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Query: UMLS:C0012739 (
disseminated intravascular coagulation
)
8,673
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Part I: Immunological assays of clotting factors in the diagnosis of liver diseases. The immunological determination of Antithrombin III is a good measure of the capacity of the liver to synthesize plasma proteins. Antithrombin III concentration in serum correlated significantly with the prothrombin time and the activity of cholinesterase. The immunological determination of factor VIII related antigen seems to be important for the early recognition of the transition of an
acute hepatitis
into a chronic course. While following uncomplicated
acute hepatitis
the level of factor VIII related antigen is normal after 40 weeks, it remains high in cases which become chronic. Immunological assay of factor XIII seems to be not very useful in the diagnosis of liver diseases. Part II: Management of coagulation disturbances in liver diseases. Except cases of hepatic coma the hemostatic abnormalities in chronic liver diseases are rarely severe enough that correction is necessary. Prothrombin concentrates are considered by most of the discussants as unnecessary and potentially dangerous. Transfusion of platelets is only neccessary when the platelet count is below 40.000 and surgery is planned. It is uncertain whether patients with chronical liver disease and laboratory signs of
DIC
benefit from heparin therapy. Although laboratory tests may be improved, prognosis, especially in cases of acute oesophageal bleeding, seems to be not changed by this treatment.
...
PMID:[Summary of work session 1: Blood coagulation in gastroenterology]. 78 39
Abnormal prothrombin was detected by latex agglutination method in the plasma of the patients with acute hepatic failure (AHF) at significantly higher rate (82% of fulminant hepatitis and 100% of subacute hepatitis) than in
acute hepatitis
(33%). The concentration of abnormal prothrombin was also significantly higher in acute hepatic failure. Since the concentration of abnormal prothrombin reversely correlated with that of hepaplastin test or prothrombin time, the measurement of plasma abnormal prothrombin seemed to be useful in monitoring the severity of acute hepatic injury. Interestingly, enzyme immunoassay which is specific for des-gamma-carboxy prothrombin (PIVKA-II) could not detect abnormal prothrombin in acute hepatic failure. Furthermore, in crossed immune-electrophoresis, the abnormal prothrombin in AHF and that in
disseminated intravascular coagulation
syndrome showed similar mobility differing from PIVKA-II. These results suggest that abnormal prothrombin can be a useful marker for AHF. Further characterization of the abnormal prothrombin may shed light on the mechanisms of severe coagulopathy in AHF.
...
PMID:[Abnormal prothrombin in acute hepatic failure: the characterization and clinical evaluation]. 185 1
Tissue plasminogen activator (t-PA) in plasma obtained from patients with
acute hepatitis
, chronic hepatitis, liver cirrhosis, hepatocellular carcinoma, drug-induced intrahepatic cholestasis, obstructive jaundice, fulminant hepatitis or
disseminated intravascular coagulation
(
DIC
), was analysed chromatographically. Liver disease cases showed a new peak (peak C) on HPLC fractionation. The protein of peak C had a lower molecular weight than ovalbumin. Lysine- and zinc- chelating affinity chromatography revealed that the peak C consist with the light chain (L-chain) of t-PA. The L-chain was also found in patients with
DIC
, but disappeared after improvement of
DIC
. Therefore, it was suggested that appearance of the L-chain would be related to acceleration of secondary fibrinolysis in plasma. The L-chain was especially high in plasma obtained from patients with decompensated liver cirrhosis. These results indicated that high increase of the L-chain in cases of severe liver disease may be due to either impaired clearance of t-PA in the liver or secondary hyperfibrinolysis accompanied by
DIC
. We concluded that determination of the L-chain of t-PA may contribute to clarify the mechanism of hyperfibrinolysis in liver diseases.
...
PMID:[Qualitative analysis of tissue plasminogen activator in plasma obtained from various liver diseases by gel filtration and affinity chromatography]. 210 95
Previous studies have demonstrated that plasma tissue plasminogen activator (t-PA) level was elevated in patients with liver disease. In this study, t-PA antigen levels were investigated in patients with
acute hepatitis
(AH; N = 12), chronic hepatitis (CH; N = 8), compensated liver cirrhosis (CLC; N = 40), decompensated liver cirrhosis (DLC; N = 23) and hepatocellular carcinoma (HCC; N = 35). The increased t-PA levels (higher than 14 ng/ml) were found in 33% (4/12) of AH on the early hospital days, 25% (2/8) of CH, 45% (18/40) of CLC and 91% (21/23) of DLC, and 60% (21/35) of Hcc cases. In patient with LC, the correlations between t-PA levels and serum total bilirubin (T.Bill) and hepatic synthetic functions were investigated. The results were that the t-PA levels correlated positively with T. Bil and negatively with liver synthetic functions such as albumin, protein C and choline-esterase, indicating that t-PA increased almost in proportion to the deterioration of hepatic function. Serial determination of t-PA in patients with HCC treated by transcatheter arterial embolization (TAE) revealed that TAE failed to normalize the t-PA levels. In one case of HCC complicated with
disseminated intravascular coagulation
(
DIC
), t-PA showed a marked increase at acute phase of
DIC
and subsequent decrease after the successful treatment for
DIC
by gabexate mesilate (FOY) infusion. These results suggest that increased t-PA in liver disease is due mainly to deterioration of hepatic function, and that secondary fibrinolytic state, such as
DIC
, is also a contributing factor.
...
