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)

Among 379 patients with AML with FAB type M1, 2 and M4-7 diagnosed between 1978 and 1997 in our institution, 19 (5%) had hypofibrinogenemia (HF), ie a fibrinogen level <180 mg/dl. Compared to patients with normal fibrinogen (n = 360) patients with HF had significantly elevated markers of activation of coagulation (TAT, F1.2, FPA) and fibrinolysis (D-dimer, FDP) indicating that disseminated intravascular coagulation/hyperfibrinolysis was the cause of hypofibrinogenemia. Patients with HF had significantly longer prothrombin times, thrombin clotting and reptilase times. Factor X and VIII were significantly lower than in patients without HF. With the exception of M7, HF occurred in all FAB subtypes, but was most common in M5 (12.1%). Patients with HF did not differ from those with normal fibrinogen with regard to age, sex, leukocyte count and other hematological parameters. During induction chemotherapy fibrinogen normalized rapidly (median 5 days) and there was no increased incidence of early hemorrhagic death. The overall and disease-free survival was similar to that of patients without HF.
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PMID:Hypofibrinogenemia in non-M3 acute myeloid leukemia. Incidence, clinical and laboratory characteristics and prognosis. 969 71

The pathophysiology and support of the massively transfused patient from the vantage of a blood banker is reviewed. Hypothermia, acidosis and shock must be reversed if blood component therapy is to be effective. Algorithms which employ ratios of various blood components have not proved themselves, nor are screening coagulation tests of value until they are remarkably abnormal. Thrombocytopenia, thrombocytopathy, and hypofibrinogenemia appear to be the parameters which predispose to continued bleeding and microvascular hemorrhage in these patients. A large part of the impaired hemostasis is due to a consumption coagulopathy rather than the anecdotal assumption that dilution of the hemostatic elements is to blame. Hypocalcemia, hypomagnesemia and hyperkalemia are rarely observed nor do they pose a problem for this group of individuals. The logistics of blood supply to the clinical areas are addressed by describing one system that has proved itself.
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PMID:Massive blood transfusion: the blood bank perspective. 1014 40

Induction of tissue factor (TF) activity by endotoxin and cytokines is an important mechanism for initiation of disseminated intravascular coagulation (DIC) seen in patients with gram-negative sepsis. Based on data from an in vitro study in which dithiocarbamates abrogated endothelial cell TF activity by inhibition of the NF-kappaB pathway, we investigated whether dithiocarbamates had in vivo activity in an animal model of DIC. Dithiocarbamates ameliorated the adverse clinical and histological effects of endotoxin-induced DIC, including morbidity, hypofibrinogenemia, and target organ damage, especially in the liver and kidney, even when given up to 1 hour after administration of endotoxin. This pilot study confirms the key role of the nuclear factor-kappa beta (NF-kappaB) pathway in induction of TF activity in initiating sepsis-associated DIC and suggests that dithiocarbamates may be useful in treatment of DIC associated with excessive TF expression because of gram-negative sepsis. Additional studies of dithiocarbamates in DIC models are warranted.
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PMID:Dithiocarbamates ameliorate the effects of endotoxin in a rabbit model of disseminated intravascular coagulation. 1054 75

