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Biomedical subjects

A Deguchi

Publications and source records attributed to A Deguchi.

At least 19 recordsLinked to original sources

Plasma level of IL-1 beta in disseminated intravascular coagulation.

The plasma level of interleukin-1 beta (IL-1 beta) was determined in normal individuals, patients with disseminated intravascular coagulation (DIC), patients in the pre-DIC period (within 7 days before the onset of DIC), and non-DIC patients to examine the relationship between DIC and the plasma IL-1 beta level. The plasma IL-1 beta level was 0-0.085 ng/ml in normal individuals, with little difference being seen according to related age. It was significantly higher in the DIC group (0.19 +/- 0.19 ng/ml) than in the pre-DIC group (0.05 +/- 0.08 ng/ml) or the non-DIC group (0.09 +/- 0.01 ng/ml). The plasma IL-1 beta level was not markedly elevated in leukemia patients, even in the DIC group, but it was significantly increased in the DIC group of solid cancer patients and was generally elevated in patients with sepsis. It was markedly elevated to 0.39 +/- 0.26 ng/ml in patients with organ failure. When mononuclear cells were incubated with lipopolysaccharide, it was found that IL-1 beta, tumor necrosis factor, and tissue factor (TF) were released into the medium, and there was an increase of TF release from endothelial cells incubated with this medium. These results suggest that the increase in IL-1 beta reflected the activation of monocytes and may be an important factor in DIC and its associated organ failure.

Adult

Dynamic fluctuations in blood of thrombin/antithrombin III complex (TAT).

The dynamic fluctuation of thrombin-antithrombin III complex (TAT) was studied in blood obtained during the daytime (at 9 AM, noon, 3 PM), during extracorporeal circulation and during the course of disseminated intravascular coagulation (DIC), to certify whether the level of TAT in blood can reflect the generation of thrombin. In 10 healthy male volunteers, the mean values of TAT (micrograms/liter) were 1.74 (+/- 1.36) at 9 AM, 1.22 (+/- 0.47) at noon, and 1.25 (+/- 0.68) at 3 PM. TAT did not show a daytime fluctuation, unlike fibrinolytic factors. The mean values of TAT in 38 hemodialyzed patients were 4.83 (+/- 2.8) before the initiation, 6.59 (+/- 4.39) in the first hour, and 13.42 (+/- 10.96) at the end of a dialysis session. In 20 patients undergoing open heart surgery, the mean value of TAT was increased during cardiopulmonary bypass (CPB) and decreased with time after the end of surgery. The fibrinopeptide A (FPA) value was increased with TAT during CPB but achieved a maximum level immediately after heparin neutralization by protamine. In 20 patients with DIC, the values of TAT varied from 5.8 to 297 micrograms/liter in the blood at the onset of DIC. In seven of eight patients treated with low-molecular-weight heparin (LMW-H), the values of TAT and FPA were lower 24 hr after LMW-H than before the treatment. These results suggest that the level of TAT in blood reflected the formation of thrombin and could serve as a sensitive parameter of activated coagulation in circulating blood.

Adult

[Plasma thrombomodulin levels in elderly subjects].

Plasma levels of thrombomodulin (TM), fibrinogen, antithrombin III (ATIII) and thrombin ATIII complex (TAT) were studied in healthy young subjects (group A), healthy elderly subjects (group B) and patients with level of TM in group B tended to be higher than that in group A. Levels of TM, fibrinogen and TAT in group C suggested the presence of a hypercoagulable state. When group C was further divided into those with and without diabetes mellitus (DM), the TM level in the former tended to be higher than that in the latter. Furthermore, among the patients with DM, those with diabetic retinopathy showed significantly higher levels of TM than those without retinopathy. Thus, high TM levels indicate the presence of endothelial injury. In groups B and C, TM correlated positively with fibrinogen, and negatively with ATIII, which also indicates that a high TM level is related to a hypercoagulable state. In conclusion, the TM level is considered to be a potential marker of the presence of endothelial injury.

