In the northern and western areas of Saitama prefecture, serum samples were collected from healthy voluntary blood-donors for the purpose of HTLV-I antibody detection as part of a health examination.
The antibodies were found in sera of 299 (0.8%) of 38, 253 donors. However, the frequency of HTLV-I antibody positive donors showed high rate (3.7%) in the sera which were collected from the donors who had been moved to Saitama from Kyushu district. The sera of Saitama original residents showed rate of 0.5% positive possessing HTLV-I antibody.
In an investigation of the mode of transmission of HTLV-I in family settings, we are interested in whether HTLV-I can be transmitted from mother to child via the placenta and/or breast milk and also from husband to wife via semen.
Our results suggest that placental transmission of HTLV-I is not a major route, the breast milk route is a significant mother to child transmission route of this virus.
Particularly, we must paid attention to the fact that mother to child transmission was high risk when the immunoglobulin class of mothers antibody was both of IgM and IgG.

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Three methods (lymphocyte cytotoxicity test: LCT, anti-human immunoglobulin lymphocyte cytotoxicity test: AHG-LCT, mixed passive haemagglutination test: MPHA) were used in detecting platelet alloantibodies in the sera of 89 patients received multiple platelet transfusions and employed the same three cross-match techniques to select compatible platelet donors for 13 patients (5 aplastic anemia, 6 acute leukemia, 2 chronic leukemia) who had become refractory to random platelet transfusion. In the sera of 89 patients, the frequency of positive sera by LCT, AHG-LCT and MPHA were each 42.7%, 55.1% and 36.0%. And 13 refractory patients received 116 platelet transfusions from HLA matched single donors. Of 116 transfusions, 9 incompatible by AHG-LCT cross-match alone had no increase of platelet count. The 24 hour-posttransfusion platelet increment more than 20000/mm³ was 76 (71.0%) in 107 compatible cross-match transfusions and 0 in 9 incompatible transfusions. The more HLA was matched, the more platelet count increased.

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We studied the A- and B-transferase in the plasma of leukemic patients in relation to their clinical course. The level of A- and B-transferase was obtained from the intensity of A and B antigen on the red cell membrane of blood group O converted by the use of UDP-N-acetylgalactosamine or UDP-galactose as a substrate. Significant changes of A- and B-transferase were observed in 13 of 15 patients in the study, but in none of them was seen any extreme decrease of the content of antigen A, B, or H on the red cell membrane. Besides, changes the level of transferase in the plasma were not always proportionate to nuclear cell counts of bone marrow.
In observation of blood chimeric twins and A- and B-transferase in allogenic bone marrow transplantation with ABO major miss match, main productive organ of A- and B-transferase in the plasma seemed to exist outside of the bone marrow, suggesting that A- and B-transferase in the plasma was not directly concerned with the process of red cell antigen development. Furthermore, it was found that reduction of A- and B-transferase in the plasma of leukemic patients was not always associated with reduction of A and B antigen on red cell membrane.

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It has been well established previously that adenine phosphate added into the storage fluid may prolong the life of blood. However massive use of this agent (APO₄) may produce some ill effects. In order to secure the safety in practical use of APO₄, we have reported previous studies (in Journal of the Japan Society of Blood Transfusion, 30 (2): 121-129, 1984.
As the sequel, new results of these serial experiments are presented here. It was revealed that massive dosage use of APO₄ for mice (500mg/kg etc) produced remarkable depression of various Immunological functions.
The reductions of T lymphocyte counts, atrophies of thymus or spleens and low levels of haemolysin test of these mice were observed. These phenomena suggested that various cellular or humoral immunological functions were suppressed by massive use of APO₄.
But the toxicity of APO₄ is related to the dosage of APO₄, and no remarkable ill effects were observed within usual clinical dosages.

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HLA-matched platelet concentrates, harvested from 4 family donors by plateletpheresis using the CS-3000 blood cell separator, were used in the treatment of three thrombocytopenic patients (two with aplastic anemia and one with relapse of acute myelogenous leukemia) who had become unresponsive to the transfusion of random platelet concentrastes due to HLA antibodies. During more than 2 years, 89, 98 and 151 procedures of HLA-matched platelet transfusions were performed, respectively. Mean 20-hour posttransfusion platelet recovery of HLA-matched platelet transfusions were 44%, 51% and 57%, respectively. In all patients, hemorrhagic diathesis such as gastrointestinal hemorrhage, nasal bleeding and genital bleeding were improved and no serious hemorrhage was occurred. During 23 months, donations of platelet concentrates were performed weekly on 2 family donors and two weekly on the other 2 family donors. No significant change in any donors was noted in counts of blood cells, differential leukocyte counts, lymphocyte subpopulations, serum total protein, serum albumin levels, serum immunoglobulin levels and serum complement levels.

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HLA-A, B, C, Bf, C4 gene and haplotype frequency were studied in 311 healthy apheresis donnors living in Yamaguchi prefecture of western area of Japan and the result was compared with the previous study of Japanes.
In HLA-A, B, C locus, the gene frequency of Aw33, B44, Bw54, Cw1 were decresed, and the gene frequency of B7, Cw7 were increased.
In Bf locus, the gene frequency of BfF was significantly decreased, and with regards to the distribution of Bf gene frequency, there is a similarity to the Southern Chinese.
Distribution of the gene frequency of C4 locus was not so different from average of Japanese, but C4A*4 and C4B*2 just increased.
The haplotype frequency of Aw33-CBL-B44-C4A3-C4B1-BfF was significantly decreased, and the haplotype frequency of A24-Cw7-B7-C4A3-C4B1-BfS was increased.