Objective: Acute fatty liver of pregnancy (AFLP) is an uncommon, potentially fatal disorder that usually occurs in the late third trimester of pregnancy. We present the first reported case of acute fatty liver in the second trimester of pregnancy.Methods: We report the clinical and laboratory findings in a patient with AFLP who presented in the second trimester of pregnancy.Results: A 37-year-old G5P4 woman presented at 22 weeks gestation (by 18 weeks ultrasound) with nausea and vomiting. She was normotensive, had no proteinuria, had elevated SGOT and SGPT (266 and 261, respectively), negative hepatitis studies and a normal platelet count. She was managed conservatively for presumed cholelithiasis until 24 weeks gestation when she was transferred to our facility because of worsening SGPT and SGPT (368 and 505, respectively), jaundice (total bilirubin of 8.9 mg/dL), hypoglycemia, and laboratory evidence of disseminated intravascular coagulation (DIC) (PT = 18.6, PTT = 56, hypofibrinogenemia and presence of fibrin split products). Ultrasound showed singleton fetus (EFW 450 g) with total placenta previa. Computed tomography scan of the abdomen revealed decreased hepatic density consistent with AFLP. Delivery of a nonviable fetus was effected after transfusion of fresh frozen plasma. Postoperatively, the patient had rapid resolution of DIC, jaundice, and hypoglycemia; liver transaminases normalized 5 days postoperatively and the patient was discharged home in good condition 5 days later.Conclusion: It has been traditionally stated that AFLP occurs in the late third trimester of pregnancy. This case demonstrates that, even in the second trimester of pregnancy, the diagnosis of AFLP should be considered as a cause of deteriorating liver function, jaundice, and DIC.
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PMID:Acute fatty liver in the second trimester of pregnancy. 1083 61

The authors report a case of a 70-year-old man, with repeating episodes of systemic subdermal hematoma due to consumption coagulopathy associated with abdominal aortic aneurysm and the bilateral femoral arterial aneurysms. Prior to the first operation for abdominal aortic repair, anticoagulation therapy was applied to treat thrombocytopenia and hypofibrinogenemia. Five years following the first surgery, the same treatment was required before resection of the femoral lesions. Consumption coagulopathy is seen in approximately 1-4% population of aortic aneurysms, however, repeated appearance of symptomatic coagulopathy is rarely reported. Anticoagulation therapy was effective to normalize the coagulation and fibrinolytic system and followed by uneventful surgical resection of the aneurysms.
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PMID:Consumption coagulopathy associated with aneurysms of the abdominal aorta and the bilateral femoral arteries. Report of a case. 1129 44

Treatment of hemorrhagic diathesis after saline-solution-induced abortion is discussed. A 23-year-old woman who had a therapeutic abortion by intraamniotic instillation of 23% saline solution developed uterine bleeding 2 hours after the fetus had passed. Her fibrinogen level was 125 mg% (normal 250-450 mg%) and her partial thromboplastin time was 97 seconds (normal 45 seconds). 2 units of fibrinogen, followed by immune serum globulin, were administered to the patient. Approximately 2 1/2 months later the patient developed hepatitis. The question of whether or not this was proper treatment for her low fibrinogen state was asked. The consultant (author) stated that the fibrinogen could have been kept in reserve for the unlikely emergency of increasing fibrinogenopenia or hemorrhage. The addition of the fibrinogen substrate could (rarely) exacerbate disseminated intravascular coagulation as well as inoculate the patient with hepatitis virus. In a patient such as this, usually needs are met with transient obstetric and medical support since body processes restore the depleted hemostatic and fibrinolytic mechanisms.
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PMID:Treatment of hemorrhagic diathesis after saline-solution-induced abortion. 1230 85

The paper contains the results of a retrospective analysis of causes for an intensified bleeding in patients operated on the heart with artificial blood circulation. An affected hemostasis plasma chain, i.e. insufficiency of blood coagulation factors due to hemodelution, hypofibrinogenemia etc., provoked the above disorder in 39% of patients with a higher postoperative bleeding. Additional reasons for the impaired hemostasis chain included: the "heparin-rebound" phenomenon (3.4%), activation of the secondary fibrinolysis (3.4%) and disseminated intravascular coagulation (DIC) (0.14%). Finally, an undiagnosed inadequate surgical hemostasis provoked an intense bleeding in 19.5% of cases.
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PMID:[Impaired hemostasis as a cause of intensified bleeding after heart surgery with extracorporeal blood circulation]. 1520 73

