Factor X antigen were investigated in seven patients with congenital factor X deficiency by Laurell's method and enzyme linked immunosorbent assay (ELISA).
Five patients had less than 0.1U/ml by Laurell's method were defined as CRM^-. One patient belonged to CRM^R showing 0.3U/ml, and another one with 0.54U/ml was considered as CRM⁺.
When factor X antigen was assayed by ELISA, 2 of 5 CRM^- patients had less than 0.001U/ml, but the rest ones showed between 0.033 and 0.065U/ml.
Patients with CRM^R and CRM⁺ showed a markedly prolonged Stypven clotting time. Therefore, it was considered that these two patients may have other than factor X Friuli disorder.
These findings suggested that there may be genetic heterogeneity in congenital factor X deficiency.

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A single dose of endotoxin caused an increase in cytotoxic damages of bone marrow cells, an increase in procoagulant activity (p-activity) of the cells, decrease in nucleated cell counts in marrow due to the migration into circulation, and an increase in serum FDP levels. The increase in cytotoxicity of bone marrow cells correlated well with the increase in p-activity of the cells. Most of the p-activity was found in the membrane fragments in the cells and p-activity was thought to be tissue thromboplastin.
Endotoxin induced an increase in p-activity in monocytes (6.9-fold) and granulocytes (2.9-fold).
The ddY mice were more responsive than C3H/He mice as to increase in cytotoxicity and also a decrease in nucleated cell counts in marrow. In contrast, none of these reactions were induced in C3H/HeJ mice. Endotoxin caused strain-dependent production of p-activity in mice. ddY mice and C3H/He mice responded to endotoxin with 7.0 and 2.9-fold increase of p-activity in whole nucleated bone marrow cells. In contrast, C3H/HeJ mice did not respond to endotoxin. Endotoxin also caused strain-dependent increase in serum FDP levels. ddY mice were more responsive than C3H/He mice, however, no increase in FDP was found in C3H/HeJ mice even by injection of 500μg of endotoxin. In C3H/HeJ mice, none of three endotoxin preparations which contained different amounts of protein could increase in serum FDP levels.
In endotoxemia, bone marrow cells migrate to circulation, therefore, the cells with an enhanced p-activity would participate in the manifestation of DIC. This possibility is further supported from the findings that endotoxin induced strain-dependent responses as to all of the 4 parameters and that these parameters correlated well with each other.

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This study was intended to clarify the effectiveness of heparin (Hp) on DIC and to establish successful Hp treatment. Tentative diagnostic criteria for experimental DIC (DIC≥7 points) were proposed and severe DIC was induced in mongrel dogs by the infusion of 10.0 and 12.5mg/kg/3hrs of tissue thromboplastin (T. Tpl) with the score of 7.3±2.9 and 11.2±1.2 respectively. When each of 100, 200 and 300IU/kg of Hp was administered by drip infusion with T. Tpl, these aggravations were inhibited according to the dose of Hp injected with the varying score from 0.0±0.0 to 5.3±2.9. The relation of APTT to plasma Hp concentration (PHC) differed greately from case to case. When successful inhibitions of DIC were not obtained, PHC revealed low levels and APTT prolonged markedly. When Hp therapy was achieved quite effectively with no side effects, PHC revealed 1.14±0.14IU/ml and APTT did not show any remarkable prolongation. When hemorrhagic diatheses due to Hp appeared PHC demonstrated 1.56±0.26IU/ml and APTT prolonged more than 5 times of normal levels. So, the inhibitory effects of Hp were not always estimated by the prolongation of APTT and the indiscriminate monitoring of Hp therapy by APTTalone as used was inadequate. In conclusion, sufficient dose of Hp had to be administered up to the range of about 1.2IU/ml of PHC (APTT within 5 fold prolongation of normal values) and it should be controlled by the combination of APTT and PHC for successful Hp treatment. Antithrombotic effects of Hp were closely reflected in the following indices as FPA, Fbg, plat and FDP and PHC changed significantly, in spite of the same dose of Hp administered, according to the effects of Hp and to the dose of T. Tpl. However, AT III demonstrated no significant differences in any groups regardless of the use or the effects of Hp. These results got us to consider further investigations upon the functional mechanism of Hp, AT III and thrombin.

