Thrombopoietin level in patients with chronic liver diseases

Eissa, Laila A.; Gad, Lamees S.; Rabie, Ahmed; El-Gayar, Amal M.

doi:10.1016/s1665-2681(19)31854-x

Cited by 24 publications

(12 citation statements)

References 54 publications

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“…47 Further, thrombocytopenia may develop due to antiplatelet antibodies or increased platelet consumption in disseminated intravascular coagulation (DIC) 48 and hepatitis C infection is a risk factor for the occurrence of autoimmune thrombocytopenia. 49 The production of TPO in cirrhotic patients is significantly compromised [50][51][52] and eltrombopag, as a TPO receptor agonist, can assist in the management of thrombocytopenic patients. Nevertheless, using this drug should be with caution as it can predispose to portal venous thrombosis.…”

Section: Plateletsmentioning

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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Section: Plateletsmentioning

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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“…Jadi kadar TPO di peredaran selain bergantung pada pembuatan di hati juga bergantung pada peripheral uptake. 19 Kenasaban antara IPF dan TPO terkait derajat keparahan penyakit Pada penelitian ini, untuk menentukan derajat keparahan penyakit digunakan patokan angka Child Turcotte-Pugh (Child Turcotte-Pugh score), terdiri atas Child A (angka 5-6), Child B (angka 7-9) dan Child C (angka 10-15). Setelah dianalisis statistik ternyata tidak didapatkan hubungan yang bermakna antara IPF dan derajat keparahan penyakit.…”

Section: Pendahuluanunclassified

Immature Platelet Fraction (Ipf) Dan Trombopoietin Di Sirosis Hati

Rohani¹,

Hernaningsih²,

Ma’at³

et al. 2018

Indonesian J. Clin. Pathol. Med. Lab.

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Liver cirrhosis remains a major clinical problem worldwide when associated with significant morbidity and mortality due toits complications. The presence of liver cirrhosis state affects the production of TPO influencing the process of thrombopoiesis. Thethrombopoiesis activity can be described by the Immature Platelet Fraction (IPF) value which is young platelets. The immature Plateletfraction value increases when platelet production enhances as well, on the contrary when the production declines, the IPF value is alsodecreased. This study was performed by cross-sectional method using 31 subject samples suffering from liver cirrhosis, consisting of ChildPugh score class A 2 samples (6.4%), Child Pugh score class B 9 samples (29%) and Child Pugh score class C 20 samples (64.6%). Theexamination of TPO levels was done by ELISA method using Humans TPO QuantikineR, the IPF value was examined using Sysmex XE-2100 Hematology Analyzer. The thrombopoietin serum levels in the samples ranged from 23.5 to 96.6 pg/mL with a mean of 45.1pg/mL.The immature Platelet Fraction values varied from 1.7% to 19.1% with a mean of 6.7%. From the statistical analysis, the levels of TPO andIPF at various degrees of the disease severity were not significantly different. There was no significant correlation between the TPO leveland IPF value, r = 0.038, p = 0.837. There was no significant difference between the TPO level and the IPF value in the splenomegaly andnonsplenomegaly state. In conclusion, based on this study no significant correlation was found between the IPF value with thrombopoietinserum levels, as well as the IPF and thrombopoietin levels, and there was no association with the disease severity.

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“…[6][7][8][9][10][11][12] In particular, the results of studies that assessed TPO levels and those that described its pathophysiology in patients with various degrees of severity of chronic liver disease greatly improved our understanding of thrombopoiesis in these patients. [13][14][15][16][17][18][19][20][21][22][23][24][25] TPO is a polypeptide consisting of 353 amino acids with a molecular weight of 30 kDa, whose codifying gene is located on chromosome 3q27. Although TPO can be expressed in various organs (kidney, smooth muscle), the highest expression of TPO mRNA is found in the liver, and in adults the liver is the principal site of TPO production, although under inflammatory conditions marrow stromal cells can be induced to produce TPO.…”

Section: Introductionmentioning

confidence: 99%

“…However, although the results of studies performed in patients with hematologic diseases or chemo-therapy-induced myelosuppression reached unambiguous conclusions regarding the pathophysiology of TPO and platelet homeostasis, studies performed in patients with liver disease produced results that led to various interpretations. [14][15][16][17][18][19][20][21][22][23][24][25] The main reason for this apparent inconsistency is represented by the fact that the initial studies that were performed in patients with various degrees of liver impairment and controls analyzed TPO levels per se and did not take into account the corresponding platelet counts. In fact, although these studies reported slightly increased, similar, or very low TPO levels compared with normal subjects, in patients with liver disease TPO levels were always "inappropriately low" for the corresponding peripheral platelet count.…”

Section: Introductionmentioning

confidence: 99%

Platelet Dysfunction: Status of Thrombopoietin in Thrombocytopenia Associated with Chronic Liver Failure

Giannini

Peck‐Radosavljevic

2015

Semin Thromb Hemost

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Thrombocytopenia is a common hematological abnormality in patients with chronic liver disease, and its prevalence is higher in patients with liver failure. Although the presence of thrombocytopenia has historically been associated with portal hypertension, the characterization of thrombopoietin has improved our understanding of the determinants of platelet count in patients with liver disease. In particular, the association between thrombopoietin levels and residual liver function helped disclose the multifaceted pathophysiology of thrombocytopenia in patients with chronic liver failure. In this regard, important results were provided by studies performed in patients with chronic viral hepatitis that assessed the complex interplay between thrombocytopenia induced by the myelosuppressive effect of interferon-based treatment and thrombopoietin pathophysiology. These studies showed that successful antiviral therapy is accompanied by improved hepatic thrombopoietin production. Moreover, studies that evaluated thrombopoietin and platelet count dynamics before and after liver transplantation were instrumental in describing how restoration of liver function determines a normalization of the thrombopoietin-platelet count feedback that is deranged in patients with end-stage liver disease.

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Thrombopoietin level in patients with chronic liver diseases

Cited by 24 publications

References 54 publications

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

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

Immature Platelet Fraction (Ipf) Dan Trombopoietin Di Sirosis Hati

Platelet Dysfunction: Status of Thrombopoietin in Thrombocytopenia Associated with Chronic Liver Failure

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