Assessment of coagulation and fibrinolysis in children with chronic liver disease

El-Sayed, Rokaya; El‐Karaksy, Hanaa; El-Raziky, Mona; El-Hawary, Manal; Koofy, Nehal El; Helmy, Hanan; Fahmy, Mona

doi:10.1097/mbc.0b013e3283569297

Cited by 10 publications

(11 citation statements)

References 15 publications

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“…This finding was largely consistent with several previous studies. For instance, an Egyptian study by El-Sayed et al investigated the D-dimer levels in 67 patients with chronic liver diseases and 30 healthy controls (17). The study observed that cirrhotic patients with Child-Pugh class A and B had significantly higher D-dimer levels compared with the non-cirrhotic patients and healthy controls (class B, 147.32±114.16 ng/ml; class A, 115.3±138.4 ng/ml; non-cirrhotic liver disease, 28.86±40.03 ng/ml; healthy controls, 17.6±11.7 ng/ml).…”

Section: Discussionmentioning

confidence: 99%

D-dimer level for predicting the in-hospital mortality in liver cirrhosis: A retrospective study

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. The present study aimed to examine the correlation of D-dimer levels with the Child-Pugh and MELD scores, as well as to determine the predictive ability of D-dimer level for the in-hospital mortality of liver cirrhosis patients. All cirrhotic patients who were consecutively admitted to our hospital between January 2011 and June 2014, and underwent D-dimer tests on admission were retrospectively analyzed. Pearson's χ 2 tests were employed to evaluate the correlations of D-dimer levels with Child-Pugh and MELD scores. In addition, receiver operating curve (ROC) analysis was employed to evaluate the specificity and sensitivity of D-dimer levels for predicting the in-hospital mortality. In total, 703 cirrhotic patients were included in the study, with an in-hospital mortality of 5.4% (38/703). The D-dimer levels were correlated with Child-Pugh (correlation coefficient, 0.219; P<0.001) and MELD scores (correlation coefficient, 0.207; P<0.001). The highest D-dimer level was observed in the Child-Pugh class C patients, followed by the class B and A patients. Furthermore, D-dimer was significantly higher in the MELD score >15 group compared with the MELD score <15 group. The area under the ROC of D-dimer levels for predicting the in-hospital mortality of liver cirrhosis was 0.729 (P<0.0001), while the best cut-off D-dimer value was 0.28 µg/ml with a sensitivity of 86.84% and a specificity of 49.17%. In conclusion, the D-dimer level is significantly associated with the degree of liver dysfunction. Therefore, D-dimer testing could be employed for the prognostic stratification of liver cirrhosis. IntroductionD-dimer is a fibrin degradation product that is observed in the blood following clot degeneration. Currently, tests determining the concentration of D-dimer in the blood are widely employed in various clinical practices. Determination of D-dimer levels in combination with clinical probability assessment can be used to safely rule-out the diagnosis of pulmonary embolism (1-3). In addition, D-dimer levels are used for predicting the risk of recurrent venous thromboembolism and determining the duration of anticoagulation therapy in these patients (4-6).The levels of D-dimer in the blood are significantly increased in patients with liver cirrhosis, and are gradually elevated further as the degree of liver dysfunction increases in severity (7,8). It has been also suggested that D-dimer levels are influenced by the presence and treatment of ascites (9). Furthermore, the levels of this protein are significantly higher in cirrhotic patients with ascites compared with those without ascites, and are significantly decreased subsequently to ascite resolution (9). More recently, a meta-analysis performed by our group indicated that D-dimer levels are significantly associated with the presence of portal vein thrombosis in liver cirrhosis and may predict the development of portal vein thrombosis following splenectomy (10). Therefore, D-dimer may be a prognostic factor negatively associated with outcomes of liver cirrhosis.I...

