Coagulation Abnormalities in Liver Disease

Lechner, Klaus; Niessner, H; Thaler, Erica R.

doi:10.1055/s-0028-1087127

Cited by 101 publications

(20 citation statements)

References 56 publications

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“…The function and quantity of plasma fibrinogen can be altered by both inherited and acquired disorders [1,[3][4][5][6][7][8][9][10][11][12][13]. Increased levels of fibrinogen can be seen in pregnancy [3,4], acute or early liver disease [5], and many acute illnesses [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

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Laboratory testing for fibrinogen abnormalities

2008

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Fibrinogen is essential for the formation of a fibrin clot. Acquired and congenital disorders of fibrinogen may result in decreased concentration or altered function of fibrinogen, often leading to an increased risk of bleeding. Routine coagulation testing and specialized laboratory investigations can guide diagnosis in patients suspected of having a fibrinogen abnormality. This article summarizes the types of laboratory assays that are used to assess fibrinogen disorders, and key abnormalities found in different types of fibrinogen disorders. Am. J. Hematol. 83:928-931, 2008. V

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Section: Introductionmentioning

confidence: 99%

“…Acquired fibrinogen deficiencies can be due to consumptive states (e.g. placental abruption), fibrinolytic therapy [9], hemodilution and severe liver disease [10]. The magnitude of congenital fibrinogen deficiencies range from severe (absent fibrinogen or afibrinogenemia) to moderate and mild (hypofibrinogenemia) [11,12].…”

Section: Introductionmentioning

confidence: 99%

Laboratory testing for fibrinogen abnormalities

2008

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“…The inverse relationship of platelet count and liver disease is well known and has been associated with advanced liver fibrosis [19]. The pathogenesis of thrombocytopenia in severe liver fibrosis is likely to be multifactorial and include redistribution of platelets to an enlarged spleen [20] and increased destruction [21].…”

Section: Discussionmentioning

confidence: 99%

Predictors and Noninvasive Identification of Severe Liver Fibrosis in Patients with Chronic Hepatitis C

Metwally

Zein

2007

Dig Dis Sci

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Diagnosis of severe fibrosis (stages III and IV) in hepatitis C has clinical implications. Our objective was to distinguish independent predictors of severe fibrosis and use them to identify patients with severe fibrosis without a liver biopsy. One hundred ninety-nine hepatitis C patients were included in the initial analysis to identify predictors of severe fibrosis. Univariate and multivariate analyses of 26 predetermined variables for significance in predicting severe fibrosis were performed. Based on the coefficient regression and P values, a scoring system was developed and applied to a second independent cohort (137 patients) for validation. In multivariate analysis, low platelet count, low albumin, aspartate transaminase level, history of blood transfusion, and hepatitis B core antibody were significant independent predictors of severe fibrosis. A scoring system (range, 0-9) was developed from the three variables with the lowest P values (platelet count, aspartate transaminase, and albumin). A cutoff point of 4 had 99% specificity and 94% positive predictive value. A cutoff point of 2 had 87% sensitivity and 95% negative predictive value. We conclude that severe fibrosis in hepatitis C may potentially be identified with a high degree of certainty in a substantial number of patients with a simple noninvasive scoring system.

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“…Plasma fibrinogen is an acute-phase reactant, and remains normal or increased in patients with liver disease [24]. Lower levels due to decreased synthesis, yet above 100 mg/dL, have been reported only in patients with very severe liver disease [25].…”

Section: Fibrinogenmentioning

confidence: 99%