In terms of reversing potentially life-threatening arrhythmias, the rationale for ICD therapy is comparable in older and younger individuals.

We report a rare case of prominent purpura induced by aspirin and enhanced by alcohol. A 44-year-old woman presented with a history of generalized purpura. She drank alcohol once or twice a week and regularly took an analgesic preparation, containing aspirin and acetaminophen, for alleviation of headaches. When purpura was evident the patient's liver function was within normal limits and her coagulation time was normal but her bleeding time was prolonged. Red blood cell, white blood cell and platelet counts were normal but a poor response to platelet agonists demonstrated platelet dysfunction. After stopping the analgesic and abstaining from alcohol for 5 days, platelet aggregation, in response to the agonists, returned to normal and purpura disappeared. When the patient took further doses of the analgesic preparation for 3 days for headache relief, but did not drink alcohol, platelet aggregation was again abnormal but purpura was only slight.

A 65-year-old man was admitted to another hospital with a life-threatening brain haemorrhage, and laboratory examinations on admission revealed prolonged prothrombin time with normal activated partial thromboplastin time. To establish the cause of his abnormal coagulation, he was referred to our clinic. Neither the patient nor his family had any previous history of bleeding symptoms. His liver function was within normal limits but coagulation tests showed increased plasma activities of factors II, VIII, IX, X, with reduced activities of factors V and VII. The activity of factor VII was less than 2% but no inhibitor of factor VII was detected in the plasma. We concluded that the patient had a rare congenital isolated factor VII deficiency although he had not shown earlier bleeding problems, presumably because of compensation for the factor VII deficiency by enhanced activities of components of the extrinsic coagulation pathway, factors II, VIII, IX and X.

A 62-year-old female was admitted to our hospital with suspected acute leukaemia and after investigation we diagnosed acute myeloblastic leukaemia (AML-M1). The patient's blood type was found to be the very rare Bombay type and surveillance of her relatives showed the same blood type in her male cousin on her mother's side. Alongside chemotherapy the patient received 4000 ml of frozen Bombay-type red cells, 1400 ml of concentrated red cells in manitol adenine phosphate solutions and 360 units of type O concentrated platelets without marked effects. The anti-H antibody was initially at 128 dilution but for unknown reasons increased to 2048 dilution after remission of AML-M1. About 3 months after hospitalization the patient died of Cryptococcus neoformans pneumonia despite strict precautions against infection. Although AML-M1 is a common adult leukaemia and is chemosensitive to anti-leukaemic drugs, neither AML-M1 in a patient with Bombay-type red cells nor its treatment with chemotherapy and transfusion with type Oh frozen red cells have previously been reported.

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Simultaneous treatment with peripheral blood stem-cell (PBSC) transplantation and intensive chemotherapy was evaluated in a case of non-Hodgkin's lymphoma (NHL) with poor prognosis. A 59-year-old male diagnosed with a high-grade, anaplastic large-cell (Ki-1) NHL, involving fractures in the left hip, underwent computed tomography and gallium scintigram surveillance. The patient received chemotherapy with epirubicin hydrochloride, cyclophosphamide, vincristine and prednisolone, and the fractured hip bone was repaired following the first course of chemotherapy. After the second and third courses of chemotherapy, PBSCs were harvested and cryopreserved. The patient then received a further course of chemotherapy and PBSC transplantation was conducted using infused cells consisting of 9.63 x 10(6)/kg CD34 cells and 2.24 x 10(5)/kg granulocyte macrophage colony-forming units. Recovery of platelet and white blood cell counts occurred 10 and 8 days, respectively, after PBSC infusion and the patient remains well.

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