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)

The study included 28 infants with infectious gastroenteritis who evolved with disturbances of coagulation and in whom laboratory tests were practiced by micromethods through capillary puncture. The most frequently seen abnormality was a combination of vitamin K dependent factors deficiency with thrombocytopenia. Another observation in our study is that hypofibrinogenemia in infants with infectious gastroenteritis is not always secondary to disseminated intravascular coagulation. A decrease in fibrinogen in these cases is explained by a lack in synthesis of this factor in infants with malnutrition since out of 16 malnourished infants, 75% evolved with hypofibrinogenemia, while eutrophic infants evolved with normal fibrinogen. The disseminated intravascular coagulation syndrome was seen more frequently in patients with infectious gastroenteritis complicated with septicemia and shock, 57% of the patients did not show manifestations of bleeding nor of thrombosis which justifies in these cases a systematic investigation of the coagulation mechanism.
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PMID:[Blood coagulation disorders in infants with infectious gastroenteritis]. 91 59

Protein C (PC), a 62,000-molecular weight vitamin K-dependent serine protease zymogen, is a natural anticoagulant that occurs in plasma at 4 mg/L. Activated PC inactivates clotting factors V and VIII and is also profibrinolytic. Activated PC is enhanced in its anticoagulant activity by protein S (PS), another vitamin K-dependent protein. Protein S is found in platelets and endothelial cells as well as in plasma. Inherited PC deficiency and PS deficiency have been associated with venous thrombosis. Both heterozygous PC and PS deficiency appear to be inherited in an autosomal dominant manner in some families. Homozygous PC deficiency presents as neonatal purpura fulminans and results in massive venous thrombosis of the skin and other organs within the first few days of life. Symptomatic heterozygous PC deficiency and PS deficiency have been treated with oral anticoagulants, successfully minimizing recurrence of thrombosis. Coumarin-induced skin necrosis, a rare complication of oral anticoagulant therapy usually seen within three to five days of initiation of therapy, has also been associated with heterozygous PC deficiency. The short half-life of PC (six to eight hours) compared with most of the vitamin K-dependent clotting factors (greater than 30 hours) is the probable reason for this paradoxical response to oral anticoagulants in some PC-deficient patients, since a transient imbalance of procoagulant and anticoagulant factors may exist during initiation of oral anticoagulant therapy. Acquired deficiency of the PC pathway occurs in disseminated intravascular coagulation and possibly other diseases such as those associated with a lupus anticoagulant.
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PMID:Coumarin necrosis, neonatal purpura fulminans, and protein C deficiency. 296 8

Protein C is a potent inhibitor of blood coagulation, and, in addition, appears to be a profibrinolytic agent. In a first step, protein C must be converted to a serine protease. This activation is catalyzed by a complex formed between thrombin and thrombomodulin, an endothelial cell surface protein. Activated protein C exhibits its anticoagulant activity through the proteolytic inactivation of two blood coagulation cofactors, factors Va and VIIIa. This reaction requires phospholipids, originating from platelets or endothelial cells, and a cofactor protein, protein S. Protein S enhances the binding of activated protein C to phospholipids. In addition, activated protein C stimulates fibrinolysis, through the inactivation of the tissue plasminogen activator (tPA) inhibitor. An isolated constitutional, quantitative or qualitative, protein C or protein S deficiency increases the risk of thrombosis, the clinical features are different in the rare cases of homozygous protein C deficiency (neonatal purpura fulminans) or in the heterozygous patients (recurrent venous thrombosis in young adults). Acquired deficiency in protein C and S had been observed in liver disease, during vitamin K antagonists or L-Asparaginase treatment, and in disseminated intravascular coagulation.
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PMID:[Protein C, protein S]. 303 76

Antithrombin III (AT III) is a plasma protein which acts as the principal inhibitor of thrombin and is a major modulator of intravascular coagulation. Hereditary deficiency of AT III leads to recurrent episodes of thromboembolism. Acquired deficiency of AT III occurs in persons with a variety of conditions, including severe liver disease and disseminated intravascular coagulation. Replacement of AT III may be important in some deficient persons. To determine if cryoprecipitate is a useful source of AT III, we measured the AT III content of cryoprecipitate prepared from citrate phosphate dextrose blood using coagulation and fluorogenic assays and immunoassays. Using the fluorogenic assay, we also determined the effect of adding heparin to blood on the cryoprecipitation of AT III. Functional and antigenic AT III levels were similar to those of normal plasma in all citrate phosphate dextrose blood units tested, indicating that AT III is not concentrated in cryoprecipitate. Heparin had no effect on the cryoprecipitation of AT III.
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PMID:The antithrombin III content of cryoprecipitate prepared from blood collected with and without heparin. 640 59

Coagulation studies were performed on 16 children with gram-negative septicemia without the complications of septic shock, liver disease, malnutrition, or laboratory evidence of classic disseminated intravascular coagulation (DIC). Ten (63%) of the 16 cases were found to have abnormal partial thromboplastin and/or prothrombin times. The coagulopathy was caused by a reduction in the vitamin K-dependent coagulation factors. The mechanism that produced this coagulopathy was not known, but evidence was found that suggested that endotoxin may interfere with the vitamin K-carboxylation reaction. The data indicated that abnormal coagulation screening test results in children with gram-negative septicemia were not specific for DIC and that a significant number of patients had a coagulopathy not related to DIC.
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PMID:Vitamin K-dependent coagulation factors in gram-negative septicemia. 670 67