Adult

[Studies on C1 inactivator resistant fibrinolytic activity].

The fibrin lysis activity in the presence of enough quantity of C1 inactivator (C1.INA) is called C1.INA resistant fibrinolytic activity (C1.IRFA). C1.INA inhibits the activation of intrinsic fibrinolysis, therefore C1.IRFA is considered to reflect the extrinsic fibrinolytic activity mainly. We studied the effect of C1.INA using fibrin plate assay on fibrin lysis activity (FLA) and C1.IRFA in normal individuals and pregnant women, and studied the fluctuation of FLA and C1.IRFA during venous occlusion test (VO) or 1-deamino-8-D-arginine vasopressin (DDAVP) administration. After VO or DDAVP administration, the euglobulin lysis time (ELT) was reduced, FLA increased and C1.IRFA also increased. The increase in C1.IRFA accounted for most of the increase in FLA. Therefore, the increased fibrinolytic activity during VO or DDAVP administration is due to extrinsic fibrinolytic activity. In the pregnant women, the fibrinolytic activity was decreased during pregnancy and the low fibrinolytic activity is suggested to be involved in the low extrinsic fibrinolytic activity. The measurement of C1.IRFA is considered to be useful.

Complement C1 Inactivator Proteins

[Measurement of FDP-D-dimer in DIC and pre-DIC].

We measured FDP-D-dimer value in disseminated intravascular coagulation (DIC), pre-DIC (within 7 days before onset of DIC) and suspected DIC (not completely satisfying the DIC criteria). The level of FDP in many patients with pre-DIC was normal, but the level of FDP-D-dimer in most patients with pre-DIC was increased. FDP was markedly increased one day before onset of DIC but FDP-D-dimer was increased 7 days before the onset. FDP was significantly higher in DIC than in pre-DIC, but it was not higher in pre-DIC than in suspected DIC. In patients with hematological malignancies, FDP-D-dimer was statistically higher in DIC than in pre-DIC and in pre-DIC than in suspected DIC, but in non-hematological malignancies, FDP-D-dimer was not significantly different among the 3 groups. The peak increase of FDP-D-dimer was noted at a DIC score of 7 or 8. The correlation of FDP-D-dimer with FDP was better in pre-DIC than in DIC, and the ratio of FDP-D-dimer to FDP was higher in pre-DIC. FDP-D-dimer was not correlated with fibrinopeptide A or B beta 15-42 in pre-DIC. It is speculated that pre-DIC is a hypercoagulable state and FDP-D-dimer may be useful to the diagnosis of pre-DIC.

Disseminated Intravascular Coagulation

[Elevated levels of cytokines in plasma from patients with disseminated intravascular coagulation].

We measured blood concentrations of tumor necrosis factor (TNF), interleukin-1 beta (IL 1-beta), soluble interleukin 2 receptor (s-IL 2r), and interferon alpha (IFN alpha) in 30 patients with disseminated intravascular coagulation (DIC) and compared the results to those of 25 patients without DIC. Plasma levels of TNF, IL 1-beta, and s-IL 2r were higher in patients with DIC than in those without DIC. In one case of acute promyelocytic leukemia, plasma levels of TNF and IL-1 beta increased at the onset of DIC but decreased upon DIC improvement. These findings suggest that activation of the immune system is involved in the development of DIC. However, these concentrations were not markedly increased in patients with leukemia, although blood TNF and s-IL 2 r were markedly elevated in patients with solid cancers. Especially in patients with solid cancers, hyperactivation of the immune system may cause an increase in blood TNF and IL-1 beta and the development of DIC.

Cytokines

[Plasminogen activator in leukemic cell homogenate].