PMID:[Evaluation of plasma tissue plasminogen activator (I-PA) levels in patients with liver diseases]. 210 6
With a quantitative blood endotoxin assay using a chromogenic substrate with a perchloric acid pretreatment (PCA-LCT), endotoxemia in various liver diseases was studied. With PCA-LCT, recovery of added endotoxin in human plasma was nearly 90%, as evidenced by an intra- and inter-assay coefficients of variation of 5.7% and 11%, respectively. Because the recovery of endotoxin was not affected in severely icteric plasmas, PCA-LCT proved to be applicable to patients with liver diseases where various degree of jaundice exist. In none of the plasmas from patients with chronic hepatitis,
acute hepatitis
without hepatic failure or liver cirrhosis without ascites did the endotoxin level exceed the normal range of less than 5 pg/ml. With the presence of ascites, however, endotoxemia became detectable, but at low levels and not in all cases. At the stage of hepatic failure complicated with renal failure or
disseminated intravascular coagulation
, endotoxemia was more frequent and endotoxin concentration greater. It is uncertain, at present, whether endotoxemia itself is deteriorating factor in hepatic failure or is merely concomitant phenomenon resulting from Kupffer cell failure.
...
PMID:Endotoxemia in liver diseases: detection by a quantitative assay using chromogenic substrate with perchloric acid pretreatment. 300 75
Four cases on non-A, non-B
acute hepatitis
have been observed in infants of the same family. No evidence of hepatitis A or B (HBs-Ag, anti-HBs antibodies, HBe-Ag, anti-HBe and anti-HBc antibodies) could be detected in sera. Virological investigations showed no evidence of cytomegalovirus, Epstein-Barr virus, infection, etc. The two younger infants developed
disseminated intravascular coagulation
and died. The other two recovered without sequelae.
...
PMID:[Severe and fatal non-A non-B hepatitis in 4 young and children]. 623 41
To investigate the pathogenesis of fibrinolysis in liver disease, antithrombin III (AT III) activity, prothrombin fragment (F1 + 2) and d-dimer (D-DI) were measured in 50 patients with liver disease and in 17 healthy controls. Moreover, 4 patients with cirrhosis were randomly assigned to receive either an intravenous infusion of AT III (at two different dosages) or placebo, with a crossover design. Increased levels of D-DI were detected in patients with cirrhosis and hepatocellular carcinoma in comparison both with control subjects and with patients with
acute hepatitis
or mild chronic liver disease. An inverse correlation was observed between AT III and D-DI (r = -0.755, P < 0.001, simple linear regression), while no correlation was found between D-DI or AT III and F1 + 2. The correlation of the deficiency of AT III activity by infusion of human AT III did not result in any significant change (P0.10, analysis of variance for repeated measures) of the plasma concentration of either D-DI or F1 + 2, in comparison to placebo. Thus, advanced forms of chronic liver disease, but not
acute hepatitis
and mild forms of chronic liver disease, are associated with increased plasma concentrations of markers of fibrinolysis, which are inversely correlated with AT III activity. However, the correction of the deficient AT III activity does not affect the plasma concentration of either D-DI or F1 + 2, thence not supporting the hypothesis that enhanced fibrinolysis in advanced liver disease is the result of low-grade
disseminated intravascular coagulation
.
...
PMID:Deficient antithrombin III activity and enhanced fibrinolysis in patients with liver disease: evidence against a cause-effect relationship. 757 84
"Ecstasy" or 3,4-methylenedioxymethylamphetamine, is a synthetic amphetamine which is increasingly consumed in Spain as a "recreational" drug. It has been associated with serious medical and psychiatric side effects, though, it is popularly considered, as a non dangerous drug. The development of
acute hepatitis
associated with the use of "ecstasy" has been reported by other authors from areas where its use is widely spread. We report the development of
acute hepatitis
associated with use of "ecstasy" in a young man with successful recovery and spontaneous resolution. In other cases the
acute hepatitis
may have a torpid evolution with slow resolution, fulminant liver failure, and death with hepatic encephalopathy,
disseminated intravascular coagulation
and adult distress syndrome. An idiosyncratic toxic hepatitis might be due to either 3,4-methylenedioxymethylamphetamine or a metabolite, a contaminant in 3,4-methylenedioxymethylamphetamine manufacture, or to an additive in tablet or capsule formulation.
...
PMID:[Acute hepatitis due to ingestion of Ecstasy]. 757 30
Symptoms of endogenic hepatic coma were observed in the course of
acute hepatitis
in 17 patients admitted to the I Clinic of Infectious Diseases of Silesian Medical School between 1987 and 1992. Five of them were treated with the arterialization of portal blood. At least one exchange transfusion preceded the arterialization in four cases. Recovery was obtained in 3 patients. Two patients died because of complications which occurred during the twenty-four hours after the intervention. In the first case the reason of the death was the extensive myocardial infarction, in the second one-
DIC
and ARDS. As it has been observed, the prothrombin rate should not be lower than 30% in these patients who are to undergo the arterialization of portal blood. This value of the prothrombin rate is provided by at least one exchange transfusion.
...
PMID:[Endogenic hepatic coma in the course of acute hepatitis treated with arterialization of portal blood]. 823 45
We studied four patients who presented a striking elevation of blood transaminases suggesting
acute hepatitis
. The post mortem histological examination of the liver revealed centrolobular necrosis that is commonly diagnosed as ischaemic hepatitis. The liver necrosis arose from heart failure which was worsened by an acute anaemia in one patient and by a severe hypoxemia, due to respiratory failure, in another. In three subjects there was evidence of
disseminated intravascular coagulation
that may be responsible for aggravating the condition of liver hypoxia. The authors also review the literature on the various aspects of ischaemic hepatitis.
...
PMID:[Ischemic hepatitis. Description of 4 cases and review of the literature]. 836 7
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