Rinsho Ketsueki
Online ISSN : 1882-0824
Print ISSN : 0485-1439
ISSN-L : 0485-1439
Volume 8, Issue 1
Displaying 1-9 of 9 articles from this issue
  • K. Nagai, E. Kakishita, H. Hara
    1967 Volume 8 Issue 1 Pages 11-20
    Published: 1967
    Released on J-STAGE: October 20, 2008
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    From biochemical studies the authors previously pointed out that in the reactive erythroid hyperplasia, proerythroblasts and basophilic erythroblasts possessing nuclei of high metabolic activity are accumulated in the bone marrow. The authors also pointed out that “reticulocyte crisis” occurred when these immature erythroblasts, not following the normal heteroplastic process, disappeared from the bone marrow either after their rapid maturation or through the extrusion of their nuclei.
    In this paper, the erythroid reaction was studied quantitatively from the view point of karyometrial findings of erythroblasts.
    Each erythroblast compartment was first determined by the method of Weicker.
    From observations on the interrelation between the mode of reaction in erythroblast compartments and the reticulocyte crisis, it would be concluded that reticulocytes are directly originated from intermediate erythroblasts (K1, K1/2, K1/4). The large-sized reticulocytes which were thought to be formed by the abortion of more immature erythroblasts (mainly K1), were fragile and short-living.
    It is also suggested that O-Ebl or K1/8 produces non-reticulated normocytes not through reticulocyte formation.
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  • II. Clinical observation on the acute exacerbation
    Kiku NAKAO, Keiji KINUGASA, Fumimaro TAKAKU, Yasusada MIURA, Yoshito Y ...
    1967 Volume 8 Issue 1 Pages 21-26
    Published: 1967
    Released on J-STAGE: October 20, 2008
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    Incidence of the acute exacerbation has been markedly high when the cases died of such complication as infection were excluded, in the 32 cases of chronic myelogenous leukemia who have been observed until their death in our clinic since 1937.
    Although the incidence was not higher among myleran treated cases as compared to the cases receiving other treatments, among 11 cases who had been treated with myleran and developed the acute exacerbation, 5 cases (45%) showed the signs of the acute exacerbation within 20 months after the establishment of the diagnosis of chronic myelogenous leukemia.
    This percentage was apparently higher than that observed in cases treated with X-irradiation or another chemicals. Therefore, a possibility that the myleran therapy could accelerate the development of the acute exacerbation was speculated from our present study.
    The acute exacerbation tended to occur more frequently in the period of myleran induced remission than in the relapsing phase of chronic myelogenous leukemia.
    Hematological changes suggesting the acute exacerbation occurred first in bone marrows followed by similar changes in peripheral blood. In one case of acute exacerbation, however, an increase in the number of blasts in peripheral blood preceded, and the bone marrow examination did not reveal any signs of acute exacerbation at that time.
    Prodromal signs of the acute exacerbation were arthralgia, bone pains, anemia, and thrombocytopenia. Increase in the serum CRP-titer was also noted in our cases suggesting its diagnostic significance.
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  • Jun KUBONOYA, Isamu UMEZAWA, Atushi HONGO, Hiroshi HASHIMOTO, Michio F ...
    1967 Volume 8 Issue 1 Pages 27-32
    Published: 1967
    Released on J-STAGE: October 20, 2008
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    Experiment was done on 28 cases of blood diseases to determine tissue activator by the method of bone marrow puncture. The results were as follows.
    Bone marrow smear was made by sternal aspiration 0.05 ml of the remaining blood was placed on fibrin plate and the tissue activator was determined after incubating for 4 hours at 37°C.
    1) It was in the hemorrhagic diseases as aplastic anemia, thrombocytopenia, monocytic leukemia, myeloma, lymphosarcoma, etc. that the increase in activator was noticed with standard plate method.
    In these blood diseases increase of plasmin was also observed when the bone marrow blood was applied to the heated plate.
    2) Among the cases where the increase of plasmin and activator in the bone marrow blood was observed, there were some cases where the increase were not found in the venous blood.
    3) There was no relation between nucleated cell count and fibrinolysis. Fibrinolysis increased when thrombocytes were below 5×104/mm3.
    4) Fibrinolysis of bone marrow was inhibited by intravenous injection of t-AMCHA, antiplasmin agent.
