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)

It has been noticed that hyperamylasemia occurs after hepatic resection. Between July 1973 and April 1991, hyperamylasemia was observed in 57 (42%) of 136 patients with hepatocellular carcinoma and 13 (32%) of 41 patients with metastatic liver cancer. The incidence was not correlated with extent of resection, blood loss, hypoxemia, disseminated intravascular coagulation, liver cirrhosis, or hepatitis B virus infection. There were three patterns: salivary-type dominant hyperamylasemia (type I), pancreatic-type dominant hyperamylasemia (type II), and a mixture of types I and II (type III). The point at issue is whether types II and III indicate postoperative pancreatitis. Although the pathogenesis remains unclear, surgeons should be alert to this complication and take reasonable measures with regard to the types of hyperamylasemia.
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PMID:Hyperamylasemia after hepatic resection. 768 77

The coagulation parameters of fourteen patients with advanced liver cirrhosis (3 in Child class B and 11 in class C) were prospectively determined quarterly for one year in order to evaluate the possible relationship between high D-dimer levels and incidence of disseminated intravascular coagulation (DIC) and of gastrointestinal bleeding. The values of D-dimer, fibrin(ogen) degradation products, platelets, fibrinogen, prothrombin activity and antithrombin III were fairly stable in almost all patients and no patient developed an overt DIC; one patient had a significant increase in D-dimer three months after the first control. During the one year follow-up, four patients died, one by the occurrence of hepatocellular carcinoma and three by digestive bleeding. Overall, four patients had upper digestive tract bleeding, three from esophageal varices and one from hemorrhagic gastritis. Hemorrhage was more frequent in patients with high D-dimer levels (3/7, 43%) than in patients with normal D-dimer levels (1/7, 14%). In conclusion, the detection of high D-dimer levels in patients with advanced cirrhosis is not predictive for the occurrence of a overt DIC but seems to be related with an increased risk of gastrointestinal bleeding.
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PMID:High D-dimer levels: a possible index of risk of overt disseminated intravascular coagulation and/or digestive bleeding in advanced liver cirrhosis? 801 48

Gammacarboxyglutamic acid (gla) is a non essential amino acid synthesized in presence of vitamin K, predominantly found in coagulation and bone proteins. In 14 cases of deep vein thrombosis and in 11 cases of disseminated intravascular coagulation, compared to 19 normal subjects and 9 patients hospitalized for leg pain, free plasma gla levels were found significantly elevated (respectively 372 +/- 244 and 559 +/- 361 versus 146 +/- 34 and 120 +/- 40 pmol/mL). In six paired plasma and serum, gla levels were similar. These results suggest an involvement of blood coagulation in gla generation with need of a catabolism of the activated factors. A significant decrease was noticed during vitamin K antagonist therapy and liver disease, both instances in which the synthesis of gla containing coagulation factors is affected. During hepatocellular carcinoma with elevated desgamma carboxyprothrombin, gla was found normal, denying an global impairement of the vitamin K metabolism.
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PMID:Increased plasma free gamma carboxyglutamic acid levels during deep vein thrombosis and intravascular disseminated coagulation. 819 12

A 67-year-old Japanese male, suffering from liver cirrhosis with hepatoma, was admitted to the Yokohama National Hospital because of ascites retention. On physical examination, his abdomen was massively distended with ascites and his lower extremities were edematous. Laboratory findings on admission revealed hypoalbuminemia, moderate icterus, pancytopenia and hepatitis C virus antibody positivity. After admission, abdominal distention and edema were improved with the use of diuretics. On the 15th day of hospitalization, the patient noted diarrhea and bowel movements that occurred 10 times a day. On the following day, his body temperature rose to over 39 degrees C. On the morning of the 17th day, he complained of severe pain in the right lower extremity. Swelling and erythema over his right lower leg were evident. The skin lesion spread rapidly over the knee and became necrotic. His right leg became increasingly swollen with the development of edema and hemorrhagic bullae. About 4 hrs after the emergence of the skin lesion, his blood pressure fell to less than 60 mmHg. Laboratory findings suggested disseminated intravascular coagulation and multiple organ failure due to serious bacterial infection. In spite of vigorous treatment including administration of antibiotics, dopamine, gabexate mesilate and plasma, he did not recover from the state of shock and died about 14 hrs after the appearance of leg pain. Bacterial culture of the blood and contents of the bullae grew a gram negative rod identified as Edwardsiella tarda (E. tarda). Histological findings showed necrotizing fasciitis. E. tarda has recently become recognized as a pathogenic bacteria, particularly in patients with an underlying illness. This is the first reported case of E. tarda septicemia with necrotizing fasciitis.
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PMID:[A fulminating case of Edwardsiella tarda septicemia with necrotizing fasciitis]. 874 15

