Thirty two bacterial infections in 22 patients with acute leukemia which causative organisms, inflammatory foci and responsible antibiotics were established in the 1st Department of Internal Medicine of Nagoya University Hospital from January, 1971 through September, 1974 were investigated and reported.
As to the incidence, pneumonia, septicemia, pharyngo-tracheitis and gingival abscess were frequent in this order and gram-negative bacilli were identified predominantly in 31 infections, in which Klebsiella was most frequent and followed by Pseudomonas and Escherichia coli.
Cephalosporin (Cephalothin, Cefazolin) was most effective to Klebsiella and Penicillin (Carbenicillin, Sulbenicillin) to Pseudomonas.
An interesting case of acute pneumonia in patient with acute monocytic leukemia was reported, which showed alternate growth of Pseudomonas and Klebsiella according to the antibiotics administered in the periodical sputum cultures.

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Ristocetin-induced platelet aggregation was studied in normal subjects and in patients with von Willebrand's disease (vWd), thrombasthenia and essential athrombia. The aggregation ranged between 38.2 and 71.2% (mean ± sd, 55.0 ± 10.3) in 10 normal subjects, 47.6 and 64.4% in 4 patients with essential athrombia and 45.5% in one patient with thrombasthenia, whilst 10 patients with vWd showed very poor aggregation between 7.4 and 36.4% (mean ± sd, 20.6 ± 9.7).
The defective aggregation in vWd was corrected by addition of a small amount of normal platelet poor plasma (PPP), crude AHF concentrate or hemophilic PPP. A rabbit antibody to human AHF completely inhibited the aggregation in normal subjects, which was corrected by further addition of either normal PPP, highly purified AHF or hemophilic PPP.
Fresh plasma transfusion to a patient with vWd resulted in a rise of the AHF-like antigen reactive to a rabbit antibody only for the first 12 hrs., and in a delayed elevation of AHF-procoagulant activity in excess which lasted for 72 hrs. after the transfusion. The correction of Ristocetin-induced platelet aggregation was noted for the first 12 hrs. after the transfusion and correlated well with the amount of AHF-like antigen.
These results suggest that a plasma factor deficient in vWd and necessary for Ristocetin-induced platelet aggregation could be AHF-like antigen itself or at least some part of the molecule and that AHF molecule essential for procoagulant activity would not be responsible for the defective platelet function in vWd.

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Two cases of typical di Gugulielmo syndrome showed the same findings as positive PAS staining, siderophilic and megaloblastoid erythroblasts in peripheral blood and bone marrow at their hospitalization and during their clinical course and followed in erythro-leukemic stage.
Their hematological morphology showed megaloblastoid anemia with giant platelets, hypersegmented neutrophilic cells and megaloblastoid cells, but was denied it because of normal levels of vitamin B₁₂ and folic acid in erythremic stage.
We thought that the above mentioned hematological changes revealed the aberration of DNA and RNA in stem cells of erythropoietic, granulopoietic and megakryopoietic system, probably induced by aromatic agents polluted in their occupation.
We obtained the results to have the abnormality of hemoglobin synthesis that caused deficiency or utilization disturbance of vitamin B₆ as co-enzyme of ALA synthetase and Heme synthetase.

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A 9-year-old girl developed clinical manifestations of rubella on May 20, 1974. The skin eruptions faded away by the fourth day of the disease. On the eighth day petechial bleeding was first noted on the lower extremities with an accompaniment of moderate epistaxis. Because these hemorrhagic manifestations tended to aggravate, she was hospitalized on June 12. She had no history of purpura and had taken on drugs in the preceding months. Generalized petechial bleeding with an involvement of oral mucosa and superficial lymphadenopathy were found on physical examination. Platelet count was 20,000/cmm. Neither anemia nor hepatosplenomegaly was present.
Rapid resorption of the petechiae ensued without any particular treatments. At the same time platelet count started to recover gradually and attained normal level in two months.
The preceding infection was confirmed as rubella by the high antibody titer in her serum. From the close clinical correlation, the marked thrombocytopenia observed in this patient was considered to be related with rubella virus infection.

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A hemorrhagic diathesis has been observed in patients with GSD-I. Some studies suggested that platelet dysfunction of patients with GSD-I could account for this phenomenon, but the mechanism of this phenomenon has not been clearly investigated in detail.
In the present report we studied three patients and their families with regard to platelet function, platelet aggregation, blood coagulation activity and fibrinolysis.
Three patients and only one of their families showed abnormalities in the collagen induced platelet aggregation, but the ADP induced platelet aggregation and other examinations indicated above were all normal.
According to these results, the bleeding tendency of a patient with GSD-I may be due to the failure of the release of intrinsic ADP from platelets by collagen. But at the present time we have not been clarify the mechanism of the release-lesion of intrinsic ADP from the platelets of patients.

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A 20-year-old male patient with acute lymphoblastic leukemia, who showed a rapid increase in blood leukocyte count despite of the administration of prednisolone 20 mg/day from March, 1974 to May 17, 1974, was treated with prednisolone 30 mg/day while simultanously treated by leukapheresis three times using a continuous blood cell separator, Celltrifuge, AMINCO during 40 days of admission.
After removal of a large amount of abnormal cells from peripheral blood by leukapheresis, the patient responded well to the small amount of cytostatic agent (prednisolone 30 mg/day), with the following results: (1) a marked decrease in peripheral leukocyte count including pathologic cells (2) a decrease in uric acid values, and (3) an increase in platelet count and percentage of neutrophile leukocytes. However, four bone-marrow aspirates remained unchanged morphologically during his admission.
These findings suggest that leukapheresis may be considered to be an useful tool for treatment of acute leukemia especially accompanied with a marked increase in abnormal cells in the peripheral blood, although remission cannot be induced by leukapheresis alone.

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A 41 year-old man was admitted to the Akita University Hospital on 6 Jan. 1971, because of paresthesia and weakness of the lower legs.
On physical examination, skin of the patient was hirsute and pigmentary, lymph nodes slightly enlarged on the neck, axilla and inguinal area. The abdomen was distended and undulatory, and edema of lower extremities was observed.
Blood examination showed RBC 486x10⁴, Hb 14.9 g/dl, WBC 5,600 and Platelet 134,400. On the bone marrow smear, plasmocytoid cells were seen at 11.8%. The serum protein analysis revealed total protein 6.7 g/dl, γ-gl. 16.0%, Ig G 1,300 mg/dl, Ig A 425 mg/dl and Ig M 63 mg/dl. By the immunoelectrophoresis, M component showed Ig A (λ) type. Any osteolytic or osteoclastic lesion was not seen on the X-ray examination. Papilloedema was seen in the fundus.
Treatment with diuretica was tried but did not effective and patient died in 9 months after administration. This case correspond to “a new syndrome of plasma cell dyscrasia” which has advocated by K. Takatsuki.
In this paper, we described outline of the case and discussed about relationship to multiple myeloma.

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