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It is well known that the thrombotic episodes are observed not at childhood but at adulthood, in the cases with antithrombin III (AT III) deficiency or its abnormality. To clarify the causes of these complications, it is necessary to investigate on the interaction between AT III and each factors in the presence of heparin.
Firstly, we have purified heparin cofactor II (HC II) from human plasma by own method and investigated on its activity compared with that of AT III. Results were as follows:
(1) We could obtain HC II by using ammonium sulfate fractionation, heparin-Sepharose and DEAE-Sepharose column chromatography, with less time consume and higher yield; recovery rate 8%, specific activity 1, 200units/mg and purification fold 840-times.
(2) Both AT III and HC II showed antithrombin activity in the presence of heparin, but only HC II showed antithrombin activity in the presence of dermatan sulfate. This antithrombin activity of HC II and dermatan sulfate was not affected by the co-existence of AT III. Therefore, it would be possible to estimate HC II activity in the human plasma, by using dermatan sulfate.

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Levels of VIIIR: AG and plasminogen activator (PA) in the venous blood before and after 5 minutes' tourniquet were measured to evaluate function of the vascular endothelial cells in 25 patients with acute myocardial infarction, 17 patients with cerebral infarction (patient group) and 26 healthy subjects (control group). Mean level of VIIIR: AG in the venous blood before tourniquet was significantly higher and that of PA was significantly lower in these patients, as compared with control group. After 5 minutes' tourniquet, mean amount of VIIIR: AG released was significantly higher in patient group than in control group, although no difference was observed in PA release. In patients complicating diabetes mellitus or hypertention, more VIIIR: AG was released than in patients without these complications. In patints complicating hypertention, PA release was significantly lower than in patients without the complication. The significance of the results obtained was discussed.

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We attempted to elucidate the cause of the shock during the treatment of the patients with esophageal varices by thrombin using endoscopic embolization. Shock was occured a few minutes after infusion of thrombin, but general condition was immediately recovered without any complication.
On the other hand the initial sign of disseminated intravascular coagulation (DIC) was observed 30min. later. Then DIC reached to maximum 180min. later, improved without any treatment on the next day and recovered completely on 7th day. In the relationship between shock and DIC, the shock was recognized at the earliest stage of DIC.

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Plasma fibrinopeptide A (FPA), Bβ 15-42 and bradykinin (BK) concentrations were determined in 46 patients with glomerulonephritis and the nephrotic syndrome by radioimmunoassay. An increase in plasma FPA, Bβ 15-42 and BK was noted in patients. Intravascular coagulation with subsequent fibrinolysis and activation of kinin system may occur in patients. A positive correlation was found between Bβ 15-42 and BUN or serum creatinine concentration, suggesting that plasma Bβ 15-42 is influenced not only by plasmin action, but also by renal dysfunction.

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We have studied on some Wakan Yakus (traditional herbal drugs) from the viewpoint of blood coagulation, and found that Gaiyoh (Artemisiae Folium) had the strongest anti-coagulation and anti-fibrinolytic effects.
In this paper, we reported the characterization, and purification of Gaiyoh. Inhibitory effects of Gaiyoh were assayed by the synthetic substrates; S-2238 (for thrombin) and S-2251 (for plasmin). Gaiyoh inhibited thrombin and plasmin does-dependently. The effect to thrombin was more slowly but strongly than that to plasmin. Both of the inhibitory effects were observed to be competitive on Lineweaver-Burk plot.
Gaiyoh contained two or more inhibitory components to the blood coagulation analyzed by Sephadex G-50 gel filtration. Since both of them were able to be eluted by acidic ethanol solution (lN HCl:EtOH=1:1) on DEAE-Sepharose column, those components had acid groups in their molecules.

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Recently, it has been pointed out that platelets play a role in thrombosis and atherosclerosis, and attention has also been focused on the relation between platelets and polyvalent unsaturated fatty acids. Therefore, arachidonic acid (AA), eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and other fatty acids in the plasma of cases of thrombotic disease (TD) were analyzed.
The conclusions were as follows:
(1) The EPA/AA ratio in the TD group was 0.40±0.22 (M±SD) which was significantly lower than that of the control group (0.87±0.48) (P≤0.01). (2) The DHA/AA ratio in the TD group was 0.77±0.20, less than the 1.12±0.40 value of the control group.
From these results, it is assumed that the low values of the EPA/AA and DHA/AA ratios in the plasma are risk factors in the onset or worsening of thrombotic disease.

