Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have recently experienced a case of Vibrio vulnificus septicemia which occurred in a patient with hepatic cirrhosis, and as we were able to give early antibiotic treatment, the patient survived. We would like to report this case here together with another case experienced 2 years ago. Case 1 was a 58-year-old male who was attending our hospital as an outpatient for hepatic cirrhosis. At 5:30 pm on August 8, 1987, he consumed abalone and giant clam and at 9 pm complained of high fever with shaking chills. He was admitted to our department as an emergency case. Cefoperazone was administered resulting in a decline of fever on the following day. During the course of treatment he fell transiently into pre-DIC, but due mainly to the administration of antibiotics his condition was subsided. Case 2 was a 53-year-old male who was under medical care in our hospital for grave hepatic cirrhosis. On October 11, 1985, he consumed sushi and two days later suffered chills and pyrexia. A blood culture revealed Vibrio vulnificus. His condition improved transiently with administration of Cefazolin, but oliguria, hypotension and ascites occurred subsequently, and finally the patient died on the 22nd day.
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PMID:[Two case reports of septic shock due to Vibrio vulnificus with liver cirrhosis]. 250 32

DIC in patients affected by cirrhosis, accompanied by portal hypertension and splenomegaly, has been suspected in the past. The main aim of this study is to ascertain the incidence of this phenomenon. We carried out coagulation and fibrinolytic tests in 113 cirrhotic patients and 20 healthy control persons. We found chronic consumption coagulopathy at analysis level in 28 cases (24.8%) with a decrease of fibrinogen, factor V, kallikrein, platelets, prothrombin complex activity, increase of PDF, partial thromboplastic time and euglobulin lysis. 25 cases had active cirrhosis, with ascites, variceal bleeding and/or hepatic encephalopathy; 3 were non-active cirrhosis. Only 7 patients had clinical DIC. We observed that coagulation disorders increased with more active cirrhosis.
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PMID:[The incidence of consumption coagulopathy in liver cirrhosis]. 256 20

Malignant ascites is often refractory to therapy and rapidly deteriorating the nutritional and physical state of the cancer patient. Nevertheless, ascites does not always implicate preterminal state of the cancer process (e.g. ovarian carcinoma). A short review is made of the pathophysiology of ascites in cirrhosis and in malignancy, and different modes of treatment are discussed. The results of medical therapy of malignant ascites (salt and water restriction, diuretics, intraperitoneal cytostatics or radiocolloids) are not convincing. The immunotherapy with OK-432, as worked out by Katano (16-46) has to prove its value. The best and most hopeful results in cases of massive previously resistant ascites, are obtained with a peritoneojugular shunt, improving immediately the nutritional status and life condition, providing excellent palliation. The superiority of the Denver shunt versus the Le Veen shunt has been assessed recently, especially for malignant ascites. Some technical and perioperative details merit more attention, to limit the high risk ratio. Control of the intrathoracic position of the catheter tip, the maintenance of the bloodflow in the jugular vein, the intramuscular tunnelisation of the peritoneal catheter, the discard of 3 or 5 liters ascitic fluid and the substitution of part of it by physiological fluid, perioperative prophylactic antibiotics and heparinisation, flow-rate control in the postoperative period by changing patients position, respiratory exercises, daily flushing, all those measures limit the risk of fibrinolysis (DIC), shunt occlusion, fluid overload and infection. The fear of metastasis by shunt is unfounded, since the survival of the primary tumor is mostly too short (41). The postoperative follow up in an intensive care unit is necessary during 24-72 hours.
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PMID:[The Denver shunt in malignant ascites]. 258 Apr 8

Personal experience of 31 patients suffering from intractable ascites due to advanced liver cirrhosis between 1978 and 1987 is reported. Seventeen patients were selected for a peritoneojugular shunt: in 3 patients the Le Veen shunt was performed and in 14 the Denver shunt was preferred. The high postoperative morbidity and mortality due to liver failure, DIC, hepatorenal syndrome, bleeding, sepsis and cerebral thrombosis is pointed out. Careful selection of patients to be submitted to this surgical procedure is essential because of the high morbidity due to ascites reinfusion. DIC has to be diagnosed as soon as possible and, when severe, the prompt interruption of the peritoneojugular shunt is mandatory.
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PMID:[The Denver peritoneojugular shunt. Current indications]. 272 37

Coagulation studies were performed in patients who underwent abdominal surgery. One hundred and twenty six patients with cholelithiasis, peptic ulcer and gastric cancer were examined. Although fibrinogen increased up to 560 mg/dl postoperatively, DIC did not occur among these patients, at all. For 30 patients who underwent hepatectomy, esophageal transection or pancreatoduodenectomy, HPT, PT, fibrinogen, platelet count, alpha 2-PI, AT-III, plasminogen and DIC score were investigated until 10 postoperative days. As for 13 patients without liver cirrhosis in this group, deterioration of HPT, PT and AT-III was noted on the second postoperative day, however these parameters improved on the fifth postoperative day and all patients recovered uneventfully. On the contrary, as to patients with liver cirrhosis, changes of coagulation parameters were drastic. Significant decrease of HPT, PT, AT-III, plasminogen and increase of FDP and DIC score were noted after operation and these values deteriorated with time in certain cases. Seven patients out of 17 died of DIC and multiple organ failure. More than half of these patients received Gabexate Mesilate (GM) injection in a dose of 1200 mg/day postoperatively for more than 5 days to prevent DIC. In patients who underwent hepatectomy due to hepatocellular carcinoma with liver cirrhosis, the increase of FDP and DIC score seemed to be inhibited by GM on the fifth postoperative day.
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PMID:[Coagulation studies in patients after abdominal surgery]. 308 4

