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)

Histopathological lesions due to rabbit haemorrhagic disease (RHD) and European brown hare syndrome (EBHS) were studied in 35 rabbits and seven hares. Both rabbits (Oryctolagus cuniculus) and hares (Lepus europeus) regularly showed severe necrotizing hepatitis. In RHD, coagulation necrosis, mainly confined to the periphery of the lobules, was consistently found. In EBHS, lytic necrosis affecting the whole lobule was conspicuous, at least in severe cases. Particularly in EBHS, necrotic hepatocytes exhibited a special kind of karyorrhexis. In rabbits with a subacute or subclinical form of disease, early liver cirrhosis was observed. Depletion of lymphocytes was a regular feature in spleens of rabbits and was frequently found in hares. In RHD, disseminated intravascular coagulation (DIC) and haemorrhages in different organs, especially in kidneys and lungs were constant findings. DIC was never seen in EBHS and haemorrhages were an infrequent finding.
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PMID:Comparative histopathological study of rabbit haemorrhagic disease (RHD) and European brown hare syndrome (EBHS). 143 Mar 43

A 63 year old man underwent MCA aneurysmal neck clipping under O2-N2O-enflurane anesthesia. On the 46th postoperative day after the first operation, he had cranioplasty under O2-N2O-sevoflurane anesthesia. Hepatic injury occurred after the operation, and GOT, GPT and bilirubin increased above 700 IU.l-1, 800 IU.l-1 and 15.0 mg.dl-1 respectively but consciousness disturbance, hyperammonemia and DIC did not appear. His hepatic injury improved on conservative therapy. It seems that his hepatic injury was not caused by hepatitis viruses or hepatotoxicity of any drugs, but caused by cross sensitization between halogenated inhalation anesthetics, especially enflurane and sevoflurane, judging from drug induced lymphocyte stimulating test (DLST). We have to select an anesthetic method considering potential hepatic injury by halogenated anesthetics in a case of repeated anesthesia and operations during a short-term.
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PMID:[A case of postoperative hepatic injury after sevoflurane anesthesia]. 146 Jul 59

An autopsy case of fulminant hepatitis caused by herpes simplex virus type 1 in a healthy adult is presented. The clinical course was characterized by hepatic failure, disseminated intravascular coagulation and acute renal failure. Many small ulcerations were present in the tongue and tonsils, and there were foci of hemorrhagic necrosis in the liver. Herpes simplex viral antigen was identified in the liver, tonsils, spleen, tongue, pharynx, larynx, esophagus, stomach, intestine, adrenal glands, and lymph nodes with immunohistochemical staining using antibodies to herpes simplex virus type 1. The electron microscopic examination revealed many virions in the hepatocytes. Herpes simplex virus was isolated from the liver, and viral DNA, which had some distinctive features of herpes simplex virus type 1, was examined. We discuss possible reasons for this opportunistic infection occurring in a healthy adult.
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PMID:Disseminated infection of herpes simplex virus with fulminant hepatitis in a healthy adult. A case report. 165 35

Obstetric hysterectomy was performed on 121 women at Ramathibodi Hospital, Bangkok, between 1969 and 1987, an incidence of 1:875 deliveries. Of 88 women whose records were available, 91% had emergency hysterectomy, with uterine atony as the most common indication (32.5%), followed by placenta accreta (26.2%), uterine rupture (10.0%), extension of cervical tear to the lower uterine segment (8.7%), broad ligament hematoma (6.2%) and placenta previa (5.0%). The intraoperative and postoperative problems included febrile morbidity (52%), intraoperative hypotension (41%), and disseminated intravascular coagulation (5.7%). Late complications included Sheehan's syndrome (3.4%), post-transfusion hepatitis (2.3%), hematoma (2.3%) and wound infection (2.3%).
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PMID:Obstetric hysterectomy: Ramathibodi's experience 1969-1987. 168 51