We examined fibrinolytic substances in homogenate of leukemic cells, normal granulocyte or mononuclear cells fraction. Plasminogen activators (PA) were significantly low in normal cells, but they were slightly increased in lymphoblastic leukemia cells and markedly increased in myeloblastic leukemia cells. In almost leukemic cells homogenate, the antigen ratio of tissue type PA (t-PA)/urokinase type PA (u-PA) was about 2.0. In especially AMMoL and AMoL, PA activity had discrepancy between euglobulin lysis time and amidolytic assay using chromogenic substrate. As PA inhibitor (PAI)-II was markedly increased in them. PAI might effect the PA assay. PA activity of leukemic cells homogenate was similar to that without t-PA stimulator and leukemic cells homogenate significantly stimulated t-PA. As both PA activity and antigen were statistically increased in leukemic cells homogenate of patient with disseminated intravascular coagulation (DIC), PA and PA stimulator in leukemic cell might play an important role in hypofibrinogenemia or DIC.

Afibrinogenemia

[Availability of DDAVP in hemostasis control for the breast tumor resection in a patient with thrombasthenia (type II)].

We reported a 33-year-old woman with thrombasthenia (type II) in whom 1-deamino-8-D-arginine vasopressin (DDAVP) was available for the hemostasis control during breast tumor resection. She has had recurrent nasal bleeding and purpura since 2 years old. On the first admission to our hospital because of hematuria at 18 years old, she was diagnosed as thrombasthenia (type II) from hemostatic studies. At 20 years old, she had a healthy baby by the cesarean section with transfusion of fresh blood and platelet concentrates. On the 5th admission for the breast tumor resection, defect of glycoprotein II b-III a of her platelets was confirmed by using SDS gel electrophoresis. Recently, there are some reports on availability of DDAVP for hemostatic control in platelet dysfunction of various etiologies as well as mild hemophilia and von Willebrand disease. So, DDAVP (0.4 microgram/kg) was used for hemostasis control. After 1 hour, the bleeding time was shortened from over 10 to 4 min, platelet adhesiveness to glass beads increased from 1.8 to 37%. Furthermore, the levels of Ristocetin cofactor and von Willebrand factor antigen (especially large multimer) also increased. But platelet aggregation with various inducers remained unchanged before and after infusion. Breast tumor (fibroadenoma) resection.

Adult

Coagulation and fibrinolysis in patients with chronic renal failure on maintenance hemodialysis.

Alteration of the coagulation-fibrinolysis system was examined in patients on maintenance hemodialysis. The mean values of fibrinogen, factor V, factor VII, factor VIII, vWF (activity and antigen), factor IX and factor XI were significantly higher in these patients than in control subjects (p less than 0.01), but factor XII alone was significantly lower. Fibrinolytic parameters (euglobulin lysis time, fibrin plate lysis, fibrin degradation products and alpha 2-plasmin inhibitor-plasmin complex) suggested a hyperfibrinolytic state and plasmin generation in the patients' circulation. These findings suggest that the alteration of the coagulation-fibrinolysis system is aggravated by repeated hemodialysis, either by the influence of the dialyzer itself or heparin.

Adult

Anticoagulant activity in cell homogenate of adult T cell leukemia.

The hemostatic abnormality in 18 patients with adult T cell leukemia (ATL) was studied. Activated partial thromboplastin time (APTT) was slightly prolonged and prekallikrein activity was markedly low in these patients. The leukemic cell homogenate from these patients prolonged the recalcification time (RCT) of normal plasma; homogenates containing more than 3 x 10(3) cells/microliter prolonged it, although a lower cell concentration shortened it. The crude anticoagulant fraction from the gel filtration, with a molecular weight of about 34,000, prolonged RCT. The crude anticoagulant did not affect prothrombin time (PT), thrombin activity or activated X activity at any concentration, but prolonged the contact activation test, inhibited the activation of prekallikrein and prolonged RCT of Fletcher trait, Fitzgerald trait and F XII deficient plasma. These effects of ATL cell homogenate were stronger on platelet poor plasma than on platelet rich plasma. Although ATL cells had low procoagulant activity, increase of leukemic cells made anticoagulant activity predominant, might be the cause of hemostatic abnormality or amplify the bleeding tendency in patients with ATL.

Adult