Neuropathy after cyclophosphamide high dose chemotherapy in a Morbus Werlhof patient. PERSONAL HISTORY: A 24 year old patient with longstanding autoimmune idiopathic thrombocytopenic purpura (M. Werlhof) was treated with glucocorticoids, immunoglobulins, splenectomy, immunosuppression and vincristin without lasting success. After a second treatment cycle with cyclosphosphamide and autologous peripheral stem cell transplantation she acutely develpod symptoms of a peripheral sensoric and motoric polyneuro-pathy. MEDICAL EXAMINATION: At admission she was in good general health, but had steroid-induced Cushing's symptoms, generalized petechial bleeding and thrombocytopenia (1000/ micro l). THERAPY AND COURSE: After 2.5 g/m 2 cyclophosphamide and stem cell transplantation distally pronounced polyneuropathy developed within a week with bladder insufficiency. Major bleeding or brain damage were excluded, and symptoms only partially reversed when treated with steroids, carbamazepine and amitriptyline. Thrombocytopenia persisted, and the patient died 4 month later from acute brain hemorrhage. CONCLUSIONS: Direct neurotoxicity has to be assumed as the likely causative agent in this case, illustrating the possibility of peripheral neuropathic lesions by high dose cyclophosphamide treatment.
Neuropathy after cyclophosphamide high dose chemotherapy in a Morbus Werlhof patient. PERSONAL HISTORY: A 24 year old patient with longstanding autoimmune idiopathic thrombocytopenic purpura (M. Werlhof) was treated with glucocorticoids, immunoglobulins, splenectomy, immunosuppression and vincristin without lasting success. After a second treatment cycle with cyclosphosphamide and autologous peripheral stem cell transplantation she acutely develpod symptoms of a peripheral sensoric and motoric polyneuro-pathy. MEDICAL EXAMINATION: At admission she was in good general health, but had steroid-induced Cushing's symptoms, generalized petechial bleeding and thrombocytopenia (1000/ micro l). THERAPY AND COURSE: After 2.5 g/m 2 cyclophosphamide and stem cell transplantation distally pronounced polyneuropathy developed within a week with bladder insufficiency. Major bleeding or brain damage were excluded, and symptoms only partially reversed when treated with steroids, carbamazepine and amitriptyline. Thrombocytopenia persisted, and the patient died 4 month later from acute brain hemorrhage. CONCLUSIONS: Direct neurotoxicity has to be assumed as the likely causative agent in this case, illustrating the possibility of peripheral neuropathic lesions by high dose cyclophosphamide treatment.