Thromboangiitis obliterans (TAO) was introduced by Leo Buerger as an isolated desease of chronic arterial obstructive desease (1908).
Recently, some investigators claimed that the desease bydesclibed Buerger is indistinguishable from arteri-osclirosis obliterans (ASO) or other peripheral arterial thrombosis. However, It is a fact that most cases are due to idiopathic peripheral arterial thrombosis, and it s certain etiology and pathogeneris are unknown. Present study is performed to investigate into changes of blood coagulation on TAO and ASO.
Clinical materials and methods
Blood coagulability was studied on 12 cases of TAO, 10 cases of ASO, 12 normal persons as control.
Blood samples were obtained by venous puncture to carry out blood test with respect to RBC, Ht., platelet count, bleeding time, prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen level and FDP. Platelet adhesive rate was examined by modified method of Hellem II.
Results and discussion
There were no increase in RBC, Ht., platelet count, bleeding time, PT and PTT. Fibrinogen level was slightly increased on TAO. Platelet adhesive rate was increased on TAO. There were no relation between increased platelet adhesive rate and fibrinogen level. It is indicated that TAO is primarily a desease of the blood vessels rather than of the blood itself. However, increased platelet adhesive rate may be an important factor of secondary thrombus formation in this desease. FDP was increased in two of twelve cases of TAO and three of ten cases of ASO. Platelet adhesive rate markedly increased on TAO and ASO except the cases which FDP was increased. Therefore, it is necessary to consider FDP level when platelet adhesive rate is examined.

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Since the first successful treatment by Öttgen in 1967, L-Asparagi vase has become one of the most popularly used antileukemic drugs in the world. The effectiveness of the drug upon acute leukemia, especially that of childhood, and lymp-hosarcoma is widely accepted. On the other hand, however, several side effects have also been reported, which include toxicity to liver and pancreas, disturbance of bloodcoagulation and thrombosis of the brain. We reported here a case of pulmonary infarction probably due to L-Asparaginase treatment.
S. N., a Japanese boy, born on April 27, 1960 was admitted to Hokkaido University Hospital on September 6, 1971 because of acute myelogenous leukemia. Onset of his disease was middle of August, 1971, when he had recurrent fever and lassitude. with the combination chemotherapy of Prednisolone, Daunomycin, Vincristine, he got complete remission and was allowed to go home on December 29, 1971. After about one month's duration of complete remission he relapsed.
On his second admission to our clinic on Feb. 18, 1972. hemanalysis showed moderate anemia (RBC 290×10⁴/mm³), slight increase of WBC (16, 000/mm³) with highpercentage of myeloblasts (72%) and decreased platelet count (110, 000mm³) In the bone marrow smears myeloblasts occupied 72% of whole nucleated cells. No splenomegaly was observed. CRP 3mm. ESR 22mm (1hr.), 52mm (2hrs.). After ineffective trials of several kinds of combination chemotherapy with Prednisolone, Daunomycin, Ara-C, Vincristine and Methotrexate, intravenous administration of L-Asparaginase (200U/Kg/day) was begun on June 1, 1972. On the third day of the treatment high fever subsided and the percentage of myeloblast in the peripheral blood smear decreased remarkably, but on the eighth day thrombophlebitis appeared on the back of the left foot. Three days late he began to complain of serious pain in the back on respiration and in the left arm. Next day he felt his left arm numb and blood pressure on the same arm revealed marked decrease. Inspite of the Urokinase therapy the patient died on July 11, 1972.
Autopsy revealed hemorrhagic infarct of bilateral lungs, fatty degeneration of pancreas and liver. In the treatment with L-Asparaginase, we advise careful consideration of the side effects of this drug in relation to the condition of the patients.

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