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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and laboratory evaluation of severe bleeding can detect the presence of an intrinsic or acquired coagulation disorder. The three most common inherited coagulation disorders are factor VIII deficiency (hemophilia A), factor IX deficiency (hemophilia B), and von Willebrand's disease. Vitamin K deficiency, liver disease, and disseminated intravascular coagulation are the most common acquired disorders. A thorough clinical history is crucial to diagnosis. Screening tests that measure prothrombin time, partial thromboplastin time, thrombin time, and platelet count permit initial classification and guide selection of more specific tests. Results can then be used to determine appropriate therapy.
Postgrad Med 1989 Sep 01
PMID:Potentially catastrophic bleeding disorders. Approach to diagnosis and management. 267 67

Two cases of infectious complications after liver biopsy are reported. Klebsiella pneumoniae and beta-hemolytic Streptococcus were cultured. In both cases the biopsy was obtained under laparoscopic control. A 28-year-old woman with liver cirrhosis died 24 hours after liver biopsy as a result of septic shock and disseminated intravascular coagulation. A 67-year-old man with hepatic fibrosis suffered from transient bacteremia and recovered uneventfully after antibiotic therapy. In these patients, there was evidence to implicate pre-existing cholangitis as factor predisposing to postbiopsy bacteremia.
Endoscopy 1989 Sep
PMID:Septic shock and bacteremia associated with laparoscopic guided liver biopsy, report on two cases. 267 94

Plasma antithrombin III (ATIII) levels decrease early during gram-negative septicemia, and even a moderate decrease in this major inhibitor of the coagulation system is associated with serious disseminated intravascular coagulation (DIC). Herein the efficacy of high-dose (at least 250 units/kg) ATIII supplementation in animal models of Escherichia coli endotoxemia or bacteremia is reported. An endotoxemic rat model demonstrated that: (1) DIC occurs very early, before the appearance of deleterious cardiovascular abnormalities; (2) ATIII prophylaxis attenuates DIC, metabolic dysfunction, and organ damage; (3) ATIII prophylaxis increases permanent survival; (4) ATIII treatment one hour after endotoxin challenge attenuates DIC, metabolic dysfunction, and organ damage, although not as well as when given prophylactically, and survival is not increased. An endotoxemic sheep pulmonary dysfunction model demonstrated that: (1) ATIII prophylaxis prevents the typical decrease in arterial oxygen partial pressure; (2) ATIII prophylaxis combined with alpha-1-proteinase inhibitor significantly attenuates indices of pulmonary dysfunction. An E. coli bacteremic baboon model demonstrated that ATIII prophylaxis and treatment significantly attenuate indices of DIC and organ damage and prevent death in an otherwise completely lethal dose bacterial challenge. In conclusion, prophylactic treatment with high doses of ATIII may be efficacious in disease states of impending disseminated intravascular coagulation, such as primary or secondary gram-negative septicemia.
Am J Med 1989 Sep 11
PMID:Efficacy of antithrombin III supplementation in animal models of fulminant Escherichia coli endotoxemia or bacteremia. 267 67

Hemorrhagic and thrombotic complications are common in sick preterm infants and may reflect inadequate regulation of coagulation. All neonates have low levels of the pivotal regulator antithrombin III (ATIII) compared with adults. Plasma levels of ATIII are very low in preterm infants and are further diminished in infants with respiratory distress, necrotizing enterocolitis, sepsis, or disseminated intravascular coagulation. Babies with lower levels of ATIII in the cord blood have been shown to have a worse outcome than neonates with levels appropriate for gestational age, including higher mortality and increased incidence of intracranial hemorrhages and catheter-related thromboses. The origin of severe ATIII deficiency is unknown. Therapies with plasma replacement or anticoagulation have decreased the incidence and severity of hemorrhagic and thrombotic complications in high-risk infants in several clinical trials. These data lay the groundwork and rationale for potential use of ATIII replacement in deficient preterm infants.
Am J Med 1989 Sep 11
PMID:Neonatal antithrombin III deficiency. 267 71

Phase I clinical studies of antithrombin III (ATIII) concentrate demonstrated a mean in vivo incremental recovery of functional activity of 1.4 percent per unit/kg administered, an initial 50 percent disappearance time of 22 hours, and a biologic half-life of 3.8 days. Based on these observations, a treatment regimen designed to maintain plasma ATIII levels between 75 and 120 percent of normal has been developed. None of 10 subjects with congenital ATIII deficiency treated prophylactically had evidence of thromboembolism, including four pregnant women at the time of delivery. Five subjects treated for acute thrombosis and/or thromboembolism, four of whom were pregnant, recovered without further thrombotic extension or recurrence. Heparin resistance was reversed in two subjects, both pregnant. Nine subjects with acquired ATIII deficiency also received ATIII treatment for venous or arterial thrombosis or disseminated intravascular coagulation, all with low plasma ATIII levels. Two subjects with disseminated intravascular coagulation demonstrated improvement, one clinically, the other biochemically. All patients with congenital ATIII deficiency survived, but only five of nine with acquired deficiency survived, highlighting the importance in acquired ATIII deficiency of the underlying disease in prognosis. Survival rate was especially poor in subjects with arterial thrombosis in the setting of low plasma ATIII. Administration of ATIII concentrate was well tolerated. None of the subjects who received ATIII concentrate demonstrated evidence of an infectious transmissible agent. These studies demonstrate that it is now feasible to safely replace the deficient protein in congenital ATIII deficiency, either prophylactically or therapeutically.
Am J Med 1989 Sep 11
PMID:Clinical experience with antithrombin III concentrate in treatment of congenital and acquired deficiency of antithrombin. The Antithrombin III Study Group. 267 72

