Sixty four patients with the artificial valve and 36 patients with the repaired valve were examined with respect to platelet aggregation induced with ADP and collagen, the plasma level of β-thromboglobulin (βTG), antithrombin III (AT III), ratio of factor VIII procoagulant activity to factor VIII like antigen (VIII AHF/VIII AGN), fibrinogen, fibrin degradation products (FDP), and plasmin activity.
As the result, platelet aggregation of the patients with the artificial valve was more accelerated than that of the patients with the repaired valve. βTG level in the patients with the artificial valve were mostly higher than those in the patients with the repaired valve. The levels of AT III, VIII AHF/VIII AGN and FDP were within normal range in all of the patients with the repaired valve, while they were reduced in some of the patients with the artificial valve. Specific changes were not seen in fibrinogen amount and plasmin activity.
Judging from these data, hypercoagulable states were found more frequently in the patients with the artificial valve than in the patients with the repaired valve. Although antiaggregating or anticoagulant agents were being given to the most of those patients, the data indicated that hypercoagulable states were not corrected in some of them. Therefore, these agents were thought to be not effective in some of them, and the prescription should be reconsidered.

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Granulopoietic and erythropoietic progenitor cells (CFC and CFUe) in bone marrow from childen with hematological disorders were assayed using methylcellulose clonal cell culture.
Marked reduction of CFC and/or CFUe in bone marrow were observed in the following disorders: onset or relapse in acute leukemia, smoldering acute leukemia, preleukemia, exacerbation in aplastic anemia, pure red cell anemia, congenital neutropenia, acute phase in agranulocytosis or transient pancytopenia, malignant histiocytosis, neuroblastoma with metastasis, and children received intensive chemotherapy or irradiation.
Possible mechaisms of CFC and/or CFUe reductions in each cases are discussed and a etiological classification of marrow stem cell reduction is attempted.

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1) Glucose consumption of the human peripheral lymphocytes stimulated with some mitogens increased as compared with unstimulated lymphocytes.
Stimulation indices of glucose consumption (G-SI) were correlative to those of ³H-thymidine uptake (T-SI) in PHA-and Con A-stimulated lymphocytes, whereas there was no correlation between them in PWM-stimulated lymphocytes.
2) In PHA-stimulated lymphocytes which were pretreated with actionomycin D or irradiation, glucose consumption, DNA synthesis and RNA synthesis were supressed in accordance with the dose of these agents.
In PHA-stimulated lymphocytes which were pretreated with cycloheximide, only RNA synthesis was supressed, however glucose consumption and DNA synthesis were not effected.
3) When the lymphocytes of cancer patients were stimulated with PHA or ConA, the glucose consumption and ³H-thymidine uptake were not so increased as those of the lymphocytes of normal volunteers.
Glucose consumptions in the lymphocytes which were cultured with irradiated allogeneic lymphocytes, were increased as compared with those in lymphocytes cultured with autologous lymphocytes.
Stimulation indices of glucose consumption were correlative to that of ³H-thymidine uptake in mixed lymphocyte reaction.
These results indicate that glucose consumption test of peripheral blood lymphocytes can be applied for the clinical examination of cellular immunity.

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Eighteen cases with fungal infections, complicated with acute leukemia and related disorders, were treated with 5-Fluorocytosine (5-FC). Five cases were with fungemia, 8 cases pneumonia, 3 cases disseminated fungal infections and one meningitis and one peritonitis.
Sixty percent of pathogenic organisms were Candida albicans.
5-FC, 4.5 to 10.5 g per day, was given in combination with or without amphotericin-B. Out of four cases treated with 5-FC alone, 3 were effective.
Out of 5 cases with fungemia 3 were effective. Out of 8 cases with pneumonia, 5 cases were cured. The percentage of 5-FC effectiveness was about 55%.
Twelve cases were given 5-FC without the diagnosis of fungal infections. The only one case out of 30 patients who were administrated with 5-FC, showed liver function abnormalities. None of 30 cases showed bone marrow suppression.

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The authors experienced a rare case, in which paroxysmal nocturnal hemoglobinuria (PNH) was followed by acute myeloid leukemia (AML). Signs of PNH were disappeared at the onset of leukemia, reappeared on its remisson, and then disappeared again at the recurrent period.
The patient was a 38-year-old male. When admitted in June 1973 on account of gastric ulcer, PNH was strongly suspected because of hemoglobinuria in the early morning and various examinations. When admitted in August 1977 due to palpitation and dyspnea, he was diagnosed as AML by recognition of leukemic cells with Auer bodies in peripheral blood and marrow, but hemoglobinuria was not observed. Upon the complete remission by DCMP treatment, hemoglobinuria was reappeared. As the sugar water test and the Ham's test were positive, it was diagnosed as PNH. After the recurrence of AML in April 1978, signs of PNH were disappeared again, and the patient was died of sepsis.

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A 64-year-old female was admitted to the Juntendo University Hospital with complaints of fever, vomiting, and right hypochondralgia in Sept. 1976.
Physical examination revealed severe pallor, tenderness, and resistence over the right hypochondrium.
Hematological examination on admission showed hemoglobin 5.3 g/dl, red blood cells 187×10⁴/mm³, white blood cells 9,000/mm³ with a small number of the immature granulocytes and the partial hypochromia of the red cells.
Bone marrow aspirate revealed an erythroid hyperplasia with numorous ringed sideroblasts but no megaloblastic change. PAS stain was negative.
A chromosomal analysis showed no abnormality with negative Ph¹ chromosome.
E. coli was cultured from her blood and bile, and a diagnosis of primary acquired sideroblastic anemia complicated with sepsis was made.
The sepsis was successfully treated with antibiotics and the external biliary drainage. She was placed on folate and pyridoxine with no improvement of anemia.
On Oct. 1977, a small number of myeloblasts and erythroblasts appeared in the peripheral blood. The bone marrow specimen obtained in Nov. 1977 showed an increase in atypical myeloblasts and a megaloblastic change in erythroid cells.

