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Query: UMLS:C0012739 (
disseminated intravascular coagulation
)
8,673
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A patient with
chronic active hepatitis
developed vomiting, dyspnoea, tachycardia, diarrhoea and diffuse pains. For several years she had been treated with azathioprine and for a few weeks before admission with phenformin for mild diabetes. Laboratory examination revealed acute
disseminated intravascular coagulation
and lactacidaemia. Despite intensive treatment the patient died a few hours after admission, the post-mortem examination revealing diffuse pulmonary haemorrhages. The present case report and those published in the literature suggest that phenformin should not be given to diabetics who also have renal or hepatic disease. In any case, if phenformin is given, it should be stopped if hepatic, renal, infectious or thrombotic complications occur. In these cases and those of sudden unexplained deterioration in diabetics, hospitalisation is essential and lactic acid levels should be determined and coagulation tests performed.
...
PMID:[Lactacidaemia and disseminated intravascular coagulation associated with phenformin medication (author's transl)]. 114 86
In liver disorders alterations of the coagulation system are mainly due to a reduced synthesis of coagulation proteins. In addition, an enhanced intravascular consumption of coagulation factors is discussed controversely in liver diseases. By measuring factor IXiAT- and TAT-complexes we tried to find out, whether coagulation activation in liver patients leads to activation of the complete coagulation cascade followed by
DIC
or whether in some diseases a futile partial coagulation activation develops. In all liver diseases examined, elevated factor IXiAT-complexes were demonstrated, while TAT-complexes were only elevated in
chronic active hepatitis
, metabolic decompensated liver cirrhosis and in patients suffering from end stage liver disease. We conclude that all liver diseases examined lead to an activation of the coagulation cascade. A complete activation followed by
DIC
only occurs in patients with very severe liver disorders.
...
PMID:Coagulation activation in liver diseases. 181 43
A method of apheresis of plasma euglobulin fraction, cryoglobulins and Willebrand factor was developed. In one session of plasmapheresis 1500-1700 ml of patient's plasma were removed, fractionated and returned. The method was used in 2 patients with immune complex vasculitides. In one of them the disease developed against a background of
chronic active hepatitis
, in the other patient it manifested itself in cryoglobulin- and cryofibrinogenemia. Clinical improvement was noted in both cases: the absence of myalgia, arthralgia, hemorrhagic eruption, and ulcerative-necrotic skin changes. The normalization of increased ristomycin-cofactor activity of Willebrand factor and CIC levels was noted in one case. A decrease in the content of plasma cryoglobulins, cryofibrinogen, and urine protein concentration (from 1.5 up to 0.03%) was noted in the other case. A possibility of the use of the method in other pathological conditions (
DIC
-syndrome, unstable angina, atherosclerotic angiopathy) accompanied by endothelial damage, was discussed. Willebrand factor multimers form complexes with low density lipoproteins therefore the removal of these complexes may be useful in the treatment of hypercholesteremia and atherosclerosis.
...
PMID:[Apheresis of euglobulins, cryoglobulins and the von Willebrand factor in vasculitis]. 295 14
The clinical and pathologic features of Epstein-Barr virus (EBV) hepatitis in 3 children are described. Manifestations included fever, hepatomegaly,
disseminated intravascular coagulation
, and failure of uptake of technetium by the reticuloendothelial system of the liver. Histologic features may mimic
chronic active hepatitis
and lymphoid malignancy. Two patients underwent exploratory laparotomy because of suspected tumor. Recognition of the wide spectrum of hepatic involvement in infectious mononucleosis is important in the differential diagnosis of hepatomegaly. Diagnosis should be made by measurement of IgM-specific EBV antibodies.
...