The Fps/Fes tyrosine kinase has been implicated in the regulation of hematopoiesis and inflammation. Mice expressing an activated variant of Fps/Fes (MFps) encoded by a gain-of-function mutant transgenic fps/fes allele (fps(MF)) exhibited hematological phenotypes, which suggested that Fps/Fes can direct hematopoietic lineage output. These mice also displayed marked hypervascularity and multifocal-hemangiomas which implicated this kinase in the regulation of angiogenesis. Here we explored the potential involvement of Fps/Fes in the regulation of hemostasis through effects on blood cells and the vascular endothelium. Hematological parameters of fps(MF) mice were characterized by peripheral blood analysis, histology, and transmission electron microscopy. Hemostasis parameters and platelet functions were assessed by flow cytometry and measurements of activated partial thromboplastin time, prothrombin time, thrombin clot time, platelet aggregation, bleeding times and in vitro fibrinolytic assays. Hematological and morphological analyses showed that fps(MF) mice displayed mild thrombocytopenia, anemia, red cell abnormalities and numerous hemostatic defects, including hypofibrinogenemia, hyper-fibrinolysis, impaired whole blood aggregation and a mild bleeding diathesis. fps(MF) mice displayed a complex array of hemostatic perturbations which are reminiscent of hemostatic disorders such as disseminated intravascular coagulation (DIC) and of hemangioma-associated pathologies such as Kasabach-Merritt phenomenon (KMS). These studies suggest that Fps/Fes influences both angiogenic and hemostatic function through regulatory effects on the endothelium.
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PMID:Hemostatic and hematological abnormalities in gain-of-function fps/fes transgenic mice are associated with the angiogenic phenotype. 1555 33

Green pit viper (Trimeresurus albolabris) is the most common venomous snake responsible for bites in Bangkok. It causes local edema and systemic hypofibrinogenemia resulted from the thrombin-like, as well as the fibrinolytic effects of the venom. However, the amino acid sequences of these venom proteins have never been reported. In this study, we have cloned five novel serine proteases from the Thai T. albolabris venom gland cDNA library. They were all closely homologous to the corresponding serine proteases from Chinese green viper (Trimeresurus stejnegeri), suggesting the evolutionary proximity of the two species. In addition, their functional activities could be deduced. There were predicted to be two thrombin-like enzymes (GPV-TL1 and GPV-TL-2), two isoforms of a fibrinogenolytic enzyme (albofibrase) and a plasminogen activator (GPV-PA), suggesting that defibrination syndrome in patients is a combination of these enzymatic effects. By multiple sequence alignment, no conserved residue or motif responsible for distinct functions of snake venom serine proteases could be observed. Moreover, one Lys 49 and one Asn 49 phospholipase A2 (PLA2) genes were cloned. Lys 49 PLA2 was predicted to devoid of catalytic activity, but showed a carboxy terminal cytotoxic region. No Asp 49 PLA2 was found in 150 clones screened. This explains the marked limb edema but no hemolysis in patients. These novel serine proteases have potentials to be therapeutic anti-thrombotic and thrombolytic agents in the future.
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PMID:Molecular cloning of novel serine proteases and phospholipases A2 from green pit viper (Trimeresurus albolabris) venom gland cDNA library. 1637 75

We report three maternal deaths which might be in possible association with the use of intravaginal dinoprostone for cervical ripening and induction of labor. All cases occurred at our institution between January 2006 and December 2007. Uterine atony and profuse bleeding followed by disseminated intravascular coagulation (DIC), characterized by severe hypofibrinogenemia developed shortly after delivery of the first two patients. The third patient developed respiratory symptoms in the active labor followed by hemodynamic changes manifested by tetanic uterine contractions and fetal heart rate decelerations. Cardiac arrest developed in all patients shortly after the occurrence of symptoms with no response to any medical intervention. The pharmacologic induction of labor with dinoprostone may be in association with increased risk of maternal death because of increased risk of postpartum DIC and amnionic fluid embolism. Further investigations seem to be needed.
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PMID:Is dinoprostone safe? A report of three maternal deaths. 1967 92


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