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A case of thrombotic thrombocytopenic purpura (TTP) was reported. The symptoms of this twelve-year-old girl were microangiopathic hemolytic anemia, thrombocytopenia, headache, hemiparesthesia and dysarthria. Fever and renal involvement were not observed.
Transfusions of whole blood or fresh frozen plasma were not effective, but she responded promptly to the antiplatelet therapy (aspirin, 20 mg/kg/d. and dipyridamole, 4 mg/kg/d.). She has been in complete remission for sixteen months.
The titer of serum circulating immune complexes (CIC) was very high before therapy, but CIC turned to be negative along with the disappearance of the symptoms.
It has been suggested that CIC could cause vascular lesions and had platelet aggregating activity. Although neither immunoglobulins nor complement were demonstrated in the biopsy specimen of the gingiva, CIC might have played a role on the pathogenesis of TTP in this case.

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A 37 year-old male, who had complaints of tarry stool and hemorrhagic diathesis, was diagnosed as chronic myelocytic leukemia from the peripheral and bone marrow smears, a low score of leucocyte alkaline phosphatase activity, and a positive Ph¹ chromosome in August 1975. He was treated with Carboquone.
In July 1978, he was admitted to our hospital with a diagnosis of blast crisis. He had been treated with DCVP (D: daunomycin, C: cytosine asabinoside, V: vincristine, P: prednisolone) and CVP schedule and got a complete remission.
The end of January 1979, he complained of severe headache, nausea, vomiting. His second admission to our hospital was February 1979. Lumbar puncture showed xanthochromia without myeloblasts. CT scanning showed high density area at the rt-temporal cerebral lobe. Finally, he died of a symptom of an increased intra cranial pressure and complicated disseminated intravascular coagulation.
At post morten examination, the hard tumor adhesive to the dura was observed on the right temporal lobe. The tumor was a walnut sized and gray colored. A thumb tip sized tumor of the right third costal cartilage was observed. There were multiple nodular infiltrations, up to soy bean sized, in the bilateral kidneys. Microscopic examination revealed a diffusely proliferated blastic cells with strong positive peroxidase reaction (myeloblastoma). Severe leukemic cells were infiltrated in the bilateral testes. A fungus ball consisted of Aspergillus was seen in the left upper pulmonary lobe.

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A 29-year-old male noticed pain and swelling in the left thigh without any notable history of trauma in early February 1979. Hevisited a local hospital and was first found to have extremely high leukocyte count, and referred to our hospital for further examination on March 15 of the same year. On admission, his left thigh was swollen about twice the right one. The liver was palpable two fingerbreadths below the right costal margin and the spleen five fingerbreadths below the umbilicus. No lymphadenopathy was observed. The initial blood study showed sever anemia and marked leukocytosis at all stages of maturation in the myeloid series. The bone marrow aspirate revealed a marked myeloid hyperplasia with 0.8% myeloblasts. The cytogenetic study of bone marrow cells demonstrated metaphases characterized by 46, XY, Ph¹ (+), and the leukocyte alkaline phosphatase activity was definitely reduced. Blood coagulation and platelet function were normal. The femoral arteriography performed on the 35 th hospital day proved a saccular aneurysm in the ramus descendens of the left lateral femoral circumflex artery. Since repeating formation of hematoma was thought to be ascribable to rupture of this aneurysm, aneurysmectomy was carried out on the 44th hospital day. Histological examination of the excised aneurysm showed an entire lack in normal architecture of the arterial wall, and massive infiltration of myeloid cells at all stages of maturation and a few megakaryocytes and eosinophils in the muscle and fat tissue around the aneurysm. The hematoma as aninitial sign in this patient with chronic myelocytic leukemia would have been caused by ruprure of the arterial wall directly invaded by leukemic cells which were nonmyeloblastic in nature.

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A 69-year-old man with hemorrhagic tendency caused by a specific inhibitor against factor V was described.
He was admitted because of severe hematuria. Coagulation studies showed a factor V level of 1% and cross correcting experiments showed a presence of factor V inhibitor in his plasma. The inhibitor was suggested to belong to IgG fraction, because it was found on the second peak of the Sephadex-G 200 gel filtration of the plasma and precipitated by 33% saturation with ammonium sulfate. On admission, antinuclear antibody and rheumatoid factor were present, but LE cells were absent. A high level of FDP was also present, but no orther signs of DIC were present. He was treated with fresh frozen plasma for one week, but no improvements were observed in coagulation studies. Then he was treated with predonisolone, which resulted in a disappearence of the inhibitor. At the same time, antinuclear antibody, rheumatoid factor and FDP also disappeared. Although the occurrence of the inhibitor in this case was assumed to be associated with some “autoimmune” mechanisms, few evidences were found to show the presence of the underlying disorder.

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A 32-year-old male developed lactic acidosis at the stage of blastic crisis of CML. This complication may have resulted from the high production rate of lactate by the marked proliferation of blasts, tissue hypoxia due to microemboli of blast aggregates and liver damage by the infiltration of blastic cells. The liver damage may have prevented the removal of lactate from the circulation. The complication of lactic acidosis in the patients with blastic crisis of CML has rarely been reported. One case with this complication was reported as far as we know. As to the morphology of leukemic blasts, only two reports of AML with lactic acidosis were available. It is interesting to note the blastic cells of our case and theirs resembled each other. In other words, the blastic cells were large and bizzare with many vacuoles in the cytoplasm. It still remains to be clarified if blastic cells which induce lactic acidosis have common surface markers and/or cytochemical characteristics.

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