PMID:The spectrum of Epstein-Barr virus hepatitis in children. 302 40
Serious hepatotoxicity is uncommon with the proper therapeutic use of non-narcotic analgesics but experience with new non-steroidal anti-inflammatory drugs (NSAIDs) is limited. Drugs such as ibufenac, fenclofenac and benoxaprofen were withdrawn from the market because of hepatotoxicity, and liver damage has been reported on occasion with virtually all non-narcotic analgesics. However, a clear pattern of toxicity with characteristic clinical, biochemical and histopathological abnormalities has emerged with relatively few. With the exception of acute hepatic necrosis following overdosage of paracetamol, little is known of the mechanisms of liver injury induced by non-narcotic analgesics. Involvement of the liver in a generalised drug reaction does not imply specific hepatotoxicity. About 50% of patients given aspirin regularly in anti-inflammatory doses develop mild, dose-dependent reversible liver damage as shown by elevation of the plasma aminotransferase activity. Liver damage is more severe in a small minority and it may rarely be complicated by
disseminated intravascular coagulation
and encephalopathy with a fatal outcome. There have also been isolated reports of
chronic active hepatitis
associated with the use of salicylates. Salicylate hepatitis has been reported most often in young females with connective tissue diseases. Many patients with Reye's syndrome have been given aspirin during the prodromal phase, and this serious condition closely resembles subacute salicylate intoxication in children. Salicylate probably has a causal or contributory role in Reye's syndrome, but many refuse to accept this and the issue is the subject of heated debate. Paracetamol in overdosage causes acute hepatic necrosis, and liver damage has been attributed to its therapeutic use. However, most reports have involved chronic alcoholics who took excessive doses and in these patients the clinical, biochemical and pathological findings were typical of paracetamol overdosage. Many authors have failed to make the distinction between therapeutic use and a therapeutic dose. In other cases liver damage could have been caused by exposure to other agents, viral infection or naturally occurring liver disease. If these cases are excluded, there are very few reports of liver damage associated with the proper therapeutic use of paracetamol. In some cases, the picture resembled
chronic active hepatitis
but no causal relationship has been established between this condition and paracetamol use. Paracetamol does not cause deterioration in liver function in patients with chronic liver disease.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Effects of non-narcotic analgesics on the liver. 355 80
Plasma fibronectin concentrations were significantly (P less than 0.001) below the reference range in dogs with
disseminated intravascular coagulation
(
DIC
) secondary to nonlymphomatous neoplasia, acute necrotizing pancreatitis, sepsis,
chronic active hepatitis
, and heat stroke. There was no statistical evidence of a group effect. Decrease in fibronectin concentration was associated with severe
DIC
, although no attempt was made to correlate fibronectin concentration with prognosis. These findings parallel those reported for severely ill human beings with diseases associated with
DIC
. They exemplify the potential of spontaneous diseases in animals as models for the study of human disease.
...
PMID:Plasma fibronectin concentrations in dogs with disseminated intravascular coagulation. 400 93
An analysis was made of 41 cases of
disseminated intravascular coagulation
in dogs, with the objective of evaluating routine and nonroutine laboratory tests used in making the diagnosis. The dogs were grouped on the basis of underlying disease, which included neoplasia (39%), pancreatitis (30%),
chronic active hepatitis
(15%), heat stroke (12%), and sepsis (4%). Of the diagnostic tests evaluated, those for determination of activated partial thromboplastin time, antithrombin III activity, prothrombin time, and the platelet count were the most valuable. Of the clotting factors, factor V activity was decreased more frequently than the activity of factor VIII:C (factor VIII: procoagulant). The factor VIII:C activity was in conflict with prevailing dogma that reflects depression of this factor in
disseminated intravascular coagulation
. Factor VIII:C activity was decreased in only 29% of dogs studied. Activation of the fibrinolytic system was manifested by decreased plasminogen activity in 49% of the dogs studied. Sixty-one percent of the dogs had increased amounts of fibrin (ogen) degradation products.
...
PMID:Disseminated intravascular coagulation: antithrombin, plasminogen, and coagulation abnormalities in 41 dogs. 726 67
We report on a 70-year old woman with
chronic active hepatitis
and portal gastropathy who was treated with TIPS. On day 28 after TIPS implantation hemobilia occurred and radiological examination of the abdomen showed migration and kinking of the portal stent. During an emergency intervention the dislocated stent was splinted with a further stent. The suspected portobiliary fistula, however, could not be detected. The subsequent angiography of the hepatic artery showed an arteriobiliary fistula in the area of the dislocated stent. By means of microparticles and coils this fistula could be occluded angiographically; the bleeding stopped completely. Three days after the successful occlusion of the arterio-biliary fistula the patient died of
disseminated intravascular coagulation
. We therefore recommend in case of hemobilia after TIPS placement an immediate evaluation of the bleeding to exclude an arterio-biliary communication. In order to avoid stent dislocation it is advisable not to use combination of stents with a different design (e.g., Wall-stent and Palmaz-stent).
...
PMID:Arterio-biliary fistula after transjugular intrahepatic portosystemic shunt: a life-threatening complication of the new technique for therapy of portal hypertension. 761 Jun 93