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Membrane phospholipid turnover in human platelets activated by tumor promoting agent (TPA, 12-o-tetradecanoylphorbol-13-acetate) was investigated. Dispite the induction of irreversible aggregation and serotonin release, TPA enhanced neither the production of 1, 2-diacylglycerol (DG) and phosphatidic acid (PA) nor the incorporation of [³²P] phosphate into phosphatidylinositol (PI) and PA, indicating the failure to enhance PI-turnover. Stimulation of phospholipase A₂, monitored by the production of lysophospholipids and arachidonic acid liberation, was not observed upon activation of platelets by TPA. These results which are much different from those observed in thrombin-activated platelets appear to suggest that the turnover in membrane phospholipids is not required for process of platlet activation by TPA. It was also found that TPA-induced Ca²⁺ influx was enhanced by ionophore A 23187 without further producing serotonin release.

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PAF-induced platelet aggregation and the effect of anti-platelet drugs (aspirin and ticlopidine) on PAF-induced platelet aggregation were investigated in various diseases and normal volunteers to reveal the role of PAF in human platelet aggregation.
In various diseases, there was a close correlation between PAF-induced platelet aggregation and ADP-induced aggregation (Fig. 1). In a case of primary thrombocytemia, PAF-induced aggregation was remotely correlated with ADP-induced aggregation (Fig. 1).
In thrombotic diseases, PAF-induced aggregation (the maximum aggregation rate), as well as ADP, was not remarkably affected by the aministration of aspirin (250-330mg/day), but was affected by ticlopidine (300-600mg/day). Collagen-induced aggregation which was inhibited by aspirin, was not remarkably affected by ticlopidine.
In vivo, the administration of aspirin (1g) inhibited the second wave of PAF-induced aggregation and ATP secretion. But these inhibition was observed only in the restricted concentration of PAF.
In vitro, aspirin did not inhibit PAF-induced aggregation and ATP secretion (Fig. 2).
These results suggest that, in human platelet aggregation, PAF plays a role different from ADP and induces the aggregation mainly via the pathway different from the cyclooxygenase pathway.

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We have examined a quantitative relationship between platelet aggregation and release reaction using 20 subjects including healthy women and gynecological patients. We have determined the released amount of ATP on luminescence curve which was observed during platelet aggregation using a lumi-aggregometer. The peak of this curve was measured and the released amount of ATP was calculated. Because the luminescence curve declined with time course, the amount of ATP was corrected with a comparison to standard luminescence curve which was obtained by an addition of 10μM of authentic ATP. A slope in luminescence curve was also calculated with correction against time course, and a lag time before the onset of luminescence was measured. The above three values were compared against the intensity of platelet aggregation. The stimulants were as follows; 1, 3 and 10μM ADP, 0.1, 1 and 10μg/ml of adrenaline and 1, 3 and 10μg/ml of collagen.
Significant positive correlations were observed between the intensities of 5 minutes aggregation and the amounts of released ATP induced by the above reagents except 10μg/ml of collagen. Furthermore, closer correlations were obtained between the intensities of 5 minutes aggregation and logarithmic amounts of released ATP. Close correlations were also observed when the intensities of 5 minutes aggregation was compared against slopes in ATP release curves induced by ADP and collagen except in high concentrations, and lag times in ATP release induced by adrenaline except in low concentration. ADP and adrenaline in low concentrations did not induce platelet release reaction in quite a number of cases. According to the results, 3μM ADP, 1μg/ml of adrenaline and 1 and 3μg/ml of collagen were deemed suitable as stimulants to observe the relationship between aggregation and release reaction of platelets.

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It was reported that platelet aggregation was enhanced after surgical operation. The phenomenon was related to an increase of appearance rate of secondary aggregation. In a previous report, the author devised a method to compare an intensity of platelet aggregation and an amount of released ATP from platelets using a lumi-aggregometer. Using this method, the author has observed changes in aggregation and release reaction of platelets collected from 16 gynecological patients before and 1 day, 1 week and 2 weeks after laparotomy. Three μM ADP, 1μg/ml of adrenaline and 3μg/ml of collagen were used as stimulants. At 1 day and 1 week after laparotomy, primary and 5 minutes aggregation were intensified with statistical significances. The released amount of ATP from platelets increased significantly (P<0.05-0.01) at 1 day after operation when platelets were stimulated with ADP and collagen. The slope of luminescence curve in release reaction showed steeper curve when compared with that before laparotomy, and the lag time of release reaction showed shorter time, after laparotomy. These findings suggested that ATP was released more rapidly and early from platelets under the influence of surgical stress. Before laparotomy, there were good positive correlations between the intensities of 5 minutes aggregation and the amounts of released ATP induced by above reagents. But at 1 day after operation, the correlation coefficients showed lower values, suggesting decrease in platelet ATP content and/or change in platelet population. In conclusion, it was found that platelet aggregation was intensified and platelet ATP release reaction was enhanced simultaneously after surgical operation.

