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

The striking mortality in viral hepatitis associated with pregnancy, regularly observed in developing countries, has shown a significant decrease in Saudi Arabia during a period of unprecedented economic growth. However, the risk of fatal hepatitis in the pregnant Saudi woman remains approximately four times that for the nonpregnant woman. The explanation for the observed mortality trend is not apparent, but is unlikely to be the result of improved nutritional status of the population alone, or because of treatment of severe hepatitis with adrenal corticosteroids. Disseminated intravascular coagulation may be one factor that decisively influences the outcome of hepatitis in the pregnant woman.
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PMID:Viral hepatitis complicating pregnancy: mortality trends in Saudi Arabia. 3 43

A case of a 26-year-old woman who presented at 38 weeks of gestation with severe hepatitis B complicated by disseminated intravascular coagulation (DIC) and hypoglycemia is reported. The clinical features of the illness suggested acute fatty liver of pregnancy. Cesarean section was followed by resolution of the coagulopathy and the hypoglycemia. Both mother and infant survived and remain well. The diagnosis of hepatitis B was confirmed by a transiently positive hepatitis B surface antigen and percutaneous liver biopsy. This case emphasizes the difficulty in distinguishing acute viral hepatitis from acute fatty liver of pregnancy. In addition, the predominant features of DIC and hypoglycemia in our case are reported.
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PMID:Viral hepatitis in pregnancy with disseminated intravascular coagulation and hypoglycemia. 63 35

Patients with liver disease have a variety of coagulation abnormalities. These derangements are of uncertain origin and do not always correlate with disease severity or activity. We have measured the levels and proportions of the total fibrin-related and fibrinogen-related antigens, the principal fibrin (D-dimer) and fibrinogen (D-monomer) degradation fragments and intermediates of fibrin formation (fibrin monomers) in patients with a variety of acute and chronic liver diseases in whom all known other precipitating causes of disseminated intravascular coagulation had been excluded. Fibrin-related and fibrinogen-related antigens were extracted from serum using antihuman fibrinogen-IgG covalently bound to activated amino-phenylthioether paper disks and were subjected to 4% to 11% sodium dodecyl sulfate-polyacrylamide gel electrophoresis under nonreducing conditions. Fibrin-related and fibrinogen-related antigen proportions were determined by densitometry, and their levels were measured by radioimmunoassay. Levels of total fibrin-related and fibrinogen-related antigens (and D-dimer) were significantly elevated (p less than 0.01) in patients with cirrhosis (121 to 641 ng/ml) and hepatocellular carcinoma (416 to 8,786 ng/ml) when compared with patients with acute viral hepatitis (84 to 322 ng/ml) and control subjects (38 to 186 ng/ml). In addition, D-monomer levels were elevated. These findings strongly suggest that disseminated intravascular coagulation is a component of the coagulopathy of certain liver diseases. Because fibrin-related and fibrinogen-related antigens have anticoagulant, vasoactive and immunosuppressive properties, their elevated presence may be biologically significant in these patients.
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PMID:Elevated fibrin-related and fibrinogen-related antigens in patients with liver disease. 132 11

In contrast to the type of bleeding encountered in congenital hemophilia with inhibitors, the diathesis toward bleeding exhibited by patients with spontaneously acquired factor VIII (FVIII) inhibitors often is severe and life threatening. Large hematomas and retropharyngeal or central nervous system hemorrhage may appear suddenly. Thus, a high premium is placed on rapid therapeutic intervention. Several treatment options are at the physician's disposal. The role of factor IX (FIX) complex concentrates, both standard and purposely activated, is discussed. The FIX products are also known as prothrombin complex concentrates (PCCs). Prudent choice of any treatment modality requires weighing its benefits and shortcomings. Advantages of PCCs--particularly the activated products--include availability, ease of reconstitution and administration, and at least partial efficacy; control of bleeding episodes can be achieved with PCCs in many (but not all) instances. One salient disadvantage of therapy with FIX complex concentrates is that they are not subjected to such rigorous viral-attenuation processes as are most of the currently marketed FVIII products. Therefore, a small but definite risk of infection with hepatitis B or C (HBV, HCV) remains. An assay that detects antibodies against HCV has been licensed and is being used to screen blood donors. Nevertheless, up to the present time the U.S. Food and Drug Administration (FDA) has ruled that HCV screening of plasmapheresis donors should not be performed for plasma collections destined to be pooled for fractionation and that units of HCV-positive source plasma (e.g., that provided by American Red Cross donors) found to be HCV positive be sent for fractionation. The starting plasma from which FIX complex concentrates and human FVIII concentrates are made thus contains some HCV and may also contain some HBV. Because nonhemophiliacs with acquired antibodies against FVIII are unlikely to have had prior exposure to blood products and are unlikely to have been vaccinated against HBV, they are at risk of viral hepatitis and its sequelae when treated with FIX complex concentrates. Furthermore, therapy with FIX complex concentrates is not always effective in controlling bleeding in persons with FVIII inhibitors, its mechanism of action in bypassing the need for FVIII remains unclear, very large doses are required, and it has an attendant risk of several adverse effects when used in large, repeated doses. These include disseminated intravascular coagulation, thromboembolism, and acute myocardial infarction. Thus, FIX complex concentrates may play a useful role in the treatment of bleeding in nonhemophiliacs with acquired inhibitors against FVIII, but one must carefully consider their disadvantages profile.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Perspectives on the use of factor IX complex concentrates in the treatment of bleeding in persons with acquired factor VIII inhibition. 174 94

