Blood Coagulation Changes in Liver Diseases

Deutsch, Erwin

doi:10.1016/b978-1-4831-6756-5.50011-6

Cited by 52 publications

(31 citation statements)

References 44 publications

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“…We found no increase o f physiological antithrombins (antithrombin III levels were actually low in our patients, in accordance with the literature) [6,14], and no pathological anticoagulants acting at this level, since cirrhotic serum had no effect on the thrombin time o f normal plasma.…”

Section: Discussionsupporting

confidence: 75%

Impaired Fibrin Formation in Advanced Cirrhosis

Dettori¹,

Ponari²,

Civardi³

et al. 1977

Pathophysiol Haemos Thromb

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The process of fibrin formation was systematically investigated in 25 patients with severe alcoholic cirrhosis. Results of functional tests are reported. A significant lengthening of the thrombin time was found which could not be completely attributed either to hypofibrinogenaemia or to an increase in physiological anticoagulants or to the presence of pathological antithrombins. A defect in fibrin polymerization was seen in the absence of significant levels of antipolymerizing agents. Indirect evidence pointed to an abnormal fibrinogen function. This was mainly suggested by the ‘polymerization curves’ of mixtures of normal and pathological plasmas and the changes in physico-chemical properties of the clot (optical and elastic properties; tensile strength). Altered synthesis in hepatocytes may lead to an ‘acquired dysfibrinogenaemia’ in the late stages of liver cirrhosis, although alteration of a normal fibrinogen molecule after secretion cannot be definitely excluded.

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Section: Discussionsupporting

confidence: 75%

Impaired Fibrin Formation in Advanced Cirrhosis

Dettori¹,

Ponari²,

Civardi³

et al. 1977

Pathophysiol Haemos Thromb

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“…Although contact factors are thought to be synthetized by the liver [16][17][18], the impairment of this organ in thalassemia is un likely to be the most important mechanism of the decreased levels found in these patients. In fact, the vitamin K-dependent factors and factor V, which are known to be earlier and more markedly affected in liver disease [5], were normal or less severely decreased.…”

Section: Discussionmentioning

confidence: 98%

“…Factor XII (Hageman factor) is also known to play a key role in the activation of the kinine system, fibrinolysis and pla telets [5,16,20]. Although contact factors are thought to be synthetized by the liver [16][17][18], the impairment of this organ in thalassemia is un likely to be the most important mechanism of the decreased levels found in these patients.…”

Section: Discussionmentioning

confidence: 99%

Screening Coagulation Tests and Clotting Factors in Homozygous β-Thalassemia

Caocci¹,

Alberti²,

Burrai³

et al. 1978

Acta Haematol

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In 30 children with homozygous β-thalassemia the hemostasis screening tests (bleeding time, PT, PTT), platelet count and specific assays of clotting factors were carried out 25 days after their last transfusion. PT, PTT, and bleeding time showed minor variations; considerable thrombocytosis was found in splenectomized patients. Factors IX and XII were decreased in a high proportion of patients, the vitamin K-dependent factors (II, VII, IX, X) were slightly reduced and factors I, V and VIII remained within the normal range in a majority of patients. Hepatic failure resulting in defective protein synthesis does not explain the more marked impairment of factors XI and XII, which might be secondary to activation of the intrinsic coagulation and/or kallikrein systems following intravascular haemolysis and multiple blood transfusions.

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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%

“…Increased levels of fibrinogen can be seen in pregnancy [3,4], acute or early liver disease [5], and many acute illnesses [6][7][8]. Acquired fibrinogen deficiencies can be due to consumptive states (e.g.…”

Section: Introductionmentioning

confidence: 99%

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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Blood Coagulation Changes in Liver Diseases

Cited by 52 publications

References 44 publications

Impaired Fibrin Formation in Advanced Cirrhosis

Impaired Fibrin Formation in Advanced Cirrhosis

Screening Coagulation Tests and Clotting Factors in Homozygous β-Thalassemia

Laboratory testing for fibrinogen abnormalities

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