Acquired Dysfibrinogenaemia in Acute and Chronic Liver Disease

Lane, David A.; Scully, M F; Thomas, Duncan P.; Kakkar, V. V.; Woolf, I. L.; Williams, Roger

doi:10.1111/j.1365-2141.1977.tb00586.x

Cited by 73 publications

(23 citation statements)

References 20 publications

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“…6 The mechanism by which abnormal fibrinogen molecules are produced is not known. Barr et al 7 postulated that dysfibrinogenemia in liver disease results from derepression of fetal gene coding of hepatocytes for fibrinogen production.…”

Section: Discussionmentioning

confidence: 99%

“…The synthesis of abnormal fibrinogen molecules has been reported in hepatocellular carcinoma 7 and in acute and chronic liver diseases. 6 The abnormal fibrinogen molecule is synthesized by regenerating liver cells, and it consistently interferes with fibrin monomer polymerization, resulting in prolonged PT and APTT tests. Results of plasma mixing tests, done by mixing various amounts of the patient's plasma and normal plasma pool and performing PT and APTT tests on each specimen of mixed plasmas, show that with the 50/50 mix the PT time was corrected to 14.5 sec from 25 sec and the APTT time corrected to 38 sec from 110 sec.…”

mentioning

confidence: 99%

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Clinicopathologic Conference

1983

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Clinicopathologic Conference

1983

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“…Most workers agree that the defect of fi brin formation in liver disease is due to abnormal FMP [3,11]. Recent reports have suggested that the DF of liver disease is char acterised by an increase in fibrinogen-bound sialic acid content [8.…”

Section: Discussionmentioning

confidence: 99%

Fibrinogen-Bound Sialic Acid Levels in the Dysfibrinogenaemia of Liver Disease

Francis¹,

Armstrong²

1982

Pathophysiol Haemos Thromb

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Fibrinogen-bound sialic acid levels were determined in 75 normal controls and 80 patients with liver disease. Patients with abnormal fibrin monomer polymerisation (FMP) had sialic acid levels significantly higher than normal controls or patients with normal FMP. Enzymatic removal of sialic acid from the abnormal fibrinogens corrected the abnormal FMP and thrombin-clotting times to the range of desialated controls. The accelerating effects of calcium ions, protamine sulphate and Polybrene were largely abolished by desialation, suggesting that these cations accelerate FMP by neutralising the negatively charged sialic acid residues.

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“…Acquired disorders in fibrinogen (dysfibrinogenaemia) are sometimes caused by liver disease, biliary tract disease and certain malignancies, such as hepatoma and renal cell carcinoma [45,46] In addition, it has been reported that patients who underwent organ (e.g. liver) or stem cell transplantation may develop dysfibrinogenaemia [47,48].…”

Section: Acquired Disordersmentioning

confidence: 99%

Inherited and Acquired Disorders of Platelet Function

Jurk

Kehrel²

2007

Transfus Med Hemother

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Platelet function defects are caused by rare congenital or, more frequently, by acquired disorders. They may lead to bleeding or thrombotic tendencies despite of normal platelet counts. The corresponding symptoms are often quite heterogeneous. A disorder of platelet function is suspected on the basis of case and family history, physical examination and platelet function tests. The so far primary screen of platelet dysfunctions, the bleeding time, is neither very sensitive nor specific and depends very much on the skills of the person that performs the test. Therefore, other general and in addition more specialised laboratory tests have to be performed for diagnosing an isolated platelet abnormality or in most cases combined platelet function defects. An approach to diagnosing a platelet disorder is presented, which supports the high significance of flow cytometry in platelet function analysis. Furthermore, we like to elucidate that in most cases a platelet-mediated haemostatic disorder cannot be characterised by just a single function defect, but rather by a combination of platelet functional abnormalities. Detailed knowledge of the platelet disorder is necessary for adequate therapeutical management of the individual patient, including the control of the underlying disease in acquired disorders, transfusion of platelets and administration of haemostatic drugs.

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Acquired Dysfibrinogenaemia in Acute and Chronic Liver Disease

Cited by 73 publications

References 20 publications

Clinicopathologic Conference

Clinicopathologic Conference

Fibrinogen-Bound Sialic Acid Levels in the Dysfibrinogenaemia of Liver Disease

Inherited and Acquired Disorders of Platelet Function

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