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  • Fumio NAGAHAMA, Hiroshi HASEGAWA, Sigeo SUZUKI, Sadao SASAKI, Yoshitak ...
    1967 Volume 8 Issue 1 Pages 33-42
    Published: 1967
    Released on J-STAGE: October 20, 2008
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    Fourty-two cases with leukemia admitted in the First Medical Dept., Hokkaido University Hospital for the past 10 years, were reviewed clinically. 76.3% of them were with acute leukemia.
    Family history revealed 24.8% of the cases had one or more patients in their siblings with malignant tumors other than leukemia.
    Although main initial symptoms or main complaints were fever, bleeding tendency, and generalized fatigue without regards to the types of leukemia, characteristic symptoms in acute myeloblastic leukemia were anemia and changes in the oral mucosa, in chronic myelocytic leukemia, abdominal tumor and in acute lymphoblastic leukemia, they were lymph node swelling and anemia.
    33.8% of the cases with acute myeloblastic leukemia showed leukemic cells more than 90% of the total cells in the peripheral blood, in contrast with chronic myelocytic leukemia in which the leukemic cells occupied less than 30% of the total.
    In the bone marrow, the acute type had a tendency showing remarkable increase in cell count and increase in number of the immature cells, than in the chronic type.
    Thrombocytopenia was the main cause of bleeding tendency, which was the most frequent complication and the main cause of death.
    In the acute myeloblastic leukemia, 50% mortality after combined therapy with steroid and 6 MP was 5.5 months; that was the longest compared with that after other types of therapy.
    Mean duration of survival of the patients with acute myeloblastic leukemia in the last 5 years was 5.2 months, which was 3.1 months longer than that in the first 5 years.
    In chronic myelocytic leukemia 50% mortality was 15 months, but they were too small in number to be significant satistically.
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  • Hisomu YAMAGUCHI, Masahiro MURAYAMA, Kazuo CHIBA, Kiyoshi INOUE
    1967 Volume 8 Issue 1 Pages 43-49
    Published: 1967
    Released on J-STAGE: October 20, 2008
    JOURNAL RESTRICTED ACCESS
    Case 1, 44-year-old housewife, anemic since November 1963. In December 1963, pancytopenia with no immature myeloid cells. No increase in myeloblasts in the bone marrow. After a year's observation without specific treatments she was first admitted to hospital with 10% of myeloblasts in the peripheral blood and the diagnosis of acute myelogenous leukemia was made. Improvement after treatment with 6-MP and prednisolone. In December 26, 1964, she was diagnosed as pleurisy and readmitted. Recovery after two weeks' treatment with antituberculous drugs. She died suddenly on January 15, 1965. Autopsy findings: Acute myelogenous leukemia with the bilateral adrenal cortical hemorrhage.
    Case 2, 59-year-old housewife. Subcutaneous hemorrhage since 1964. In June 1965 diagnosis of aplastic anemia was made. Subjective symptoms subsided temporarily after treatment with prednisolone and blood transfusion. Fever appeared since November 1965, and enterococcus was cultured from sputum, urine and venous blood. Died on January 6, 1966. Autopsy findings: Aplastic anemia, marked hemorrhage in the bilateral adrenal glands, renal pelvis and ureters, and scattersed abscesses in the kidney and liver.
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  • Sumio MIYAZAKI, Tohru KANDA, Takeo FUJIMOTO, Hiromichi TAKE, Thizuru T ...
    1967 Volume 8 Issue 1 Pages 50-53
    Published: 1967
    Released on J-STAGE: October 20, 2008
    JOURNAL RESTRICTED ACCESS
    Deficiency of red cell glucose-6-phosphate dehydrogenase (G-6-PD) is uncommon in Japanese. Only four cases have been reported so far. Recently we have studied two cases of G-6-PD deficiency. One was a ten years old boy who was admitted with the complaints of anemia and jaundice. He was found to have a marked deficiency of erythrocyte G-6-PD, and abnormal level and stability of glutathione. The other case was a nine months old girl who was admitted because of anemia and hemoglobinuria. She was also found to have a remarkable deficiency of erythrocyte G-6-PD, and died eight days after admission. Exposure to toxins or medications was not traced in both cases.
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