Airway hyperreactivity (AHR) was studied with an astograph for 34 sequential hematopoietic stem cell transplantation (HSCT) patients before and after HSCT. The percentage of Dmin positive patients was 25.0% before HSCT and 25.0-57.1% after HSCT, while all normal subjects were negative for Dmin. The mean Dmin of post HSCT patients was 22.7u in days 501-1000 and 19.3u after 1001 days, which was significantly lower than the 45.2u of normal controls. The patients were divided into two groups according to the treatment before HSCT, strongly treated (S, acute leukemia and non-Hodgikin lymphoma) and weakly treated (W, chronic myelogenous leukemia and aplastic anemia) patients. The ratio of Dmin positive patients and mean Dmin in the W group after HSCT (38.9%, 27.8u), and the S group before and after HSCT (55.6%, 20.5u and 45.5%, 23.8u, respectively), were significantly impaired compared with the findings in the normal controls (0%, 45.2u). The mean sGrs/Grs count was higher in the W group before HSCT than in the other groups (W before and after HSCT, 0.58 and 0.19, respectively; S before and after HSCT, 0.21 and 0.22, respectively). Taken together, AHR was observed in HSCT patients, particularly for patients in the S group. These data indicate that high dose chemo-radiotherapy including conditioning regimen causes AHR. The mechanisms leading to AHR may be infection, inflammation, and remodeling of the airway.

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We treated seven refractory or relapsed myeloma patients resistant to conventional chemotherapy with thalidomide. We started thalidomide at 100 mg daily and the dose was increased up to 300 mg if the patient could tolerate it. The patients were evaluated at four weeks and 12 mg of dexamethasone was added for four days when the patient failed to respond to thalidomide treatment. One patient was excluded from the study because of general fatigue. Two of the six patients responded to thalidomide alone and three of the remaining four patients responded to the combination with dexamethasone. The most common adverse effect was sleepiness which was seen in three patients. Two patients showed pancytopenia (Grade 3), constipation and skin eruption. Of the six patients four needed reduction of the thalidomide dose to 200 mg because of adverse effects. Plasma levels of TNF-α, IL-6, bFGF and VEGF were measured before and after four weeks. High plasma bFGF levels were seen in responding patients. In conclusion, treatment with thalidomide alone or in combination with dexamethasone is feasible and effective in refractory or relapsed myeloma patients. Further study is required to clarify the role of thalidomide in the therapeutic strategy for multiple myeloma.

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It has been previously demonstrated that aging, a history of malignancy or surgery, and exposure to bovine thrombin may be related to the presence of factor V inhibitor. However, dermatomyositis (DM) and autoimmune thrombocytopenic purpura (ATP) have rarely been associated with factor V inhibitor. Here we report a patient with factor V inhibitor accompanied by DM and ATP. In January 2000, a 77-year-old woman with DM was hospitalized because of susceptibility to bleeding. At the onset of DM, she had suffered from gastric leiomyosarcoma, and had undergone gastrectomy and splenectomy without the use of bovine thrombin. Thereafter, she had been treated with prednisolone until October 1999. On admission, prolongation of both APTT and PT was seen. Her factor V activity had fallen to 6%, and factor V inhibitor was positive at 8.9 Bethesda units. Moreover her platelet count had dropped to 1.0×10⁹/l. A bone marrow aspirate showed a cellular marrow with megakaryocytic hyperplasia, and the patient's PA-IgG level was elevated at 389 ng/10⁷ cells. These findings suggested that ATP was also present. Additionally, the patient showed a positive result for Coombs test and consumption of complement. After a further course of steroid therapy, the patient's condition was markedly improved. This is a very rare case that showed factor V inhibitor and ATP simultaneously. Furthermore, the patient's clinical course suggests the relationship between the presence of factor V inhibitor and the reactivation of her collagen disease activity.

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A 50-year-old man was admitted to another hospital with epigastralgia. Malignant lymphoma was suspected because the patient had increased levels of serum LDH and an abnormal Ga scintigraphy finding in his chest. When he was transferred to our hospital, he underwent a right inguinal lymphadenopathy. The laboratory data showed increased levels of serum LDH and soluble IL-2 receptor, but there was no appearance of peripheral abnormal lymphocytes. His chest MRI indicated tumors in the right atrium (4 cm×4 cm) and in the head of his left humerus. Those tumors were enhanced by Gd-DTPA. There were no other lymphadenopathies. Histopathological and immunohisto-chemical studies showed T-cell type lymphoma in the right inguinal lymph node. Furthermore, monoclonal rearrangement of HTLV-I proviral DNA was detected from the lymph node by Southern blot analysis. Taken together, we diagnosed the patient as having ATL (lymphoma type). His condition has improved well with systemic chemotherapy. We report a rare case of lymphoma type ATL with initial massive cardiac involvement, although ATL cells sometimes involve the heart at the end of the disease course.

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A 42-year-old man was diagnosed as having refractory anemia in May, 2001. He developed overt leukemia and received allogeneic bone marrow transplantation (BMT). His younger brother, a 40-year-old man, was diagnosed as having acute leukemia with trilineage myelodysplasia in November, 2001. Although he was treated with conventional chemotherapy, he failed to achieve complete remission. He also received allogeneic BMT. We suggest that environmental factors in addition to a genetic defect in the pluripotent hematopoietic stem cells may be associated with the occurrence of this familial leukemia.

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