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Some antineoplastic agents inhibit platelet aggregation. In this study, the effects of Daunorubicin (DNR) and Doxorubicin (DXR) on platelet adhesiveness were investigated by the glass bead column method, a method of adhesiveness to Collagen-Sepharose and Baumgartner's method. And molphology of these adherent platelets were observed by electron microscope.
Also, the influence of the combination of antineoplastic agents and Dilazep (DZP), or dl-α-Tocopherol (V. E) was investigated Baumgartner's method.
In the glass bead column method, platelet retention rate was significantly reduced with DNR (10^-4 moles f. c) and DXR (10^-4 moles f, c). Scanning electron microscopy revealed that adherent platelets on the glass surface extended pseudopds and were spread out. However, the number of aggregated platelets was reduced. In the method of adhesiveness to Collagen-Sepharose, no change in morphology of adherent platelets to collagen fibers was seen as compared with the controls. The effect of DNR or DXR in this method was not significant. It was demonstrated that platelet adhesion and aggregation are inhibited by DNR and DXR, using Baumgartner's method. They inhibited spreading out of adherent platelets at the subendothelial surface, and DNR also inhibited extending pseudopods. By transmission electronmicroscopic findings, adherent platelets at the subendothelial surface of rabbit aorta were observed to retain the granules and the ring of microtubules in the marginal zone.
The effect of combination of antineoplastic agents with DZP or V. E was not significant.

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Fibronectin (Fn.) is widely distributed in human tissue and plasma. The ability of the Reticulo-endothelial system (RES) to retain normal phagocytic activity has been directly correlated with plasma levels of Fn.
It is the purpose of this study to determine the levels of Plasma Fn., platelet associated (PA) Fn. and IgG in malignancy and sepsis.
PA-IgG and PA-Fn. were measured by immunoperoxidase technique.
Plasma levels of Fn. were significantly decreased in malignancy and sepsis. PA-IgG and PA-Fn. levels were significantly elevated in the advanced stage of these diseases. Thus, PA-IgG and PA-Fn. levels showed increases in parallel with the decrease in plasma Fn., both of which were normalized in conjunction with the remission of these diseases.
It was concluded from these findings that plasma Fn. is depleted in patients with advanced malignancy and sepsis. These diseases are almost accompanied by DIC. This may be due to the removal of fibrin aggregates from blood by the RES. These state of thrombin stimulation are suggested by the levels of increased PA-IgG and PA-Fn.

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The circulating platelets are generally considered to be affected and be rapidly cleared from circulation by autoantibody to the platelets in idiopathic thrombocytopenic purpura (ITP). This study was aimed to examine the platelet shape in ITP to obtain a further information on such platelet-antibody interaction.
30 adult patients with chronic type of ITP and 2 with Evans syndrome and 5 patients with other hematological disorders who had received repeated platelet transfusions were examined. The circulating platelet shape was examined after fixing the platelets in glutaraldehyde according to our method (3). Inactivated ACD-A plasma of some patients was examined for whether it had a platelet shape changing factor (PSCF) when incubated with normal discoid platelets. Results on 26 untreated patients showed a significant spherification and pseudopod formation of the platelets as suggested in a preliminary paper (3) and further relative increases of bipolar forms and irregular forms. Analysis on 32 untreated or treated patients has revealed that the deformation of the platelets well postively correlated to the decrease in platelet counts while not to PBIgG levels, which were not correlated to platelet counts. PSCF was demonstrated in 3 out of 6 cases of ITP, 2 of Evans syndrome, and 3 out of 5 patients with repeated platelet transfusions. A monoclonal antibody to glycoprotein IIbIII caused no siginificant deformation of the native platelets. Further study is necessary to determine the nature of PSCF (antibody-related substances?). In conclusion the circulating platelets were deformed probably by some plasma factor (s) in ITP and Evans syndrome.