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A 40-year-old man had been suffered from bleeding tendency since childhood. At the age of 34, he was diagnosed as having hemophilia A when he was admitted for an operation of an uretheral stone. Two years after the diagnosis of hemophilia A, he was suspected of having factor VIII inhibitor, because the treatment of spontaneous bleeding in the right knee joint with factor VIII concentrate was unsuccessful.
Partial thromboplastin time (PTT) and factor VIII activity before and after intravenous infusion of factor VIII concentrate were over 3min and 2.9% respectively. Further examination revealed a factor VIII inhibitor titer of 4.5 Bethesda unit. Eighteen months after detecting factor VIII inhibitor, he exhibited anamnestic reaction.
Treatment with high doses of factor VIII concentrate were effective for his bleeding symptoms without improvement of PTT and factor VIII activity. Treatment with steroid, an immunosuppressive agent (azathioprine) and/or high-dose intact immunoglobulin, which were gave after the development of anamnestic reaction, did not decrease the factor VIII inhibitor titer. Therefore, it was guessed that he should be treated with prothrombin complex concentrate (PCC) and activated PCC.

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The effect of sera from cancer patients on in vitro lymphokine activated killer (LAK) induction of peripheral blood lymphocytes (PBL) was tested. The LAK activity from PBL of cancer patients in the culture medium with normal AB serum was induced, but by addition of cancer serum in the medium, LAK induction was inhibited. The degree of inhibition produced by cancer sera increased with the extent of the disease. The cytotoxic activity of LAK cells was suppressed after the incubation of LAK cells in the medium with cancer serum for 12 or 24 hours. The sera from advanced cancer patients inhibited both LAK induction and 3H-thymidine uptake of PHA-stimulated PBL. However, the sera from non-advanced cancer patients did not always show inhibiting effect on either of them. A fraction (<10, 000) which was obtained from cancer serum by diafiltration has inhibiting activity.

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We tested for the anti HIV antibody and the HIV antigen in the sera of 81 hemophiliacs (A 68 cases, B 13 cases), who have been under treatment in our department.
The anti HIV antibody was found to be present in 44.3% of the cases, including 7 cases who later changed to positive, and 6 with HIV antigen. In the sera of those 7 seroconverted cases, although the HIV antigen was negative, the p24 antibody was detected by the Western blotting method and the gp41 antibody was detected by the Confirmatory EIA (ENVACORE, Abbott Lab., USA) earlier than by the immunofluorescence method and conventional ELISA. Moreover, in 4 cases who later developed AIDS, HIV turned out positive concurrently with or shortly after the enfeeblement and/or disappearance of the p24 antibody which was associated with a progressive decrease in the CD4/8 ratio of lymphocytes and the development of recurrent oppotunistic infections.
Based on these results, it is suggested that the periodical examination for anti p24 and gp41 antibodies and HIV itself might be clinically useful for predicting the development of AIDS and thustreating them at an early stage.

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A case of delayed hemolytic transfusion reaction caused by anti-Le^a is reported. The patient was a 44-year-old woman and she had undergone cardiac surgeries in 1965 and 1981. She received a replacement of her mitral and aortic valves on February 10, 1987. During surgery she received 9 units of red blood cells. Ten days after the transfusion, she noticed a hemoglobinuria. Serologic examination revealed that she belonged to the type Le (a-b-), and had a anti-Le^a in her posttransfusion serum. The direct Cooms' test was negative. This is the very rare case of a delayed hemolytic transfusion reaction cause by anti-Le^a.

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A case of microangiopathic hemolytic anemia (MHA) associated with disseminated breast cancer is reported. A 57-year-old woman was admitted for evaluation of a tumor of the left breast. She had had lumbago for about 6 months prior to the admission. A few days after the admission, she received red blood cell transfusion and she developed a bout of hemolysis immediately after that. The hematological examinations showed hemolytic anemia in association with severe red blood cell fragmentation and leukoerythroblastosis. While clotting abnormalities or thrombocytopenia was quite mild at the height of the hemolytic crisis. On the other hand, the histology of the left breast tumor revealed papillotubular adenocarcinoma and the Ga-citrate scintigram showed diffuse RI uptake at the spine especially in the lumbar region. Taken altogether, she was diagnosed as having disseminated breast cancer and MHA without disseminated intravascular coagulation (DIC). Then she was started on combination chemotherapy using CMFVP regimen, and anti-estrogen therapy. About 4 months later, MHA was brought to remission with the remarkable reduction of the tumor bulk at both the primary and metastatic sites, and she was discharged. A month after that, however, she entered the hospital again because of the rapid progression of anemia attributable to relapsing MHA. On the 17th hospital day of this admission she died of respiratory failure.
The autopsy disclosed diffusely infiltrative, though partly nodular, metastatic tumor growth of thoracic and lumbar vertebrae. In addition, there were a number of tumor emboli in the small vessels of both lungs and severe cryptococcal infection in both pulmonary bases as well. But there were no thrombi formation in any organs to suggest the presence of DIC.
To conclude, the case depicted here is quite intriguing in view of the pathogenesis of MHA unassociated with DIC, unfavorable effect of blood transfusion for MHA and the possible efficacy of chemotherapy against malignancy-related MHA.

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