Fibrinolysis and fibrinogenolysis in liver disease

Takahashi, Hiroyuki; Tatewaki, Wataru; Wada, Ken; Niwano, Hiroe; Shibata, Akira

doi:10.1002/ajh.2830340402

Cited by 21 publications

(10 citation statements)

References 28 publications

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“…The results obtained in the current study confirm many earlier reports of prolongation of the PT in acute hepatitis [3,14], liver cirrhosis [3,8,15,16], and HCC [3]. Progressive prolongation of PT in cirrhotic patients closely relates to the severity of liver cirrhosis [8,11,[17][18][19].…”

Section: Discussionsupporting

confidence: 94%

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Haemostatic abnormalities in liver disease: could some haemostatic tests be useful as liver function tests?

Ghumlas

Gader

Faleh

2005

Blood Coagulation &Amp; Fibrinolysis

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The liver plays a central role in haemostasis, being the site of synthesis of most of the clotting factors, coagulation inhibitors and fibrinolytic parameters, in addition to its clearance of activated clotting and fibrinolytic factors. Nonetheless, no haemostatic test(s) is included among the routine liver function tests and this study aims to probe this possibility. The liver disease group (n=258) included acute hepatitis (n=25), chronic viral hepatitis (n=128), hepatitis B (HB) carriers (n=25), liver cirrhosis (n=67), and hepatocellular carcinoma (HCC) (n=13). The prothrombin time was significantly prolonged in acute hepatitis, liver cirrhosis and HCC. However, the reptilase time was prolonged in all the groups except in HB carriers, while the thrombin time was prolonged only in the HCC group. Antithrombin III and protein C levels exhibited significant reduction in acute hepatitis, liver cirrhosis and HCC. On the other hand, protein S levels (total and free) were reduced significantly in all the patients groups, including HB carriers when compared with healthy controls. Derangement of haemostatic tests is a common feature in liver disease, being most significant in acute hepatitis, liver cirrhosis and hepatocellular carcinoma. The most sensitive markers of hepatocyte malfunction are protein S (total and free) and the reptilase time as they were abnormal, in the mildest liver affections, when other biochemical tests as well as other haemostatic tests were normal. Further studies are needed to see whether these two tests qualify for inclusion among the routine liver function tests.

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Section: Discussionsupporting

confidence: 94%

“…On the other hand, the observed reduction in fibrinogen levels is a common feature of acute hepatitis and liver cirrhosis [14][15][16]19,33,34]. Fibrinogen is synthesized almost exclusively in the liver and low levels of fibrinogen in liver cirrhosis are due to a combination of factors including decreased synthesis [35].…”

Section: Discussionmentioning

confidence: 99%

Haemostatic abnormalities in liver disease: could some haemostatic tests be useful as liver function tests?

Ghumlas

Gader

Faleh

2005

Blood Coagulation &Amp; Fibrinolysis

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“…These results might be explained by the small thrombus size and/or by the low fibrinolytic activity observed in these patients [9], Neverthe less, high D dimer levels were repeatedly detected in 2 patients. It has been recently reported that patients with liver disease have elevated plasma fibrin degradation prod ucts whereas fibrinogenolysis products are normal [12]. On the other hand, Gordge et al [13] have observed high levels of D dimer in patients with chronic renal failure using a highly sensitive ELISA method.…”

Section: Discussionmentioning

confidence: 99%

Low Molecular Weight Heparin (CY-216) versus Unfractionated Heparin in Chronic Hemodialysis