Ascitic fluid reinfusion in severe cirrhosis has frequently been associated with intravascular coagulation (DIC). A low-grade DIC has been postulated to be present in liver cirrhosis. PT, APTT, fibrinogen, plasminogen, antiplasmin, fibrin degradation producers (FDP), euglobulin lysis time, tissue plasminogen activator, and fibrinopeptide A were investigated both in the plasma and ascitic fluid of cirrhotic patients before and after the concentration-reinfusion technique. Our results indicate that increased thrombin formation associated with hyperfibrinolysis is present in the plasma of cirrhotic patients. In ascitic fluid very high levels of thrombin and fibrinolysis activation were found. We conclude that (1) a DIC-like picture exists in ascites and (2) after ascites reinfusion procedures, ascitic fluid is the principal factor in the pathogenesis of DIC. During ascitic fluid reinfusion heparin treatment could be used successfully.
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PMID:A DIC-like picture on plasma and ascitic fluid of cirrhotic patients. 314 1

With the aim of temporarily assisting deterioration of liver function developing after surgery, extracorporeal blood purification therapy (EBPT) (plasma exchange and/or hemofiltration) was carried out in 26 postoperative patients. Initiation of EBPT was instituted according to the criteria of either a serum bilirubin greater than 15 mg/dl or Grade 2 or more coma. Plasma exchange was carried out 235 times in 23 patients and hemofiltration was performed 28 times for seven patients. In addition, hemodialysis and CAPD were linked in eight cases. Plasma exchange was found to control the progression of DIC and endotoxemia. Nine patients (35%) were weaned from EBPT. In the survivors the levels of blood ammonia and number of major complications were significantly lower compared to the nonsurvivors. Three patients treated only with hemofiltration were all lost. Among co-morbid factors present, incidences of renal failure, respiratory failure, and associated liver cirrhosis significantly increased poor clinical outcome on EBPT for postoperative liver failure.
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PMID:Temporary metabolic support by extracorporeal blood therapy for liver failure after surgery. 319 18

Using a new rapid coagulant method, protein C activity (PC act) was determined in liver cirrhosis and malignancies and compared with PC antigen and AT III values. PC was decreased in a more pronounced manner than AT III in liver cirrhosis, mainly due to impaired synthesis. This is of special clinical interest because PC proved to be a high sensible indicator of liver cell dysfunction. Decreased levels of PC act (PC ratio act/ag less than 1) in decompensated liver cirrhosis may be caused by the synthesis of dysfunctional PC and/or vitamin K deficiency with production of undercarboxylated PC most sensitively registered by this coagulant assay. An increased clearance of in vivo activated PC induced by DIC may play an insignificant role. In patients with liver metastases, PC act (but not AT III and immunological parameters) was significantly reduced, supporting the conclusion that in these patients liver dysfunction concomitant with synthesis of dysfunctional PC must be discussed as the main cause of this alteration.
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PMID:Immunological and functional determination of the protease inhibitors, protein C and antithrombin III, in liver cirrhosis and in neoplasia. 320 4

A simple assay method of heparin cofactor II (HC II) activity is described. The procedure is based on the following principle: Antithrombin III (AT III) in plasma is inactivated by addition of an IgG fraction of goat serum after immunization of the animals against human AT III. Complete inactivation of AT III could be shown by absence of an anti Xa-effect of heparinized plasma treated with this antibody. Thrombin was only partially inhibited after inactivation of AT III. The characteristics of this inhibition were typical for the action of HC II. This method was applied for an assay of HC II activity. After optimizing of the method practical application in clinical routine screening was carried out. A diminution of HC II was observed in liver cirrhosis and in DIC but not in AT III deficiency. In 15 out of 269 cases of recurrent DVT there were HC II activities below 70% of normal. In 4 out of these patients activities of HC II were repeatedly between 44% and 52%. In arterial obstructive disease there was an HC II activity of less than 60% in 18 out of 583 patients and in 11 of them the HC II levels were repeatedly between 45% and 54%.
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PMID:Heparin cofactor II: a simple assay method and results of its clinical application. 342 87

A study of 93 patients with liver cirrhosis showed that the most important blood coagulation disorder in this pathology resulting in hypocoagulation, was not decreased synthesis and deficit of the prothrombin complex factors but disturbance of the final stage determined by afibrinogenemia. Considerable depression of XIIa-kallikrein-dependent fibrinolysis and marked increment of an antiplasmin level in the plasma were noted. Positive paracoagulation tests were revealed in 57% of the patients, and as other signs typical of the lingering DIC-syndrome were absent, they were interpreted as the "hypercoagulation syndrome" or "pre-DIC syndrome". The problem of possible relationship of development of both thromboses and hemorrhages with acquired afibrinogenemia in liver cirrhosis was discussed.
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PMID:[Role of dysfibrinogenemia and disorders of fibrinolysis in the pathogenesis of hemostatic pathology in liver cirrhosis]. 357 61


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