The early stage of the state in which coagulation or fibrinolytic pathway is activated has been difficult to estimate. It has become possible to detect disseminated intravascular coagulation (DIC) at an early stage due to the development of highly sensitive methods which quantitate so called "molecular markers". Herein, to evaluate the clinical usefulness of plasmin-alpha 2-plasmin inhibitor complex (PIC) and tissue factor activity in plasma were examined. The first time, monitoring the plasma levels of PIC might be useful for the diagnosis of a pre-DIC condition and for effective control of therapy. We believed that combination assay for both PIC and D dimer will be adequate to differentiate whether the hemostatic abnormalities are induced mainly by DIC or hepatic insufficiency. Recently, new clinical usefulness of PIC has been reported. The PIC/thrombin-antithrombin III complex ratio was lower in patients with poor prognosis than in those with good prognosis, and it was also lower in those with organ failure than in those without it. The tissue factor is a major activator of the coagulation cascade and may play a role in initiating thrombosis. A simple chromogenic substrate assay for the quantitation of tissue factor activity in plasma samples was developed. Abnormally high levels were found in 80% of the patients with DIC, predominantly in patients with non-hematological solid tumors and acute leukemia. Serial determinations of plasma tissue factor demonstrated that plasma tissue factor changes immediately with the course of DIC. Plasma tissue factor did not correlate with hemostatic markers of DIC such as thrombin-antithrombin III complex, PIC, FDP D-dimer. Tissue factor activity correlated well with membrane anchoring region of tissue factor protein levels. Tissue factor activity correlate with tumor necrosis factor alpha levels in patients with non-hematological solid tumors without hepatocellular carcinoma. These findings suggest that the plasma tissue factor is potentially valuable for monitoring the progress of DIC in a limited population of patients.
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PMID:[Clinical usefulness of the measurements of plasmin-alpha 2-plasmin inhibitor complex and plasma tissue factor activity in patients with disseminated intravascular coagulation]. 881 61

The pathogenesis of disseminated intravascular coagulation (DIC) has, in part, been attributed to the impairment of the natural anticoagulant protein C/protein S pathway. DIC, which frequently occurs during sepsis, has been linked to cytokines that can induce or modulate procoagulant activity. Three of these cytokines, IL-1 alpha, IL-6, and TNF-alpha have been reported to be increased in the early stages of sepsis. In the present study, we have stimulated HepG-2 hepatoma cell cultures with recombinant human IL-1 alpha, IL-6, TNF-alpha, and oncostatin M (OSM). The results demonstrated that TNF-alpha, and to a lesser degree, IL-1 alpha, could significantly suppress IL-6 upregulation of protein S, whereas the effects of OSM was only suppressed by the combination of IL-1 alpha and TNF-alpha. The combination of IL-1 alpha and TNF-alpha also suppressed protein S production below that of control or basal levels. These results indicate that IL-1 alpha and TNF-alpha may play important regulatory roles in coagulation.
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PMID:TNF-alpha suppresses IL-6 upregulation of protein S in HepG-2 hepatoma cells. 892 89

To investigate the role of PAF in tumor-associated disseminated intravascular coagulation (DIC), we have established the tumor-induced DIC model in rats and examined the effect of PAF-antagonist as compared with commonly used anti-DIC drugs. Four days after the intraperitoneal inoculation of rat ascites hepatoma AH-130, DIC-like hematological parameter changes such as decrease in platelet count, prolongation of PTT and increase in FDP were observed. In addition, serum levels of GOT and GPT were increased, indicating that liver injury was provoked. PAF-antagonist SM-12502 inhibited the development of DIC (PT, PTT and FDP) and liver injury. These results indicate that PAF plays an important role in tumor-associated DIC as well as accompanying organ failure.
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PMID:Effect of SM-12502 on disseminated intravascular coagulation (DIC) in tumor-bearing rats. 913 Nov 47

