent with severe sensorimotor demyelinating polyneuropathy were evident in electromyography and nerve conduction studies. Guillain-Barre syndrome was suspected and he received immune globulin. His symptoms improved significantly and he was able to ambulate unaided by the end of May. Patient 2, a 39-year-old woman, had been previously treated with high-dose cytarabine, daunorubicin, etoposide, mitoxantrone and asparaginase [dosages and durations not stated], for recurrent acute myeloid leukaemia. Following a conditioning regimen of cyclophosphamide 60 mg/kg/day for 2 days and full body irradiation, she underwent allogeneic PBSC transplantation. After transplantation, she began receiving tacrolimus and methotrexate [dosages not stated] for graft-versus-host disease prophylaxis. Two months later, she developed diplopia; MRI suggested possible leukaemic involvement. She was generally weak but ambulatory at the time. She underwent irradiation and received cytarabine and asparaginase [dosages not stated] and donor lymphocytes, due to persistent disease. She achieved remission; however, in March 2004, she developed progressive weakness and became bed ridden. Laboratory findings revealed elevated protein (97 mg/dL) in her CSF. Electromyography and nerve conduction studies were consistent with Guillain-Barre syndrome. She received immune globulin with gradual improvement of her lower limb paralysis. However, she died 9 months after transplant of refractory leukaemia. Author comment: In transplantation, Guillain-Barre syndrome development may be related to tacrolimus. . . It has also been suggested high dose chemotherapy can directly damage neural sheaths leading to exposure of neural antigens to immune-reactive cells. . . Immunosuppressive drugs may also play a role through alteration of T-cell activation in response to peripheral myelin. Zhang L, et al. Guillain-Barre syndrome after transplantation. Leukemia and Lymphoma 49: 291-297, No. 2, 2008 - USA 801118350 1 Reactions 2 Aug 2008 No. 1213 0114-9954/10/1213-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
Transcript of Antineoplastics/tacrolimus
Reactions 1213 - 2 Aug 2008
SAntineoplastics/tacrolimus
Guillain-Barre syndrome?: 2 case reportsTwo patients developed Guillain-Barre syndrome after
exposure to high-dose antineoplastics andimmunosuppressants associated with peripheral blood stemcell (PBSC) transplantation.
Patient 1, a 47-year-old man was diagnosed with multiplemyeloma in January 2004 and received vincristine,doxorubicin and dexamethasone. After priming with high-dosecyclophosphamide [dosage not stated] and granulocytecolony-stimulating factor, PBSCs were harvested. Six monthsafter diagnosis, he underwent autologous PBSCtransplantation preceded by high-dose melphalan 200 mg/m2.He started maintenance therapy with thalidomide 3 monthslater. In April 2005, he experienced weakness and numbnessin his feet, which ascended to his thighs and upper limbs.Thalidomide was withdrawn, but his condition continued todeteriorate. Laboratory findings only revealed elevated protein(137 mg/dL) in his CSF. He was transferred to a specialinstitution; at this time he was unable to ambulate. He had adecreased sensitivity to touch and pain below the T12 level,with grade 0/5 muscle strength in distal muscles of the lowerextremities. His deep tendon reflexes were absent. Changesconsistent with severe sensorimotor demyelinatingpolyneuropathy were evident in electromyography and nerveconduction studies. Guillain-Barre syndrome was suspectedand he received immune globulin. His symptoms improvedsignificantly and he was able to ambulate unaided by the endof May.
Patient 2, a 39-year-old woman, had been previously treatedwith high-dose cytarabine, daunorubicin, etoposide,mitoxantrone and asparaginase [dosages and durations notstated], for recurrent acute myeloid leukaemia. Following aconditioning regimen of cyclophosphamide 60 mg/kg/day for2 days and full body irradiation, she underwent allogeneicPBSC transplantation. After transplantation, she beganreceiving tacrolimus and methotrexate [dosages not stated] forgraft-versus-host disease prophylaxis. Two months later, shedeveloped diplopia; MRI suggested possible leukaemicinvolvement. She was generally weak but ambulatory at thetime. She underwent irradiation and received cytarabine andasparaginase [dosages not stated] and donor lymphocytes, dueto persistent disease. She achieved remission; however, inMarch 2004, she developed progressive weakness andbecame bed ridden. Laboratory findings revealed elevatedprotein (97 mg/dL) in her CSF. Electromyography and nerveconduction studies were consistent with Guillain-Barresyndrome. She received immune globulin with gradualimprovement of her lower limb paralysis. However, she died9 months after transplant of refractory leukaemia.
Author comment: In transplantation, Guillain-Barresyndrome development may be related to tacrolimus. . . Ithas also been suggested high dose chemotherapy can directlydamage neural sheaths leading to exposure of neural antigensto immune-reactive cells. . . Immunosuppressive drugs mayalso play a role through alteration of T-cell activation inresponse to peripheral myelin.Zhang L, et al. Guillain-Barre syndrome after transplantation. Leukemia andLymphoma 49: 291-297, No. 2, 2008 - USA 801118350
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Reactions 2 Aug 2008 No. 12130114-9954/10/1213-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
