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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reports in the literature on the difficulty of differential diagnosis between Disseminated Intravascular Coagulation (DIC) Pseudo-DIC and Primary Fibrinolysis (PF) in patients with liver disease, stimulated a study of various coagulation parameters (PT, PTT, Platelets, Fibrinogen, FDP) in 28 cirrhotic patients. The study confirmed reports in the literature on the high incidence of circulating FDP among liver disease patients. The vital role these play in maintaining alterations in haemostasis means that cirrhosis cases must be approached with extreme caution, avoiding any therapeutic or instrumental procedure liable to worsen the already disturbed coagulation pattern in such patients.
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PMID:[Evaluation of several parameters of coagulation in liver cirrhosis: disseminated intravascular coagulation or pseudo-disseminated intravascular coagulation?]. 336

Blood platelets were assayed in 56 cirrhosis patients divided into two groups: alcoholic cirrhosis (20 cases) and non-alcoholic cirrhosis (36 cases). Each group was also divided into two sub-groups: with and without clinical signs of portal hypertension. Low platelet counts were found in both groups (greater than 70%), the incidence being high in the sub-group with clinical signs of portal hypertension. Alcohol appeared to have no influence on the development of platelet insufficiency which was rather correlated with the severity of the hepatopathy, the presence of splenomegaly (splenic sequestration), immunological factors, (presence of circulating antiplatelet antibodies) and "consumption" phenomena (significant incidence of circulating FDP, and indicator of chronic Disseminated Intravascular Coagulation).
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PMID:[Thrombopenia and cirrhosis. Study of 56 cases]. 367 Jun 96

It is now possible to pinpoint the biochemical processes responsible for liver damage in alcoholics and to monitor detoxication from a biological point of view. Cirrhosis of the liver is a direct consequence of chronic alcoholism in 60-80 % of cases, and most alcoholics, after several years of drinking, cannot escape the ravages of alcohol, although it is not yet known why a small proportion are not affected biochemically. Psychological deterioration can be explained biochemically, due to the neurotoxic effects of acetaldehyde, formed by alcohol but 20-30 times more toxic, which acts on catecholamines and serotonin with, inter alia, depressant, habit-forming, hallucinogenic and convulsive properties. Hepatic symptoms depend on the stage the alcholic has reached - acute, subacute or the chronic and final stage of cirrhosis of the liver, and include disturbances of transaminases, gamma-GT, serum proteins, immunoglobulins, specific proteins, lipids (including very interestingly an increase in cholesterol-HDL which needs to be investigated further) and hematic changes with FDP and thrombocytes affected, and often anaemia.
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PMID:[Biological profile of liver damage in alcoholics (author's transl)]. 611 Mar 11

Current management of hemorrhage in cirrhotic patients is disappointing, probably because it deals only with the portal hypertension, while the coagulation disorders are neglected. Some new suggestions can be made : 1) Hemorrhage originates in coagulation disorders. The mechanical lesion of the mucosa is only the opportunity for these disorders to become apparent. The lesion may be : infrequently, a ruptured esophageal varix or a gastroduodenal peptic ulcer ; a lesion of the cardia (hiatal hernia, reflux, esophagitis, minimal traumatic tears) ; a gastric anomaly (hemorrhagic gastritis, superficial ulcerations, petechiae) ; in some cases no mucosal lesion is apparent. 2) Any widespread liver disease results in lasting hypercoagulability which is responsible for : permanent lysis, consumption, DIC. The spleen is responsible for the functional alteration of the platelets. Splenectomy is followed by permanent recovery. 3) Changes involving the platelets are responsible for most hemorrhages. Thrombopenia and severe anomalies of platelet aggregation are common findings in liver cirrhosis. Further deterioration can be induced by acetylsalicylic acid, especially if it is absorbed after an immoderate ingestion of alcohol. Emergency treatment consists in platelet transfusions. 4) Stasis in the portal system may, however, result in permanent activation of coagulation. 5) Cirrhosis results in chronic hypercoagulability and severe platelet deterioration. Any stress involving coagulation mechanisms may therefore induce hemorrhage : infection, acetyl salicylic acid, respiratory distress, estrogens, massive transfusion. It is always dangerous to "feed" consumption or to restrain lysis. 6) Coagulation tests should be performed rapidly, in order to evaluate hypercoagulability, consumption, lysis, and evidence of DIC ; FDP can probably be responsible for inflammatory changes in the liver and spleen. 8) Coagulation disorders are permanent since the hepatic alterations are irreversible.
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PMID:[Hemorrhage in liver cirrhosis : new suggestions (author's transl)]. 627 81

