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)

Using a new rapid coagulant method, protein C activity (PC act) was determined in liver cirrhosis and malignancies and compared with PC antigen and AT III values. PC was decreased in a more pronounced manner than AT III in liver cirrhosis, mainly due to impaired synthesis. This is of special clinical interest because PC proved to be a high sensible indicator of liver cell dysfunction. Decreased levels of PC act (PC ratio act/ag less than 1) in decompensated liver cirrhosis may be caused by the synthesis of dysfunctional PC and/or vitamin K deficiency with production of undercarboxylated PC most sensitively registered by this coagulant assay. An increased clearance of in vivo activated PC induced by DIC may play an insignificant role. In patients with liver metastases, PC act (but not AT III and immunological parameters) was significantly reduced, supporting the conclusion that in these patients liver dysfunction concomitant with synthesis of dysfunctional PC must be discussed as the main cause of this alteration.
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PMID:Immunological and functional determination of the protease inhibitors, protein C and antithrombin III, in liver cirrhosis and in neoplasia. 320 4

A coagulopathy due to vitamin K deficiency was discovered in 42 hospitalized patients, most of whom had been misdiagnosed as having disseminated intravascular coagulation. Factors contributing to vitamin deficiency included inadequate diet, malabsorption, failure of physicians to prescribe vitamin K supplements, antibiotic therapy, renal insufficiency, hepatic dysfunction, recent major surgery, and possibly pregnancy. Sixteen patients (34%) bled sufficiently to need red blood cell transfusions and ten patients (24%) ultimately died. Of 18 patients who also had thrombocytopenia, three did have disseminated intravascular coagulation. The deficiency, a contributor to morbidity and mortality, can be prevented by prophylactic administration of vitamin K to severely ill patients who are eating inadequately and receiving antibiotics.
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PMID:Coagulopathy caused by vitamin K deficiency in critically ill, hospitalized patients. 365 2

The prevalence of vitamin K deficiency in newborn infants and the influence of perinatal risk factors were studied prospectively in 934 infants. A noncarboxylated prothrombin assay to detect proteins induced in vitamin K absence (PIVKA-II) was used to determine the presence of vitamin K deficiency; of 934 cord blood samples assayed, 2.9% were positive for PIVKA-II (0.015 to 0.15 U/ml). All infants found to have detectable PIVKA-II were born at term. The number of infants positive for PIVKA-II was greater in the group small for gestational age (7.4%) than in those appropriate (2.7%) or large (3.1%) for gestational age. Nine categories of perinatal risk groups were defined: however, the majority of infants who were PIVKA-II positive (63%) were normal. All infants received prophylactic vitamin K, and no infant with PIVKA-II in the cord sample subsequently had clinical bleeding. In two patients the rate of 50% disappearance of PIVKA-II after vitamin K administration approximated 70 hours. Two PIVKA-II positive patients with active bleeding or disseminated intravascular coagulation had an accelerated disappearance of 20 to 40 hours. The long disappearance time of PIVKA-II in a steady state may allow detection of vitamin K deficiency despite administration of vitamin K. The majority of cases of neonatal vitamin K deficiency occurred in normal newborn infants. Therefore, all infants should receive prophylactic vitamin K at birth.
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PMID:Vitamin K deficiency in the newborn infant: prevalence and perinatal risk factors. 376 Oct 86

An outline has been given of the major abnormalities of coagulation which can occur secondary to diseases in previously normal individuals. First, the disorders due to deficiency of the vitamin K-dependent clotting factors are described. Vitamin K deficiency can occur in the newborn, or at later stages in life when there is intestinal malabsorption. The malabsorption disorders, such as coeliac disease, together with major abdominal surgery or prolonged use of broad-spectrum antibiotics can give rise to vitamin K deficiency. Additionally, in obstructive jaundice the lack of secretion of bile salts into the upper intestine causes vitamin K malabsorption. The use of oral anticoagulants is associated with haemorrhage in a small proportion of patients. These patients usually have an excessively prolonged prothrombin time, due to overdosage with anticoagulants, but occasionally haemorrhage can occur from a localized bleeding site, such as a duodenal ulcer, in patients under good anticoagulant control. The large number of drugs which can interact with anticoagulants are listed, from which it can be seen that careful monitoring of all patients on oral anticoagulants must be carried out. The haemostatic defects associated with liver disease are then tabulated. In this situation abnormalities may be due to deficient synthesis of coagulation factors in hepatocellular failure, by failure of vitamin K absorption, and also by disseminated intravascular coagulation (DIC). DIC occurs in hepatocellular failure, because the liver cells are normally responsible for clearing activated products of the coagulation and fibrinolytic enzyme systems. The presence of clinical haemorrhage and haemostatic breakdown in hepatic disease usually indicates a serious prognosis, but appropriate replacement therapy is indicated in this situation. Disseminated intravascular coagulation embraces a large number of clinical haemorrhagic syndromes, where intravascular activation of the coagulation system takes place accompanied by compensatory fibrinolytic activity. DIC can be initiated by intravascular release of procoagulant substances, such as tissue thromboplastin, or by damage to vascular endothelium and platelets. The main clinical conditions associated with DIC comprise the severe infections and septicaemias, obstetric accidents, shock and trauma, neoplasia and snake-bite envenoming. In all instances, the pathophysiological disorder of haemostasis is managed by treating the underlying disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acquired coagulation disorders. 389 41