We evaluated the efficacy of recombinant factor VII to correct impaired haemostasis in a patient with liver cirrhosis requiring an invasive procedure. A test intravenous bolus of 80 microg/kg of recombinant factor VII was given to a Jehovah's Witness, with a solitary 4.4-cm hepatocellular carcinoma and underlying hepatitis C virus cirrhosis, in an attempt to correct his haemostatic disorders and safely inject the tumour with alcohol. An extensive portal block had precluded consideration of liver transplantation. Haemostasis was evaluated by clotting assays, bleeding time and thromboelastography 10 min before and 10 min and 1, 2, 4, 8 and 24 h after factor VII infusion. Parameters of both coagulation (prothrombin time) and platelet function (bleeding time and the alpha and ma parameters of thrombelastography) were improved 10 min after factor VII infusion; improvements lasted 4 to 8 h or more. Platelet count did not change and there was no evidence of disseminated intravascular coagulation. The improvements in haemostatic parameters correlated significantly with the increases in factor VII plasma concentrations (p<0.04). Factor VII clearance was 25.1 U/h/kg and its half-life was 5.8 h. The same dose of recombinant factor VII was given to the patient 1 week later, just before the alcohol injections. The patient had no subsequent bleeding or other complication, with no change in haemoglobin levels over 24 h. Thus, recombinant factor VII represents a therapeutic advance, as it can correct fully both coagulation and platelet function defects in cirrhosis and allow invasive procedures to be performed safely.
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PMID:Correction of both prothrombin time and primary haemostasis by recombinant factor VII during therapeutic alcohol injection of hepatocellular cancer in liver cirrhosis. 1055 1

Peritoneovenous shunt placement has been reported as a treatment of refractory ascites by general surgeons, but without a clearly established role. The authors successfully inserted shunts under ultrasonographic and fluoroscopic guidance in 12 patients who had symptomatic refractory ascites (nine men, three women; mean maintenance duration, 88.5 d). Nine patients had advanced liver cirrhosis (five with superimposed hepatoma). Other patients had stomach cancer, colon cancer, and complicated polycystic kidney disease. The mortality rate was 83%. Causes of death included bleeding from preexisting varices, sepsis, hepatic failure, rupture of hepatoma, and disseminated intravascular coagulation. The authors describe the feasibility, technical details, and short-term results of percutaneous peritoneovenous shunt placement.
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PMID:Percutaneous peritoneovenous shunt creation for the treatment of benign and malignant refractory ascites. 1174 23

A 63-year-old male with liver cirrhosis due to type-C hepatitis virus was admitted on June 14, 1999 to our hospital with complaints of dyspnea, and blisters, swelling and purpuras on his legs. He had consumed raw fish one or two days before. He was already in a state of shock with sepsis and disseminated intravascular coagulation shortly after the admission. Although treatment with MEPM and MINO for sepsis, and daltepalin sodium, antithrombin III and gabexate mesilate for disseminated intravascular coagulation was begun within 12 hours, he died only 30 hours after admission. The causative organism was detected from the blood and the contents of blisters, and was determined as Vibrio vulnificus. On autopsy, Vibrio vulnificus was also detected from skin and muscular tissue of his legs, but necrotizing fasciitis were not apparently revealed. Coagulating necrosis and acute tubular necrosis were verified in intestine and kidneys respectively probably due to ischemic changes. Pseudolobuli were formed and a small hepatocellular carcinoma was detected in the liver. Vibrio vulnificus has two infection channels; one is oral intake and the other is an external wound. The former is said to become serious. It has a rather short period from the starting of the symptom to death, and is highly fatal. If this bacteria is suspected by the clinical coarse of the patients or the laboratory examinations, it is necessary to dose effective antibiotics in its early stage. And for prevention, susceptible patients must be informed of the existence of this disease and the necessity of adequately heating raw seafood.
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PMID:[An autopsied case of septicemia due to Vibrio vulnificus]. 1185 76


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