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At least 1,405 records · Page 78Linked to original sources
PubMed1990

[Acquired dysfibrinogenemia in a child in the course of a liver disease].

This report documents the results of coagulation studies in a 15-year old boy with hepatic disease of possibly autoimmune origin. Thrombin- and reptilase clotting times were prolonged. The results of fibrinogen determinations with different methods (heat precipitation, kinetic assay according to Clauss) lead to the assumption of a qualitative anomaly of fibrinogen (dysfibrinogenaemia). Investigations with purified fibrinogens from the patient and a healthy control confirmed this assumption. The thrombin clotting time of purified fibrinogen from the patient was clearly prolonged in comparison to the purified fibrinogen from a healthy control. The fibrin monomers of the patient exhibited impaired polymerization. No structural abnormalities were detected by electrophoretic techniques, particularly the thrombin-induced release of fibrinopeptides was found to be normal. The coagulation abnormalities resolved after glucocorticoid administration.

Adolescent↗
PubMed1990

[Transient dysfibrinogenemia and cerebral thrombosis following remission induction therapy for acute lymphoblastic leukemia].

A 38-year-old female with acute lymphoblastic leukemia developed monoplegia of the left upper extremity following chemotherapy for remission induction consisting of vincristine, prednisolone, cyclophosphamide, adriamycin and methotrexate. Hemorrhagic infarction due to thrombosis of the right cortical vein was diagnosed by brain images using computed tomography and magnetic resonance imaging in addition to the clinical course. At this time, a plasma level of fibrinogen measured by the thrombin time method had decreased to 84 mg/dl, while its antigenicity was 276 mg/dl. There was no evidence of activation of the blood coagulation and fibrinolysis system nor of abnormal liver function. A mixing test with normal plasma disclosed the absence of an inhibitory factor against fibrin polymerization in her plasma. Fibrinogen levels as assessed by the thrombin time method recovered to the antigenicity level one and half months later. The discrepancy between the activity and antigenicity of fibrinogen indicated the occurrence of acquired dysfibrinogenemia, probably induced by antileukemic agents. Thus, it is suggested that dysfibrinogenemia is a possible cause of cerebral thrombosis in this patient.

Adult↗
PubMed1990

[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↗
PubMed1989

Congenital afibrinogenaemia.

A case of congenital afibrinogenaemia in a young female child is described. She had haemorrhagic tendency since birth in the form of markedly prolonged umbilical bleeding and easy bruising afterwards. Two of her brothers had bleeding tendencies, one died shortly after birth due to uncontrollable umbilical bleeding and other died at the age of 12 years from internal haemorrhage. The family study indicates the mode of inheritance to be probably autosomal recessive. The principal laboratory findings are complete non-coagulability of blood, grossly abnormal coagulation tests, zero ESR value, failure to detect fibrinogen by heat coagulation or chemical precipitation tests and biuret reaction and correction of thrombin time after fibrinogen infusion.

Afibrinogenemia↗
PubMedDate not supplied

[Prolong bleeding after extraction from green pit venom].

A case of prolonged socket bleeding after extraction is reported to have been caused by a recent green pit viper snake bite. The snake is a common tropical creature. Several cases bitten are seen in general medical clinic yearly. Pain and local symptoms lead most patient to doctor's attention; while coagulopathy, the other clinical features are usually not being aware of. The 66-year-old patient who had been bitten by the snake a day earlier, of having tooth extraction was referred to Rachaburi Hospital Dental clinic of having post-extraction delayed haemostasis. A routine heamostasis as of gel foam with adrenalin pack and vitamin K injection was unsuccessful. Further laboratory investigations confirmed that he had hypofibrinogenemia as the pathogenic cause. Fresh frozen plasma was administered, haemostatis was satisfactory within 24 hrs.

Afibrinogenemia↗
PubMed1989

[Transient hypofibrinogenemia induced by prednisolone in a case of acute lymphoblastic leukemia].

