Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Improved factor VIII preparations have made major surgery feasible for hemophiliac patients, as well as increasing their survival. In a hemphoiliac undergoing prostatectomy, the effects of local or systemic fibrinolysis and possible disseminated intravascular coagulation must be considered, in addition to the factor VIII deficiency. We successfully treated an octogenarian with benign prostatic hypertrophy and mild hemophilia during and after suprapubic prostatectomy by infusions of antihemophilic factor (factor VIII) concentrate. Cessation of infusion on the 15th day resulted in bleeding two days later. This ceased after resumption of antihemophilic factor infusion. Tests for abnormal fibrinolysis and fibrin split products gave negative results.
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PMID:Prostatectomy in an 85-year-old hemophiliac. 5 87

Long-term determinations of haemostasis factors in a case of Osler's telangiectasia revealed the temporarily simultaneous existance of periods of thrombocytopenia, a decrease of prothrombine and a reduction of the fibrinogen and plasminogen level. These findings considered as signs of consumption coagulopathy coincided with an increased bleeding tendency of the patient. The correlation existing between the clinical symptoms and the observed disorders of coagulation may possibly be explained by the appearance of an intravascular coagulation during the late period of the haemorrhagic diathesis, which could be proved by the simultaneous increase of fibrinogen degradation products. Moreover, the patient's plasma was capable of strongly inhibiting factor VIII of a normal plasma. The possible influence of plasmatic disorders of coagulation which are caused by secondary reasons on the clinical picture of a haemorrhagic diathesis primarily based on vascular conditions is discussed.
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PMID:[A case of Osler-Rendu disease with simultaneous thrombopenia and a factor VIII inhibitor]. 6 66

Coagulation and fibrinolysis studies were performed on 64 newborns; 16 premature infants with hyaline membrane disease (HMD), 17 newborns with other forms of respiratory distress syndrome (RDS) (8 of them were premature), 31 healthy newborns (11 of them were premature). All the babies were studied once in the first 48 hours of life. There was no significant difference between sick and healthy babies for 5 parameters; platelet count, factor VIII, fibrinogen, fibrin(ogen) degradation products, euglobulin lysis time. Factor II, VII and X were low in all infants, and premature infants had significantly lower levels compared to full term newborns. Factor V, plasminogen, alpha 2 macroglobulin (alpha 2M) and antithrombin III (AT III) levels were significantly lower in sick infants. Except for AT III, these deficiencies were not related to prematurity. No significant difference was found between HMD and other RDS. Of the 33 sick infants, 5 developed laboratory findings consistent with disseminated intravascular coagulation (DIC). The results indicate that the coagulation and fibrinolytic abnormalities reported are not specific to HMD.
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PMID:Haemostatic disorders and respiratory distress in the newborn. 7 54

Serial prospective studies of coagulation status have been undertaken on 73 babies with a positive Coombs test. No abnormalities were detected in the babies with mild haemolytic disease, but seven of the 36 babies with severe haemolytic disease (cord Hb less than 11 g/dl or cord bilirubin greater than 85 mumol/1) showed evidence of transient defibrination 1 d after birth and another six had evidence of coagulation failure at birth with a platelet count of less than 150 x 10(9)/1 and a severe deficiency of multiple coagulation factors. The level of factor II and factor X was less than a fifth of the normal cord blood level in these six babies and the level of I, VII and IX was severely reduced; the factor VIII level was normal or high. Exchange transfusion started within 1 h of birth corrected the immediate factor deficiency in these six babies, but evidence of defibrination then became apparent with afibrinogenaemia, a marked fall in factors II and V, less constant falls in factors VII, IX and X, and a raised fibrin:fibrinogen degradation product level. One of these six babies died with severe pulmonary hypoplasia within an hour of birth; the other five died from haemorrhage into the lung or brain 1 1/2--6 d after birth. The very low vitamin-K dependent factor levels in the cord blood of the babies who died are presumably the result of liver damage in utero, but the subsequent changes are those of a comsumption coagulopathy. Simple screening tests at birth served to indicate which babies were at risk and it is concluded that death due to haemorrhage might be reduced by more intensive factor replacement before there is overt evidence of haemorrhage in these babies.
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PMID:Coagulation failure in babies with rhesus isoimmunization. 11 26

The relationship between factor VIII (AHF) procoagulant activity and factor VIII-related antigen were examined in patients with disseminated intravascular coagulation (DIC), pulmonary embolism (PE), and coronary artery disease with or without myocardial infarction (MI). It was found that 13 of 13 patients with DIC, 17 of 17 patients with PE, and 10 of 12 patients with MI possessed a significantly elevated factor VIII-related antigen to factor VIII activity ratio (VIII-ratio). The VIII-ratio returned to normal in each of 2 patients with DIC and 1 paitent with PE after treatment with heparin, heparin and alpha-amino-caproic acid, and heparin and coumadin respectively. In contrast, the VIII-ratio was slightly elevated only in 1 of 15 patients with coronary artery insufficiency without MI. In in vitro studies, after treatment of plasma with thrombin or plasmin, factor VIII activity was lost, whereas the amount of factor VIII-related antigen remained the same or was even increased when measured by agarose quantitative immunoelectrophoresis. These observations have led us to conclude that an elevated VIII-ratio is a very sensitive indicator of intravascular coagulation.
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PMID:In vivo and in vitro effects of thrombin and plasmin on human factor VIII (AHF). 13 71