A study is presented of 159 patients with cholestatic forms of viral hepatitis and 82 patients with viral hepatitis showing no cholestasis. The disorders of the coagulation activity were found to be nonhomogeneous and depended on the clinical variant of viral hepatitis, the period and severity of the disease, premorbid background and ways of infection. It is emphasized that development of the syndrome of disseminated intravascular coagulation is characteristic of the most severe forms of hepatitis against the background of prolonged and maximal bile stasis as well as in viral hepatitis B. Use of heparine, contrical and antihemorrhagic drugs when indicated prevents or controls the DIC syndrome.
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PMID:[The hemostatic system and DIC syndrome in cholestatic forms of viral hepatitis]. 260 5

Treatment of the coagulation disturbances developing with hepatic damage following a paracetamol overdose was assessed in a controlled trial of 22 patients, one half being given heparin and fresh frozen plasma and the other fresh frozen plasma alone. No significant difference was observed either in the speed of correction of the coagulation defect or in the clinical outcome. Two-thirds of the patients had evidence of disseminated intravascular coagulation, but despite the presence of a severe coagulation defect, significant bleeding occurred in only five patients. This may be because with paracetamol-induced hepatic necrosis both the coagulation defect (and possibly other features attributable to severe hepatic insufficiency) are of shorter duration than in hepatic necrosis due to causes such as viral hepatitis in which the liver damage may be a continuing process.
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PMID:A controlled trial of heparin therapy in the coagulation defect of paracetamol-induced hepatic necrosis. 482 Jun 42

We report a 20 year-old woman with hemophagocytic syndrome. In February 1993, she developed high fever, arthralgia, salmon-like pink eruption, leukocytosis and splenomegaly. She was diagnosed as adult Still's disease and successfully treated with intravenous immunoglobulin and oral prednisolone. In September 1993, she was re-admitted to our hospital complaining of general fatigue and low grade fever and treated with oral prednisolone at a daily dose of 15 mg. On October 2, 1993, she suddenly developed high fever and salmon-like pink eruption on her leg followed by the marked increase of serum transaminase and LDH levels (GOT 3,270 IU/l, GPT 1,880 IU/l, LDH 5,480 IU/l) on October 7. Since hepatic failure progressed, we started methylprednisolone pulse therapy and plasmapheresis. However, because of the progression of pancytopenia caused by hemophagocytosis, the treatment with VP-16 was initiated. However, she died of DIC on November 2, 1993. Autopsy revealed submassive necrosis of the hepatocytes with moderate infiltration of histiocytes. She was retrospectively diagnosed as hemophagocytic syndrome whose manifestations are very similar to those in adult Still's disease and acute viral hepatitis.
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PMID:[A case of hemophagocytic syndrome manifesting adult Still's disease and acute hepatitis]. 755 62

A woman aged 63 presented with septic fever, followed by hepatocellular jaundice. Viral hepatitis was ruled out by serologic tests, but no definite diagnosis could be made. Due to severe disturbance of the plasmatic coagulatory system and a serum bilirubin level above 4 mg/dl, a liver biopsy was not performed. The patient had a persistent septicemia refractory to Imipenem. In spite of intensive care measures, the patient died of disseminated intravascular coagulation and multiorgan failure caused by septic shock. The correct diagnosis of miliary tuberculosis was made only post mortem by histopathological examination of liver specimens and confirmed by detection of Mycobacterium tuberculosis DNA in the patient's liver by polymerase chain reaction.
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PMID:[Miliary tuberculosis of the liver as a cause of septic shock with multi-organ failure]. 816 13

Plasmic, platelet and fibrinolytic components of hemostasis were studied in 115 patients with severe viral hepatitis C transmitted fecally and orally. Most informative for determination of the disease severity and prognosis of onset of acute hepatic encephalopathy within 1-2 days were plasmic factor II, V, VII, X. In genesis of hemorrhagic syndrome of importance is procoagulant deficiency as a result of detective synthesis and consumption due to DIC syndrome rather than platelet disorder. In addition to procoagulant disorders there were low levels of plasminogen and its inhibitors changing with the disease severity.
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PMID:[The hemostatic system in patients with viral hepatitis C]. 864 6

40 patients with infective endocarditis (IE) abusing intravenous drugs (heroin, opium surrogates) and 9 IE patients predisposed to heart diseases were examined by Duke diagnostic criteria. IE in drug abusers is characterized by acute course of the disease with affection of the intact valves of the right heart (97.5%) and septicemia provoked by high-virulent microflora (Staph. aureus in 65%). Drug abusers showed the following principal clinical syndromes of IE: thromboembolic (65%); septic with formation of acute DIC syndrome (75%), development of pyodestructive foci in the organs and polyorganic insufficiency (23.3%); acute circulatory insufficiency (37.5%); secondary nephropathy (100%). In IE abusers with predisposition to heart diseases IE ran subacutely in the presence of bacteriemia caused by low-virulent microflora (Strept. viridans in 11%) or in the absence of microbial growth in blood seeding (78%). High IE lethality in drug abusers (40%) is explained both by severe complications and concomitant diseases (viral hepatitis B and C, HIV infection, etc.).
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PMID:[The course of infectious endocarditis in IV drug abusers and in subjects predisposed to heart diseases]. 1158 79


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