Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hereditary protein C, a primary hypercoagulable state, has not been previously associated with preeclamptic toxemia. A woman with previous preeclamptic toxemia and fetal deaths presented with recurrent deep vein thrombosis during her third pregnancy. Hereditary protein C was diagnosed but full heparinization followed by low-dose heparin failed to prevent preeclamptic toxemia.
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PMID:Hereditary protein C deficiency during pregnancy. 368 69

Protein C(PC) is the zymogen of a serine protease which regulates blood coagulation by inactivating activated blood coagulation factors V and VIII. We investigated the plasma level of PC in patients with deep vein thrombosis (DVT, n = 50), Buerger's disease (n = 34), arteriosclerosis obliterans (n = 37) and myocardial infarction (n = 17). PC in plasma was determined by rocket immunoelectrophoresis using a monospecific anti-PC antiserum raised in rabbits. Our study indicated that only in DVT the level of PC was decreased in comparison with the normal control (p less than 0.05). This decrease may be accounted for by increased utilization of PC for the regulation of continuously activated blood coagulation mechanism possibly ongoing in patients with DVT. On the other hand, among the patients with the DVT, we found a homozygous PC deficiency combined with a heterozygous dysplasminogenemia in a 22-year old male who had been suffering from recurrent venous thrombosis since the age of 14. Although the homozygous form of PC deficiency has been reported to be closely associated with fatal thrombotic disorders including purpura furminans during the neonatal period, the patient reported here had surprisingly survived the neonatal period and the childhood without any clinical manifestation relevant to thrombosis.
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PMID:[Protein C dynamics in peripheral arterial occlusive diseases and myocardial infarction: association of homozygous protein C deficiency with heterozygous dysplasminogenemia found among patients with deep vein thrombosis]. 375 30

In Japan, the various hemostatic medicines have been used after operation. On the contrary, in Europe and U.S.A., the anticoagulants are used both before and after operation because of the high incidence of postoperative deep vein thrombosis. We made inquiries about how they have been used to 566 main surgical clinics in Japan. In the half of these surgical facilities, these medicines still have been used routinely. But in 16.9% of surgery, 9.5% of obstetric & gynecological operation and 29.4% of orthopedic surgery, they have never been used at all. In the field of surgery, in 42% of cardiovascular, 32.1% of respiratory and 10.8% of general surgery, they have not been used absolutely. For the patients with liver cirrhosis, obstructive jaundice and the patients who received the massive blood transfusion during operation, more than 80% of facilities have used the hemostatic medicines. After operation, the blood becomes hypercoagulable and tends to form thrombosis, because of increasing coagulability, decreasing AT-III and protein C, hyper-function of platelet, hypofibrinolytic state and high viscosity. Especially cancer patients have the high risk of deep vein thrombosis. Also we investigated the difference of the incidence of the hemorrhagic complications after operation between in the hemostatic drug group and no drug one. No significant difference was observed. It is concluded that the use of hemostatic medicines after operation is not recommended.
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PMID:[Is it necessary to administer hemostatic medicines after surgical operation? The results of questionnaires about the use of hemostatic medicines in Japan]. 380 75

A congenital deficiency in protein C (physiological inhibitor of coagulation) was identified in 57 patients: the deficiency was quantitative (type I) in 20 families, qualitative (type II) in two families. The transmission was autosomal dominant in 21 families but was suspected to be recessive in one family: the 18 years old homozygous propositus has a severe deficiency (protein C = 16 p. 100): both parents are heterozygous (consanguinity was present) and 5 other family members with heterozygous deficiency are asymptomatic. In the 49 patients (25 women, 24 men) belonging to the 21 other families, 9 men and 4 women (27 p.100) are asymptomatic although precipitating factors had existed in 5 patients. In the remaining 36 symptomatic patients, a deep venous thrombosis was observed in 34, a pulmonary embolism in 18. Recurrent arterial thromboses were diagnosed in 3 patients. The first thrombotic episode was observed at the mean age of 27 +/- 11 years and a triggering factor was found in 26 patients (72 p. 100). Thrombosis was recurrent in 21 (60 p. 100). In the patients without oral anticoagulant treatment, mean protein C antigen concentrations were 47 +/- 9 p. 100 and mean protein C activity was 46 +/- 10 p. 100. In 4 patients with type II deficiency, protein C antigen levels were normal (113 +/- 15 p. 100), contrasting with decreased protein C activity (43 +/- 6 p. 100). Thirty-eight patients have been treated with oral anticoagulants and a skin necrosis developed in the homozygous patients only.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Constitutional protein C deficiency in 57 patients from 22 non-related families]. 381 81

A 57 year old man presented with apparently spontaneous lower extremity deep vein thrombosis and pulmonary embolism. He was treated in conventional fashion with intravenous heparin and oral warfarin. After 4 daily doses of warfarin the prothrombin and proconvertin (P+P) time was within therapeutic range, and heparin was stopped. Over the next six hours complete defibrination occurred, associated with severe bleeding complications. Functional protein C measured after normalization of routine coagulation tests averaged 40% of normal, and was only 3.5% of normal immediately prior to the episode of defibrination. We conclude that the very low functional protein C levels seen immediately prior to defibrination were caused by a combination of pre-existent protein C deficiency and warfarin therapy, and directly predisposed to defibrination once heparin was stopped, despite "therapeutic" warfarin anticoagulation. Exacerbation of intravascular coagulation should be considered a potential prothrombotic effect of warfarin therapy in protein C deficient individuals.
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PMID:Defibrination during warfarin therapy in a man with protein C deficiency. 383 6