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The effects of ticlopidine (TC) and aspirin (ASA) on the platelet aggregation were studied in ten healthy male volunteers. All subjects received oral TC (300mg/day in three divided doses) for the first three weeks. Following drug free interval of two weeks period, ASA (300mg/day once a day) was administered orally for the next three weeks. Blood samples for platelet aggregation study were withdrawn in the morning on days before drug administration, 2, 4, 7, 14, and 21 days on drug, and 3 days after discontinuance of the drugs.
The results from this study suggested as follows; (1) Both TC and ASA revealed almost equal inhibitory effects on platelet aggregation induced by collagen and epinephrine, (2) TC, however, had the more potent inhibitory effect on platelet aggregation indued by ADP than that of ASA in healthy volunteers, (3) The inhibitory effects of TC on platelet aggregtion was decreased at the 4th day during administration of the drug, (4) In TC groups, the inhibitory effect was markedly reduced at 3 days after discontinuance of the drug.

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Coronary thrombolysis or percutaneous transluminal coronary recanalization (PTCR) has recently been established as a treatment of acute myocardial infarction (AMI). This study was performed to elucidate the changes in plasma levels of β-thromboglobulin (β-TG), fibrinopeptides and prostaglandins before and after the PTCR. Twenty-six AMI patients within 6 hours after its onset, 53±12.1 (SD) years of age were subjected for the PTCR using with urokinase (680, 000±124, 000 IU). Eleven patients among 26 undergone PTCR were selected for the determination of plasma levels of β-TG, thromboxane B₂ (TXB₂), 6-keto-PGF_1α, fibrinopeptide A (FpA) and FpBβ 15-42 before and serially after PTCR.
Successful recanalization was obtained in 18 out of 26 cases (69.2%). β-TG was elevated both in successful and unsuccessful cases suggesting platelet activation in AMI. Those who achieved good recanalization demonstrated a sharp rise of β-TG probably due to wash-out phenomenon shortly after the recanalization. β-TG returned to the normal range within 1-7 days (Fig. 1) TXB₂ was increased in both groups, higher in the recanalized group and gradually returned to the normal range in several days. Two out of 5 recanalized cases demonstrated wash-out phenomenon. 6-keto-PGF_1α levels were also increased in AMI which became normalized in a day. FpA was increased in both groups in the acute stage of AMI suggesting the hypercoagulable state and gradually decreased to the normal range. FpBβ made a peak at the termination of PTCR, higher in the recanalized cases suggesting better fibrinolysis, and rapidly decreased in a day. A typical case of successful PTCR was shown in Figure 2. Marked rises in β-TG and TXB₂ shortly after PTCR may indicate recanalization of the obstructed coronary artery.

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Six cases of deep vein thrombosis were treated with intravenous batroxobin, lysyl-plasminogen and urokinase following thrombectomy by Fogarty catheter (Table 1).
Plasma fibrinogen, plasminogen and α₂-plasmin inhibitor were markedly reduced by 10 BU of batroxobin. Although fibrinolytic activity measured by plasminogen-free fibrin plate method was detected in 25% of the blood samples taken after 60mg of lysyl-plasminogen infusion following batroxobin administration, no activity was induced by urokinase given after lysyl-plasminogen administration. In other patients given lysyl-plasminogen administration more than 12 hours after batroxobin administration, a slight increase in plasma plasminogen was observed, and fibrinolytic activity was strongly induced by 120, 000 IU of urokinase (Table 2).
Complete or partial patency of reconstructed deep veins was recognized by venography performed 6 months after operation.
These results suggested that even moderate dosages of uorkinase can induce fibrinolytic activity under conditions of low α₂-plasmin inhibitor levels cused by batroxobin and additional lysyl-plasminogen.