Systemic hemostatic agents are reviewed. Among the agents discussed are vitamin K preparations (phytonadione, menadione, menadione sodium bisulfite, menadiol sodium diphosphate); and blood products (whole blood, plasma, cryoprecipitate, factor VIII concentrates, factor IX concentrates and fibrinogen concentrates). Normal and abnormal hemostasis and fibrinolysis are discussed, as is the general management of systemic hemostatic defects. Specific disorders covered are clotting factor deficiencies, hemophilia A, factor VIII inhibitors, von Willebrand disease, hemophilia B (Christmas disease), other congenital coagulation disorders, acquired deficiency of factors II, VII, IX and X, and defibrination syndrome.
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PMID:Drug therapy reviews: clinical use of hemostatic agents. 30 96

Serial coagulation studies were completed on six neonates with apparent or inapparent localized hemorrhage. The sites of the hemorrhages were intracranial (2), gastrointestinal (2), subperiosteal (1), and pulmonary (1). The studies revealed an increased factor VIII level, decreased platelet count, and a short PTT. Since similar findings occur in disseminated intravascular coagulation, it is possible that coagulation abnormalities associated with localized hemorrhage result from similar mechanisms. These observations suggest that occult and clinically unrecognized hemorrhage can be suspected by serial coagulation studies of sick infants.
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PMID:Coagulation abnormalities associated with localized hemorrhage in the neonate. 30 56

Forty-five patients with multiple injuries treated at an intensive care unit were studied prospectively. The patients were divided into two groups: the severely injured (no mortality) and critically injured (56% mortality). Treatment was started within two hours from the accident in all cases. The following coagulation parameters were measured for eight days: euglobulin lysis time (ELT), thromboelastography (TEG), vecalcification time (RECA), partial thromboplastin time (PTT), factor V, factor VIII, Normotest, Thrombotest, thrombin time, fibrinogen and platelets. Severe coagulation disorders were observed in one-third of the patients 12-48 hours after trauma. The abnormalities were more pronounced in patients who had sustained very severe injuries and arrived in a state of shock. The ELT was shortened 0-6 hours after the accident and accelerated coagulation was indicated simultaneously by decreased PTT, RECA, and r-values as well as by elevated Thrombotest and factor VIII values. The factor V and fibrinogen levels were initially lowered. Low platelet values at 2-4 days, prolonged thrombin and r-times, secondary decrease of fibrinogen FV, FVIII, and low Thrombotest values suggested disseminated intravascular coagulation associated with complications, such as fat embolism and "shock lung" syndromes. General bleeding tendency with high mortality was observed in 16% of the patients.
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PMID:Coagulation disorders in severely and critically injured patients. 60 16

Two drugs, 2,6-cis-diphenylhexamethylcyclotetrasiloxane (Cisobitan) and estramustine-17-phosphate (Estracyt) were given to patients with poorly differentiated metastatic carcinoma of the prostate. The effect of the drugs on blood coagulation was investigated. Some parameters showed changes during the treatment: Antithrombin III decreased in the Estracyt treated patients to a level which might imply a thrombogenic effect. Fibrinogen decreased, whereas factor VIII showed no consistent change. Normotest changes appeared to correlate with liver damage whereas antithrombin III showed no change. Increased levels of fibrinogen degradation products and fibrinopeptide A (FPA) were more frequent in the group of deteriorating patients. However, the number of FPA analyses were too small for any definite conclusions regarding possible disseminated intravascular coagulation.
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PMID:Blood coagulation studies in patients with advanced carcinoma of the prostate treated with 2,6-cis-diphenylhexamethylcyclotetrasiloxane or estramustine-17-phosphate. 66 37

Nine patients with severe classic hemophilia and inhibitors against factor VIII were treated for 156 bleeding episodes with 503 infusions of Proplex, Konyne, or Auto-Factor IX, three preparations of prothrombin complex concentrates (PCCs). Approximately two thirds of the bleeding episodes were managed successfully. Although the prothrombin time (PT) and partial thromboplastin time (PTT) were shortened after most PCC infusions, there was no evidence of disseminated intravascular coagulation. The degree of shortening of PT or PTT was not related to the particular PCC preparation used, dose, or cessation of hemorrhage. All PCC preparations contained activated clotting factors, as manifested by their ability to shorten the PTT of normal plasma, factor-VIII-deficient plasma, and factor-IX-deficient plasma. Shortening, which was greater with Auto-Factor IX than with the other products, was inhibited partially by a factor IX antibody and blocked completely by prolonged incubation with plasma. Although the nature of the procoagulant material in PCCs is uncertain, these products are of proven benefit to hemophilic patients with high-titer inhibitors. Side effects have been minimal and inhibitor titers have not risen.
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PMID:Use of prothrombin complex concentrates in hemophiliacs with inhibitors: clinical and laboratory studies. 72 19


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