Already in newborns almost all congenital and acquired disorders of hemostasis can be encountered. Especially gestational age and developmental peculiarities of hemostasis influence the incidence of the different causes for hemorrhages. Due to laboratory progress the well-known question of vitamin K deficiency and related bleeding has again become a point of interest and can be answered more clearly now than some years ago. Other significant disturbances of neonatal hemostasis are disseminated intravascular coagulation, intracranial hemorrhages, and the thrombocytopenias of the newborn. Disseminated intravascular coagulation is a pathogenetically important and frequent complication of numerous diseases in term as well as particularly in preterm infants. Ultrasonography gave new information about frequency and prognosis of intracranial hemorrhages in affected newborns. Finally, qualitative and quantitative disorders of the platelets present always a true challenge for the neonatologist in terms of differential diagnosis and differential therapy.
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PMID:[Pathology of hemostasis in newborn infants. II]. 401 Jun 68

A breast-fed 25-day-old infant was hospitalized because of swelling and tenderness of the left leg, developed after mild rotary motion of the leg by his brother. Radiographic examination showed widening of the left articular hip joint space. On the day of admission, a presumptive diagnosis of septic arthritis was entertained, and antibiotic therapy was instituted. Following profuse bleeding from sites of skin punctures, coagulation studies were performed. Prothrombin time and partial thromboplastin time were prolonged. Administration of phylloquinone (vitamin K1) resulted in rapid normalization of coagulation. Differential diagnosis between hemarthrosis resulting from vitamin K deficiency and septic arthritis with disseminated intravascular coagulation is a matter of great importance in such patients.
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PMID:Vitamin K deficiency presenting with hemarthrosis. 649 Aug 91

The frequency, nature, and management of chemotherapy-associated oral hemorrhages were studied in 1,093 adult inpatients undergoing treatment for acute leukemia or the blastic phase of chronic leukemia. Of this number, 163 (14.9%) manifested gross bleeding from the mouth during the course of treatment. The most common oral bleeding sites were the lips, tongue, and gingiva. Thrombocytopenia was the underlying cause in 88% of the cases, disseminated intravascular coagulation in 6%, and combinations of thrombocytopenia and hypofibrinogenemia and of thrombocytopenia and vitamin K deficiency in 5.5% and 0.6%, respectively. The vast majority of the patients with mouth bleeding had platelet counts below 40,000/mm3. Approximately 50% had indirect evidence of a coagulation factor deficiency in the blood. The oral hemorrhages were best managed by transfusions of HLA-compatible fresh platelets and fresh frozen plasma, together with topically applied clot-promoting agents, until hemostatic control was restored.
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PMID:Chemotherapy-associated oral hemorrhages in adults with acute leukemia. 661 Jan 54

A simple and rapid assay for the detection of PIVKA-II is described. The principle of the assay is based on agglutination of antihuman prothrombin rabbit IgG coated latex with absorbed plasma which is treated with barium carbonate. This assay is expected to be useful as a screening test to differentiate whether or not vitamin K deficiency is present in various clinical cases such as newborn infants, patients with liver diseases, disseminated intravascular coagulation, and so on.
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PMID:A simple and rapid test for PIVKA-II in plasma. 706 27

Appropriate management of the bleeding newborn is easily accomplished by first assessing the clinical circumstances under which the bleeding occurs. Having determined the clinical circumstances, knowledge of the pathophysiology of disseminated intravascular coagulation, liver failure, vitamin K deficiency, and hemophilia coupled with knowledge of the normal levels of coagulation factor activities at birth leads to selection of appropriate laboratory tests to confirm the etiology of the bleeding. Once the etiology is confirmed, treatment requires management of associated clinical conditions and replacement of vitamin K and/or deficient coagulation factors.
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PMID:Diagnosis and treatment of coagulopathy in the newborn. 730 61

Twenty cases of hemothorax in newborns, including 4 of our own patients, are reviewed in detail. This unusual cause of acute respiratory distress within the neonatal period was observed in 14 males and 6 females. Most of the patients were fullterm newborns. As causal factors hemorrhagic disease of the newborn (vitamin K deficiency), disseminated intravascular coagulation, arteriovenous malformations and pleural/vascular rupture are considered. The time of occurrence of bleeding symptoms ranged from 1 to 28 days of life. Sixteen out of 20 patients survived without sequelae, but in 4 cases the outcome was lethal.
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PMID:Hemothorax in the newborn. 739 66


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