Hemostatic changes were evaluated in ten patients with acute lymphoblastic leukemia and lymphoma who received chemotherapy with L-asparaginase, vincristine, and prednisolone for 1 week. Following treatment, prothrombin time and activated partial thromboplastin time were significantly prolonged, while a marked decrease in fibrinogen levels was observed. The values for cross-linked fibrin degradation products, however, remained within normal limits during treatment, which excluded the possibility of disseminated intravascular coagulation. The concentrations of coagulation inhibitors (antithrombin III, protein C, and protein S), plasminogen, and alpha 2 antiplasmin also significantly decreased; however, levels of both tissue-type plasminogen activator and plasminogen activator inhibitor, which are synthesized in endothelial cells, increased during the treatment. Although a decrease was observed in concentrations of many coagulation factors, including subunits A and B of factor XIII, the activity and antigenicity of factor VII significantly increased following the treatment. From this study, we concluded that these hemostatic abnormalities caused by the administration of L-asparaginase produced a labile condition that easily inclines to bleeding or thrombosis.
Am J Hematol 1989 Sep
PMID:Changes in hemostatic and fibrinolytic proteins in patients receiving L-asparaginase therapy. 275

Twenty cases of fetal death complicating a multiple pregnancy after 20 weeks' gestation are reviewed. We evaluated gestational age at diagnosis and delivery (29.3 +/- 0.7 and 31.8 +/- 0.9 weeks, respectively), interval from diagnosis to delivery (2.6 +/- 0.6 weeks), and cause of fetal death as a group and by type of placentation (76.5% monochorionic). Eighty-five percent of the surviving fetuses were delivered preterm, and the four neonatal deaths were all due to extreme prematurity, with a mean (+/- SEM) birth weight of 794 +/- 237 g. Perinatal mortality was 585 per 1000, 450 for twin A and 750 for twin B. The causes of fetal death varied. Maternal disseminated intravascular coagulation was not diagnosed in any pregnancy in the present series. The high risk of complications related to preterm birth, compared with the low risk of problems related to continuation of a multiple pregnancy after diagnosis of a fetal death, argues in favor of conservative management in this setting.
Obstet Gynecol 1989 Sep
PMID:Multiple pregnancy with late death of one fetus. 276 7

Placental separation in the third trimester of pregnancy may be associated with coagulopathy, fetal distress, or intrauterine death. We report a case of vaginal bleeding due to placental separation at 17 weeks' gestation associated with disseminated intravascular coagulation. After treatment with blood, fresh frozen plasma, and fibrinogen, the pregnancy progressed uneventfully for another 12 weeks, when delivery by emergency cesarean section was performed.
Obstet Gynecol 1989 Sep
PMID:Fetal survival following coagulopathy at 17 weeks' gestation. 229 14

The microgranular form of acute promyelocytic leukemia (APL) was described in the late 1970s and adopted by the French, American, and British classification system in the early 1980s. Morphologically, this form shows distinct differences from the classic form of APL, but clinically it shares many of the same traits. Among these is the predilection for coagulopathies, including disseminated intravascular coagulation (DIC). This DIC has been associated with one previously reported case of fatal hepatic vein thrombosis (Budd-Chiari syndrome), in association with an untreated case of APL. The authors present a case of the microgranular variant of acute promyelocytic leukemia (FAB-M3V), with autopsy and electron microscopic evidence in support. It is important to recognize this variant form of APL and its association with hepatic vein thrombosis, because any successful attempt at therapy must be instituted early in the course of the disease.
Am J Clin Pathol 1989 Sep
PMID:Hepatic vein thrombosis (Budd-Chiari syndrome) in the microgranular variant of acute promyelocytic leukemia. 277 53

This is a method for measuring tissue factor (TF, Factor III, tissue thromboplastin) activity in plasma by using a chromogenic substrate. As pretreatment, the euglobulin fraction of plasma was prepared by removing endogenous inhibitors and heated at 60 degrees C for 3 min to remove fibrinogen. This allowed us to measure the low TF activity in plasma that could not otherwise be measured. Neither phospholipids nor coagulation factors VII, IX, X, or Xa in the samples interfere. Within-run and day-to-day reproducibility were both good. The mean value obtained by this method for normal persons was 1.02 (SD 0.91) arbitrary units/L. A markedly high plasma TF activity of 20 arb. units/L or more was observed in patients with some types of disseminated intravascular coagulation.
Clin Chem 1989 Sep
PMID:Measuring tissue factor (factor III) activity in plasma. 277 13


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