In order to assess the true incidence of haemostatic disorders in cirrhotic gastro-intestinal haemorrhage, a comparative prospective study of primary haemostasis, coagulation and fibrinolysis was carried out in 37 patients distributed into two groups: cirrhotics with gastro-oesophageal varices that had never bled (Group A = 22), and cirrhotics who had had an intestinal bleed from "ruptured" gastro-oesophageal varices (Group B = 15). Combination of thrombocytopenia (less than 100 10(9)/l) and a bleeding time greater than 8 mn was more frequent in Group B (80%) than in Group A (45%) (p = less than 0.05). On the other hand, no significant difference between the two groups was found in the activated cephalin time, thrombin time, prothrombin complex factors (II, V, VII-X), fibrinogen, antithrombin III, Factor VIII complex factors, FDP levels or plasminogen. In conclusion, these results suggest that disorders of primary haemostasis may be involved in bleeding from gastro-intestinal varices in cirrhosis. However, coagulation disorders and anomalies of fibrinolysis would not seem to play a determining role.
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PMID:[Importance of disorders of primary hemostasis in the occurrence of upper digestive hemorrhage in cirrhosis]. 633 45

Ascitic fluid from patients with ovarian cancer contains high levels of fibrin(ogen) degradation products (FDP). Crosslinked fibrin derivatives were isolated by precipitation and separated by PAA-gel-electrophoresis. In order to evaluate the submolecular structure the total precipitate and single derivatives were investigated after cleavage of the disulfide bonds. The findings are related to the radioimmunological measurements of certain fibrinopeptides. Tumor ascites contains approximately ten times higher levels of crosslinked fibrin derivatives than cirrhosis ascites. The fibrinopeptide A content is similar, whereas the levels of plasmin-induced alpha-chain fragment are significantly higher in tumor ascites. The findings suggest a catabolism of fibrinogen in ascitic fluid via coagulation and fibrinolysis. In tumor ascites fibrinogen is catabolized to a significantly higher degree via the degradation of crosslinked fibrin. Crosslinked fibrin derivatives may therefore be usable as non-carcinoembryogenic tumor markers.
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PMID:[Markerfunction of crosslinked fibrin derivatives in ascitic fluid from patients with ovarian cancer: a comparison with ascitic fluid in liver cirrhosis]. 655 32

The authors report the results obtained investigating PT - PTT - Fbg - Alcohol test - FDP - AT III in the serum and FDP in the ascitic fluid of 18 patients with ovarian cancer, 2 patients with pelvic relapse of cervical cancer and 10 patients with cirrhosis of the liver. It is pointed out the presence of FDP in the ascitic fluid in large amounts, so it not seems to be an ovarian cancer specific marker, but an aspecific marker of malignancy.
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PMID:Evaluation and comparison of hemocoagulation parameters both in serum and in ascites from patients with gynecologic malignancies. 716 71

We evaluated coagulation and fibrinolytic parameters in both plasma and ascitic fluid of 39 patients with ascites secondary to liver cirrhosis and in 14 cirrhotic patients without ascites, in order to verify if the peritoneal compartment could be involved in the pathogenesis of the hyperfibrinolytic state of the disease. An activation of fibrinolysis, as suggested by increased levels of FDP, D-dimer and tissue plasminogen activator (t-PA) was demonstrated in both ascitic fluid and to a lesser extent in plasma. A positive correlation was also observed between plasma and ascitic fluid plasminogen, anti-plasmin and fibrinogen, while a negative correlation was found between plasma and ascitic fluid plasminogen activator inhibitor-1 (PAI-1). Moreover, plasma PAI-1 was significantly lower in patients with ascites than in those without ascites and among ascitic patients in those who had bleeding into soft tissues when compared to those who did not present haemorrhagic events. Finally, a significant association was also shown between positivity for plasma D-dimer (> 200 ng/ml) and the presence of ascites. Taken together, our data suggest an exchange of some coagulation and fibrinolytic proteins between plasma and ascitic fluid and point out the key role of PAI-1 in regulating plasma fibrinolytic potential and in bleeding complications in cirrhotic patients.
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PMID:The hyperfibrinolytic state of liver cirrhosis: possible pathogenetic role of ascites. 806 Dec 56

Clinical and laboratory findings were studied in 56 patients with liver disease (10 acute hepatitis, 10 fulminant hepatitis and 36 cirrhosis). Spontaneous bleeding occurred in 19 patients (8 fulminant hepatitis, 11 cirrhosis) and another 8 cirrhotic patients had variceal bleeding. There were 22 deaths (36%), 12 of these patients had spontaneous bleeding. Depletion of antithrombin III (AT III) occurred in fulminant hepatitis (mean +/- S.D. = 27 +/- 16%) and cirrhosis (49 +/- 23%) but thrombin-antithrombin III complexes (TAT) were significantly higher in the former (45 +/- 22 vs 8.6 +/- 7.0 ng/ml; p = 0.006). Within subgroups of cirrhosis (with or without spontaneous bleeding or with variceal bleeding), there were no significant differences in levels of AT III or TAT. Of all patients, those with spontaneous bleeding had persistently lower AT III levels but had variable changes of other coagulation parameters (PT, PTT, TT, FDP, fibrinogen and platelet counts). This study showed that coagulopathic consumption is an important cause of AT III deficiency in fulminant hepatitis but not in cirrhosis. Serial changes in AT III levels correlated with bleeding risk in patients with liver disease.
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PMID:Haemostatic abnormalities in patients with liver disease associated with viral hepatitis. 899 5


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