We report here a patient with acute lymphoblastic leukemia (ALL) in whom hypofibrinogenemia developed during chemotherapy. The patient was a 65-year-old female who was diagnosed as having common ALL, and she was treated with BHAC-DMPV (enocitabine: 160 mg, daunorubicin : 40 mg, 6-MP: 35 mg, prednisolone (PSL): 60 mg, and vincristine: 2 mg). Hypofibrinogenemia appeared promptly each chemotherapy, including PSL was given. To ascertain a correlation between hypofibrinogenemia and the drugs given in this patient, a trial administration of PSL was attempted during a complete remission state. The level of fibrinogen, in terms of the amount of antigen or coagulability, decreased during PSL treatment, although the levels of AT III, plasminogen, alpha 2PI.Plm complex, and FDP did not change. Thus, it is difficult to speculate that PSL induced destruction of leukemia cells and release of protease from the cells resulting in fibrinolysis and hypofibrinogenemia in this case. These findings also suggest that the administration of only PSL could induce hypofibrinogenemia.

Afibrinogenemia↗
PubMed1985

The effect of fibrin polymers on thrombin-catalyzed plasma factor XIIIa formation.

The effect of fibrin polymers on thrombin-catalyzed factor XIIIa formation was studied in afibrinogenemic plasma. Fibrin polymers derived from des A fibrinogen and des A,B fibrinogen increased sixfold the rate of thrombin-catalyzed factor XIIIa formation in the presence of EDTA. Calcium chloride accelerated factor XIIIa formation 14-fold in the presence of des A,B fibrinogen without increasing the rate of thrombin formation. Fibrinopeptides A and B had no effect on factor XIIIa formation in afibrinogenemic plasma. Des A,B fibrinogen reduced by 20- to 40-fold the thrombin concentration required to activate factor XIII. Glycyl-L-prolyl-L-arginyl-L-proline (gly-pro-arg-pro), a fibrin polymerization inhibitor, inhibited des A and des A,B fibrinogen from enhancing thrombin-catalyzed factor XIIIa formation. Gly-pro-arg-pro did not modify factor XIIIa formation in afibrinogenemic plasma and did not inhibit thrombin cleavage of the chromogenic substrate S-2238. These results demonstrate that fibrin polymers accelerate thrombin-catalyzed plasma factor XIIIa formation.

Afibrinogenemia↗
PubMed1986

Early hemostatic disorders in patients with gynecologic tumors.

One hundred and seventeen female subjects were studied: 23 patients with cervical carcinoma; 25 with endometrial carcinoma; 29 with benign uterine diseases; 14 with ovarian carcinoma; 26 patients with benign ovarian tumors. These patients, together with 25 healthy female control subjects, underwent several coagulation tests including Beta-Thromboglobulin (Beta-TG) and Platelet Factor 4 (PF4) plasma levels. Among all Beta-TG and PF4 exhibited the most interesting results. They were increased in four groups of patients: those with malignant 92.2% (13/14) and benign 50% (13/26) ovarian tumors and those with endometrial 64% (16/25) and cervical carcinoma 69.5% (16/23). Our study showed a high incidence of abnormalities of Beta-TG and PF4, early signs of hemostatic disorders, in gynecological malignancies especially in ovarian carcinoma. These data suggest a possible value of these tests as tumor-markers and in order to detect the patients who develop thrombo-embolic accidents.

Adult↗
PubMed1986

Blood and plasma viscosity in experimentally induced hyper- and hypo-fibrinogenaemia.

For some time now fibrinogen has been attributed considerable importance in influencing blood and plasma viscosity. This paper attempts to experimentally confirm this statement in vivo: two groups of arteriopathic patients were selected for investigating viscosity in hyper- and hypo-fibrinogenaemia induced by PTA and a cycle of fibrinolytic treatment with urokinase respectively. Although fibrinogenaemia exhibited highly significant changes under such conditions, there was no important change in viscosity. Probably the role of fibrinogen in influencing viscosity has been overestimated in the past and it is likely that there are other more important factors.

Afibrinogenemia↗