Grau

Sigüenza²,

Maduell³

et al. 1992

Nephron

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In 14 patients undergoing chronic hemodialysis, we investigated the safety and efficacy of the low molecular fragment (CY-216) in comparison to unfractionated heparin (UFH) in the prevention of clotting in the extracorporeal circuit (ECC). In this study, 168 hemodialysis sessions were undertaken with UFH in 2 bolus doses (5,437 ± 1,477 SD IU) and 231 with CY-216 in a single bolus dose [initial dose 150 anti-Xa U Institut Choay (IC)/kg]. There were no clots in the bubble trap in any UFH sessions, and 14.8% had coagulated fibers in the dialyzer. Clotting in the bubble trap was observed in 2 CY-216 sessions (0.8%) and coagulated fibers in 22.6% of the sessions. At the end of the study, the mean dose of CY-216 was 250 anti-Xa UlC/kg but a dose of 350 anti-Xa UlC/kg was needed in the 2 patients treated by recombinant human erythropoietin. Anti-Xa levels at the end of the runs were higher (0.47 ± 0.1 U/ml) in the CY-216 group than in the UFH group (0.28 ± 0.1 U/ml). There was a correlation between anti-Xa levels and efficacy in the CY-216 group. An anti-Xa activity above 0.4 U/ml was needed in order to minimize thrombus formation. Antithrombin III-protease complexes (ATM) and D dimer fibrin derivatives (D dimer) were used as thrombotic markers but they were of little value for the detection of fibrin formation in the ECC. Our findings suggest that CY-216 administered as a single bolus dose seems to be of similar effectiveness to UFH.

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“…Moreover, it is now accepted that plasminogen is also synthesized by the liver [1,2], In parenchymal chronic liver disease, especially cirrhosis, the acquired deficiencies of fibrinogen, antithrombin III and plasmino gen are mainly due to their impaired hepatic synthesis [22,[24][25][26][27], and the decrease re flects disease severity [6,7], Only a minimal share seems to be caused by their increased turnover and catabolism [26], their consump tion in disseminated intravascular coagula tion [3,25] or synthesis of abnormal proteins [24,28],…”

Section: Discussionmentioning

confidence: 99%

Circadian Rhythms of Fibrinogen, Antithrombin III and Plasminogen in Chronic Liver Diseases of Increasing Severity

Pasqualetti

Festuccia²,

Acitelli³

et al. 1997

Pathophysiol Haemos Thromb

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Acquired deficiencies of fibrinogen, antithrombin III and plasminogen are reported in liver disease, and it is known that their plasma levels fluctuate during the day. The aim of this study was to investigate the circadian rhythms of these three factors in chronic liver disease. Five groups of subjects were considered: (A) 15 healthy controls; (B) 15 patients with hepatic alcoholic steatosis; (C) 15 patients with chronic active hepatitis; (D) 15 patients with compensated cirrhosis of the liver, and (E) 15 patients with decompensated cirrhosis with ascites. The levels of fibrinogen, antithrombin III and plasminogen were determined in blood samples drawn in each subject during the span of a day every 3 h starting from midnight. The time-related values were analyzed using the ‘population-mean cosinor’ method. Groups A and B presented a significant (p < 0.05) circadian rhythm for each variable, group C a significant (p < 0.05) circadian rhythm for fibrinogen and antithrombin III and groups D and E no significant (p > 0.05) circadian rhythms. Statistically significant differences (p < 0.05) were demonstrated among the groups in the mean daily levels of the three variables by ANOVA, the concentrations decreasing with disease severity. These data confirm the existence of a significant diurnal periodicity in the circulating levels of fibrinogen, antithrombin III and plasminogen in controls and suggest that liver disease is associated with progressive circadian modifications in the temporal structure of fibrinogen, antithrombin III and plasminogen, related to the stage of the liver disease. The rhythm derangements may be considered markers of evolution in liver disease.

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Fibrinolysis and fibrinogenolysis in liver disease

Cited by 21 publications

References 28 publications

Haemostatic abnormalities in liver disease: could some haemostatic tests be useful as liver function tests?

Haemostatic abnormalities in liver disease: could some haemostatic tests be useful as liver function tests?

Low Molecular Weight Heparin (CY-216) versus Unfractionated Heparin in Chronic Hemodialysis

Circadian Rhythms of Fibrinogen, Antithrombin III and Plasminogen in Chronic Liver Diseases of Increasing Severity

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