We investigated changes in the concentrations of thrombin-antithrombin III complex (TAT) and plasmin-alpha 2 plasmin inhibitor complex (PIC) after the intravenous administration of 4000 units of antithrombin III (AT III) concentrate to patients with fulminant hepatic failure (FHF), subacute hepatitis (SH), or liver cirrhosis (LC). FHF patients showed shortening of the initial half-life of exogenous AT III. In addition, a marked rise in plasma TAT was noted 3 to 6 h after the intravenous administration of AT III, even in patients who had a normal plasma TAT level before AT III therapy. In contrast, SH and LC patients showed no marked changes of plasma TAT levels after AT III administration. No marked changes were observed in the PIC concentration in any of the patients. These findings suggest that thrombin formation is increased in FHF and that simple measurement of the plasma TAT concentration is not an adequate method for assessing thrombin formation in FHF patients who have suspected disseminated intravascular coagulation associated with an apparent decrease in AT III synthesis. Instead, it seems necessary to measure the plasma TAT concentration in FHF patients after replacement therapy with AT III concentrate has been performed, to evaluate their hypercoagulability more accurately.
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PMID:Importance of measuring plasma thrombin-antithrombin III complex levels when using antithrombin III concentrate therapy in fulminant hepatic failure. 175 55

Twelve patients developed herpes simplex (HSV) hepatitis a median of 18 days after solid organ transplantation. This is earlier than cytomegalovirus hepatitis, which usually occurs 30-40 days after transplantation. Eight recipients (67%) died, and in seven, the diagnosis was made at autopsy or less than 48 h before death. Clinical manifestations associated with mortality were hypotension, disseminated intravascular coagulation (DIC), metabolic acidosis, gastrointestinal bleeding, and bacteremia. Laboratory abnormalities at diagnosis associated with mortality were high creatinine, low platelet counts, prolonged partial thromboplastin time, and a high percentage of band forms on the blood smear. Disseminated HSV disease was noted in four of six patients who had an autopsy and included involvement of lungs in three and the gastrointestinal tract in three. Five recipients developed DIC and all died. Pathologically, HSV hepatitis has two forms, focal and diffuse. All three patients with diffuse liver pathology died. However, three of seven with focal liver pathology survived with antiviral therapy, which suggests that early diagnosis and treatment may be lifesaving. None of these patients had received prophylactic acyclovir. It is possible that acyclovir prophylaxis may be able to prevent this disease.
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PMID:Herpes simplex virus hepatitis after solid organ transplantation in adults. 185 Apr 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.
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PMID:[Abnormal prothrombin in acute hepatic failure: the characterization and clinical evaluation]. 185 1

The respective roles of intravascular coagulation (DIC) and fibrinolysis were assessed in severe chronic liver disease by measuring thrombin-antithrombin (TAT) complexes, tissue-type plasminogen activator antigen (tPA Ag) and fibrinogen and fibrin degradation products (FgDP and FbDP respectively) in 66 patients with liver disease caused by cirrhosis (n = 34) or chronic hepatitis (n = 32) as compared to findings in a control group (n = 30). There was a significant increase of TAT complexes (P less than 0.01), tPA Ag (P less than 0.002), FDP and FbDP (P less than 0.001) in patients as compared to controls. FbDP increase was more evident in patients with cirrhosis than in those with hepatitis (P less than 0.01). Significant correlations between these parameters with some liver function tests were also demonstrated. Thus, in patients with severe liver disease, an increased thrombin activity, as demonstrated by high TAT levels; followed by hyperfibrinolysis suggest that a low grade DIC may occur.
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PMID:Thrombin activation and increased fibrinolysis in patients with chronic liver disease. 190 1

A 70-year-old woman was admitted for evaluation of hepatosplenomegaly, fever and elevated serum LDH levels. A biopsy specimen of the liver revealed histiocytic proliferation at the portal triad, and a mild degree of hepatitis. A bone marrow biopsy specimen showed proliferation of histiocytes with minimal immaturity and atypism, and haemophagocytosis by the proliferated histiocytes. Fever, hepatosplenomegaly and elevation of LDH levels all disappeared spontaneously, and presumptive diagnosis of benign reticulosis with haemophagocytosis was made. One year later, fever, hepatosplenomegaly and elevation of LDH levels redeveloped, and the liver and bone marrow biopsy specimen showed proliferation of unequivocally malignant histiocytes. The patient died as a result of disseminated intravascular coagulation with shock 20 d later. We concluded that, in this case, malignant histiocytosis first presented as benign haemophagocytic reticulosis and, 1 year later, there was a typical malignant presentation.
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PMID:Unusual clinical presentation of malignant histiocytosis in a 70-year-old woman. 206 13

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.
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PMID:[Qualitative analysis of tissue plasminogen activator in plasma obtained from various liver diseases by gel filtration and affinity chromatography]. 210 95


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