Hereditary protein C deficiency, which is inherited as an autosomal-dominant trait, predisposes to venous thrombotic disease. Heterozygotes are at risk for superficial thrombophlebitis, deep venous thrombosis and/or pulmonary embolism, which may occur without apparent cause at a young age. Other manifestations are cerebral venous thrombosis and mesenteric vein thrombosis. In severe, often homozygous, protein C deficiency, a purpura fulminans syndrome may occur shortly after birth, resulting in death due to extensive thrombosis, if it is not adequately treated. The thrombotic manifestations in heterozygotes are effectively prevented by coumarin therapy. However, in the initial phase of oral anticoagulant therapy, the patients have an increased risk for the development of coumarin-induced haemorrhagic skin necrosis. The purpura fulminans syndrome can be treated with either replacement therapy or with coumarin therapy. Heparin appears to be ineffective in the prevention of both the purpura fulminans syndrome and the coumarin-induced skin necrosis.
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PMID:Hereditary protein C deficiency. 384 Jan 12

Activated protein C is a potent inhibitor of coagulation, and familial protein C deficiency has been associated with recurrent venous thrombosis. We have investigated protein C antigen levels in patients undergoing major elective abdominal surgery, to determine their relationships to postoperative deep vein thrombosis (DVT), malignancy, and preoperative treatment with intramuscular or oral stanozolol. Preoperative and postoperative protein C levels were not significantly different in patients with and without DVT (detected by 125I-fibrinogen leg scans), nor in patients with and without malignancy. In a placebo group (n = 26), a significant fall in protein C was maximal on the first postoperative day and persisted for 7 days. In a group given intramuscular stanozolol, 50 mg on the preoperative day (n = 23) stanozolol shortened the duration of the postoperative fall in protein C, but did not prevent DVT. In a group given oral stanozolol, 10 mg/day for 2 weeks before and 1 week after operation (n = 11), stanozolol significantly increased protein C levels prior to surgery, hence maintaining protein C at pretreatment levels after surgery. The effect of this regimen on the incidence of DVT is under study.
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PMID:Protein C antigen levels in major abdominal surgery: relationships to deep vein thrombosis, malignancy and treatment with stanozolol. 391 79

Protein C is a vitamin-K dependent plasma protein, whose activation is catalyzed by alpha-thrombin. Unlike vitamin-K dependent coagulation factors, activated Protein C is an anticoagulant enzyme. Purpose of the present study was to evaluate the pathophysiology of Protein C in patients undergoing minor and major elective surgery. A third group of patients were operated for cancer of the gastrointestinal tract. Protein C levels have significantly decreased in all patients in third postoperative day, while this decrease occurred since the first postoperative day in the case of cancer patients. This suggests that Protein C is consumed after surgery in its anticoagulant and profibrinolytic activity. The acquired Protein C deficiency may be related to postoperative hypercoagulability and increased risk of deep vein thrombosis.
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PMID:Protein C: a new plasma protein related to postoperative hypercoagulability. 654 3

Protein C antigen was determined by Laurell rocket immunoelectrophoresis in 225 patients with a history of venous thrombosis. Among these patients two females with protein C deficiency were detected. Additional studies in the families of the protein C deficient patients revealed further 7 family members with protein C deficiency. In 8 not anticoagulated patients with protein C deficiency the protein C ranged from 36 to 62% (median: 45%). In one patient on oral anticoagulant treatment protein C antigen concentration was less than 10%, F II and FX were 65 and 50%, respectively. The pattern of inheritance was consistent with autosomal dominant inheritance. 5 of the 9 protein C deficient patients had severe thrombotic tendency characterized by recurrent deep venous thrombosis (n = 4), pulmonary embolism (n = 1), probable mesenteric vein thrombosis (n = 1) and superficial thrombophlebitis (n = 2). All protein C deficient patients without thrombosis were less than 17 years old.
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PMID:Protein C deficiency in two Austrian families. 666 61

Resistance to activated protein C (APC) is associated with a single amino acid substitution in factor V (Arg506-->Gln, factor V Leiden) that results in delayed inactivation of the molecule by APC. The mutation is present in 20% of patients with a first episode of deep venous thrombosis. Arterial and venous thromboses are also associated with the type II protein C deficiency (protein CVermont). In protein CVermont, the substitution Glu20-->Ala alone (rPC gamma 20A) is responsible for the defective anticoagulant properties of PCVermont. It was recently established that a thrombotic episode occurred in 73% of family members who are heterozygous for both a functional protein C gene mutation and the factor V Leiden mutation. We evaluated the molecular defect that would accrue in the combined deficiency state of factor VR506Q/VaR506Q and rAPC gamma 20A using recombinant APC and natural purified factor VR506Q from patients homozygous for the Arg506-->Gln substitution. While wild-type recombinant APC (rAPC) slowly cleaves and inactivates factor VR506Q and factor VaR506Q, minimal cleavage of membrane-bound factor VR506Q and VaR506Q by rAPC gamma 20A at Arg306 and Arg679 occurs, and no loss in cofactor activity is observed. Our data demonstrate that rAPC gamma 20A cannot inactivate either factor VR506Q or factor VaR506Q at biologically relevant rates because of impaired cleavage at Arg306 and Arg679.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biochemical prototype for familial thrombosis. A study combining a functional protein C mutation and factor V Leiden. 748 40


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