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Section: Discussionmentioning

confidence: 99%

D-dimer level for predicting the in-hospital mortality in liver cirrhosis: A retrospective study

et al. 2016

Experimental and Therapeutic Medicine

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“…Reduced synthetic capability of liver cells results in decreased levels of both procoagulant and anticoagulant factors. In addition, hyperfibrinolysis may occur in children with chronic liver disease, especially if the disease is cirrhotic (El-Sayed et al 2013). Whether a pediatric patient with liver disease and loss of reserve capacity develops bleeding or thrombosis depends on the vascular bed and additional risk factors in the individual patient (Magnusson et al 2016).…”

Section: Discussionmentioning

confidence: 99%

Coagulopathy in Zellweger spectrum disorders: a role for vitamin K

Zeynelabidin

Klouwer

Meijers

et al. 2017

J of Inher Metab Disea

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IntroductionZellweger spectrum disorders (ZSDs) are caused by an impairment of peroxisome biogenesis, resulting in multiple metabolic abnormalities. This leads to a range of symptoms, including hepatic dysfunction and coagulopathy. This study evaluated the incidence and severity of coagulopathy and the effect of vitamin K supplementation orally and IV in ZSD.MethodsData were retrospectively retrieved from the medical records of 30 ZSD patients to study coagulopathy and the effect of vitamin K orally on proteins induced by vitamin K absence (PIVKA-II) levels. Five patients from the cohort with a prolonged prothrombin time, low factor VII, and elevated PIVKA-II levels received 10 mg of vitamin K IV. Laboratory results, including thrombin generation, at baseline and 72 h after vitamin K administration were examined.ResultsIn the retrospective cohort, four patients (13.3%) experienced intracranial bleedings and 14 (46.7%) reported minor bleeding. No thrombotic events occurred. PIVKA-II levels decreased 38% after start of vitamin K therapy orally. In the five patients with a coagulopathy, despite treatment with oral administration of vitamin K, vitamin K IV caused an additional decrease (23%) of PIVKA-II levels and increased thrombin generation.ConclusionBleeding complications frequently occur in ZSD patients due to liver disease and vitamin K deficiency. Vitamin K deficiency is partly corrected by vitamin K supplementation orally, and vitamin K administered IV additionally improves vitamin K status, as shown by further decrease of PIVKA-II and improved thrombin generation.

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“…Fibrinogen alternations encompass both quantitative and qualitative changes in cirrhotic children. 71 Reduced fibrinogen levels can be a result of either reduced synthesis, increased destruction, or a combination of these two. 72 The elevated levels of FDPs in cirrhotic patients demonstrate the accelerated fibrinogen consumption and/or decreased hepatic clearance rate of FDPs.…”

Section: Fibrinogenmentioning

confidence: 99%

A Review on Clinical, Pathophysiological, and Diagnostic Hematological Features in Children With Liver Cirrhosis

Shahramian

Tabrizian

Delaramnasab

et al. 2019

Int J Basic Sci Med

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Appropriate diagnostic and therapeutic measures for liver cirrhosis is critical, particularly in children. In the present review, a comprehensive approach was provided toward hematological parameters in pediatric liver cirrhosis. The literature search included MeSH terms "liver cirrhosis" and "hepatic cirrhosis" and databases such as PubMed, Web of Science, Scopus, and Google Scholar were searched up until December 2017. Hematologic changes in the liver cirrhosis mainly encompassed anemia and coagulopathies. In addition, bleeding diathesis was considered as the most clinical complication in these patients. In addition to reduced coagulation factors, hyperfibrinolysis is a common feature in childhood cirrhosis and may be an important contributor to the risk of bleeding. Based on the results, children with liver cirrhosis also demonstrated a procoagulant state at laboratory and clinical levels. This may be partly due to a reduction in coagulation inhibitors such as anti-thrombin, C1 inhibitor, and α1-antitrypsin in children with cirrhosis. The portal vein thrombosis and portal hypertension are considered as the most clinical presentations of the hypercoagulable state. Further, children with liver cirrhosis complicated with portal hypertension usually show leukopenia, anemia, and thrombocytopenia due to hypersplenism. Although the etiology of childhood and adult cirrhosis may be different, their hematological compilations and clinicopathological features are somehow similar.

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Assessment of coagulation and fibrinolysis in children with chronic liver disease

Cited by 10 publications

References 15 publications

D-dimer level for predicting the in-hospital mortality in liver cirrhosis: A retrospective study

D-dimer level for predicting the in-hospital mortality in liver cirrhosis: A retrospective study

Coagulopathy in Zellweger spectrum disorders: a role for vitamin K

A Review on Clinical, Pathophysiological, and Diagnostic Hematological Features in Children With Liver Cirrhosis

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