Nonbacterial thrombotic endocarditis is a cardiac valve lesion characterized by vegetations composed of fibrin and trapped platelets on an uninflamed valve leaflet. It is often associated with malnutrition or underlying malignancy. The vegetations may give rise to clinically significant emboli and occasionally may cause cardiac murmurs. The diagnosis should be considered in any debilitated patient who suddenly develops unexplained embolic disease, a new cardiac murmur or disseminated intravascular coagulation.
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PMID:Nonbacterial thrombotic endocarditis. 683 99

Of the 2877 patients who underwent chest surgery at our department during the 20-year period between 1973 and 1992, 9 (0.3%) developed postoperative chylothorax. The underlying disease included primary lung cancer in 5 patients, pulmonary metastasis in 1, invasive thymoma in 2, and neuroblastoma of the posterior mediastinum in 1. For the treatment of chylothorax, the thoracic duct was ligated in 2 patients with a high volume of chylous leakage. In 6 patients treated conservatively, early pleurodesis was attained by injecting 1 to 5 doses (mean: 2.2 doses) of the streptoccal preparation OK-432 intrathoracically; favorable results were achieved. In 1 patient, the diagnosis of chylothorax was delayed because of postoperative pyothorax. This patient developed nutritional deficiency, compromised immunity, and disseminated intravascular coagulation (DIC), which led to death before the chylothorax could be treated. In principle, postoperative chylothorax should be treated conservatively. Favorable results can be expected with the intrathoracic injection of OK-432 beginning at the early postoperative period to achieve pleurodesis, combined with the prevention of nutritional deficiency, electrolyte imbalance, and infection.
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PMID:Treatment of postoperative chylothorax by pleurodesis with the streptococcal preparation OK-432. 782 62

We evaluated retrospectively the causes of death from active pulmonary tuberculosis by the review of records and chest radiograohs of 364 patients (male 282, female 82) with active pulmonary tuberculosis, who were admitted to our hospital during 1995 to 1998. 43 patients (male 33, female 10) were died under anti-tuberculous chemotherapy. 20 cases were tuberculous death; death from acute progression of tuberculosis without response to chemotherapy (acute progression group) in eight cases and death from debility in spite of partial response to chemotherapy (debility group) in eight cases. 23 cases were died from underlying diseases; death from malignant neoplasmas (malignant group) in nine cases and death from complication of bacterial pneumonia (pneumonia group) in seven cases. In acute progression group, the age (mean +/- SE) was 64.8 +/- 5.2 years old and the survival period from admission was 11.8 +/- 4.2 days. Five cases were laborer or unemployed. This group was characterized with far advanced diseases presenting extensive lung lesions complicated with DIC or hepatic dysfunction, low performance status (PS), severe malnutrition and lymphocytepenia. In debility group, the age was 70.8 +/- 3.9 years old and the survival period from admission was 254.6 +/- 90.7 days. Five cases were laborer or unemployed. This group was characterized with multiple underlying diseases, low PS, previous anti-tuberculous chemotherapy and resistance to INH and/or RFP. In malignant group, the age was 69.3 +/- 3.2 years old and the survival period from admission was 99.9 +/- 21.2 days. This group was characterized with relatively well nourished, relatively good PS in comparison with other groups, and lymphocytepenia. In pneumonia group, the age was 82.8 +/- 1.7 years old and the survival period from admission was 153.3 +/- 54.5 days. This group was characterized with remarkably advanced age, low PS related to underlying disorders of central nervous system. In the causes of death with active pulmonary tuberculosis under chemotherapy, inhomogenous groups were included. Extensive disease, low PS, malnutrition, lymphocytopenia, previous chemotherapy, resistance to INH and/or RFP, and poorer social circumstances seemed to be risk factors for tuberculous death. In contrast, underlying malignant nepolasma, lower PS, and far advanced age were seemed to be the risk factors for non-tuberculous death.
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PMID:[A clinical study of causes of death from active pulmonary tuberculosis with chemotherapy]. 1002 8

A twenty-year-old woman with anorexia nervosa (body mass index=11) suffered from severe liver dysfunction (aspartate aminotransferase 5,000 IU/l, alanine aminotransferase 3,980 IU/l, prothrombin time 32%), hypoglycemia (serum glucose 27 mg/dl), and pancreatic dysfunction (amylase 820 IU/l, lipase 558 IU/l). She fell into a depressive state with irritability, which was not improved by intravenous glucose. Despite treatment with plasmapheresis for the liver dysfunction, she subsequently developed pulmonary edema, acute renal failure, gastrointestinal bleeding, and disseminated intravascular coagulation. Hemodialysis, mechanical ventilation and drug therapy including prednisolone, prostaglandin E1, and branched-chain amino acid, improved her critical condition. In this case, malnutrition may have been the cause for the liver dysfunction and subsequent complications.
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PMID:Anorexia nervosa with severe liver dysfunction and subsequent critical complications. 1043 64

Antithrombin (AT) is the most important inhibitor of activated coagulation enzymes. Deficiency of this protein can be a congenital defect. Different types have been described with a diminution of the entire molecule as well as diminution of activity only with normal concentration and normal activity and concentration but with a decreased sensitivity to heparin. There exist also different types of acquired deficiency due to a diminished production, an increased loss or an increased consumption of the inhibitor. Because AT deficiency is the cause of an increased thrombotic tendency in many cases the therapeutic and prophylactic possibilities are described. Since highly purified concentrates became available, substitution was attempted in cases of AT deficiency. It was found to be of greatest importance in cases of disseminated intravascular coagulation (DIC) which is a frequent consequence of septic or traumatic shock. In such cases an adequate AT-substitution can even be lifesaving as could be shown in different trials.
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PMID:Hereditary and acquired antithrombin deficiency. 1044 57


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