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Vascular plasminogen activator (PA) is unstable and previous attempts at isolating it from blood have been hindered by the difficulty in separation it from inhibitors and other proteins. We studied its charactor by using a Fibrin/Celite column chromatography proposed by Husain et al. PA was partially purified by taking advantage of its strong binding to fibrin. The fraction eluted by 0.2M arginine showed plasminogen activator activity on fibrin plates. Determination of amidolytic activities on chromogenic substrate S-2251 (Kabi) in the presence of plasminogen and also on S-2288 were made. PA fraction showed high activities on them which were not influenced by Trasyrol, Soybean trypsin inhibitor, AT-III and Heparin. Plasminogen and plasmin inhibitors were not detected in the PA fraction but a small amount of factor XII, prekallikrein and high molecular weight kininogen were contaminated. By the method of SDS-PAGE, three bands, molecular weight 140, 000, 80, 000 and 66, 000 have been shown in the fraction and the main activity of PA was brought about by the protein corresponding to the band of molecular weight of 80, 000. Nevertheless the breakthrough also showed a high fibrinolytic activity which contained plasmin inhibitors. It seems that a different type of PA is present in the breakthrough.

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Urokinase (UK), a human urinary plasminogen activator, was modified chemically by a covalent attachment of methoxypolyethylene glycol (PEG) #5, 000 to its lysine residues after activation of PEG with cyanuric chloride. For the evaluation of thrombolytic activity of PEG-modified UK (PEG-UK), a novel experimental thrombosis model was developed in a dog's artery.
The femoral artery of an anesthetized dog was exposed and transfusion catheter was fixed on its branch, and then the distal part was clamped at a distance of 2cm, washed with saline, and dried with oxygen to cause injury on intima. Thrombus was formed by an injection of both a fibrinogen solution and a thrombin solution into the clamped artery and thrombus formation was confirmed angiographically after removal of the clamps.
Using this model, a strong thrombolytic activity of PEG-UK was shown by periodical angiographies when administered from the catheter. However, native UK couldn't dissolve the thrombus at a dose of 100, 000iu/dog. The serum FDP level of the PEG-UK reached to 1, 280μg/ml, while that of the native UK treated dog stayed at 20μg/ml.

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The effect of cardiopulmonary bypass (CPB) on the production of prostacyclin and thromboxane was studied. Sixteen patients, who had undergone CPB with bubble oxygenator, roller pump and moderate hypothermia, were examined. We collected serial plasma samples and assayed them for thromboxane B₂ (TXB₂) and 6-keto-Prostaglandin F_1α (6-keto-PGF_1α) by radioimmunoassay, the main metabolites of thromboxane A₂ and prostacyclin respectively. And twelve mongolian dogs were studied experimentally. They had undergone normothermic CPB with bubble oxygenator and roller pump for 120 minutes. Serial plasma samples were assayed with same method.
In the clinical study, TXB₂ and 6-keto-PGF_1α increased significantly during CPB. The ratio of two prostanoids (6-keto-PGF_1α/TXB₂) did not changed in many of the cases. In experimental study of dogs, TXB₂ increased significantly on the commencement of CPB. 6-keto-PGF_1α increased gradually and continuously during CPB. The ratio of two prostanoids (6-keto-PGF_1α/TXB₂) elevated at the post CPB phase as a result. 6-keto-PGF_1α did not increased in three clinical cases despite of elevated TXB₂. These cases are not ideal from the view point of prostanoid balance during CPB.

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Although pulmonary thromboembolism is seldom seen in Japan, its incidence has been increasing.
We experienced a case of atypical pulmonary embolism, which showed diffuse multiple perfusion defects on lung scanning and was treated with high dose of urokinase (480, 000units for 1hour, 240, 000units/hour for 18hours) followed by heparin (10, 000units/day). The therapy was clinically effective and recovery of perfusion area was recognised by lung scanning. The therapy was done according to NIH protocol.
After this episode the patient repeatedly developed severe dyspnea and died three months after the first urokinase therapy. Clinical diagnoses were lymphocytosis (B cell) in peripheral blood with polyclonal hypergammaglobulinemia and plasmocytosis in bone marrow. Autopsy findings showed primary pulmonary hypertension, hypertrophic right ventricle, pulmonary arterial obstructions distal from arterioles where lymphocytic infiltration was peculiarly noted.
We examined changes in coagulation and fibrinolysis parameters of this patient. After urokinase administration, α₂-plasmin inhibitor activity decreased to 15.5%, and plasminogen activity also decreased to 46.5%. They returned to normal in 2 or 3 days after cessation of urokinase. Antithrombin III and α₂-macroglobulin of the patient were half of normal and all factors in complement system were markedly decreased, which appeared to be related to the nature of the disease itself. Activites of coagulation factors including factors II, V, VIII:C, X, XII decreased, but retuned to normal rapidly.

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