Platelet aggregation and coagulation and fibrinolysis parameters in both portal and systemic circulations in patients with cirrhosis and hepatocellular carcinoma

Kunihiro, Naoko; Kawai, Bunpei; Sanjo, Akira; Osaka, Kazuhiro; Ohnishi, Akihiro

doi:10.1016/s1386-6346(00)00078-4

Cited by 5 publications

(6 citation statements)

References 17 publications

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“…Splanchnic vasodilatation and enhanced generation of PGI2 shift the collagen (but not the ADP) aggregation curve significantly to the right in portal blood. There were no differences in coagulation and fibrinolytic parameters 82 …”

Section: Platelet Functionmentioning

confidence: 79%

“…Basal cyclic adenosine monophosphate and cyclic guanosine monophosphate, the two main inhibitory messengers, are upregulated in the cirrhotic platelet 69 . There was a normal upregulation upon stimulation indicating an increased stimulation of circulating factors in vivo like PGI2 81–83 and nitric oxide (NO) 84 for cAMP and cGMP, respectively 69 . There is one study suggesting a locoregional difference in platelet aggregation, i.e.…”

Section: Platelet Functionmentioning

confidence: 99%

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Review article: blood platelet number and function in chronic liver disease and cirrhosis

Witters

Freson

Verslype

et al. 2008

Aliment Pharmacol Ther

155

134

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Summary Background The liver plays a central role in coagulation and fibrinolysis but is also closely intertwined with the function and number of blood platelets. Aim To describe and integrate all literature concerning blood platelets and liver disease by performing a thorough literature research. Methods A thorough literature research on ‘blood platelets’ and ‘liver disease’ was performed. Results Thrombocytopenia is a marked feature of chronic liver disease and cirrhosis. Traditionally, this thrombocytopenia was attributed to passive platelet sequestration in the spleen. More recent insights suggest an increased platelet breakdown and to a lesser extent decreased platelet production plays a more important role. Besides the reduction in number, other studies suggest functional platelet defects. This platelet dysfunction is probably both intrinsic to the platelets and secondary to soluble plasma factors. It reflects not only a decrease in aggregability, but also an activation of the intrinsic inhibitory pathways. The net effect, finally, is a decreased platelet function in the various types of chronic liver diseases and cirrhosis. Finally, recent data suggest that platelets are not only affected by but can also contribute to the liver disease process, as for instance, in viral hepatitis and cholestatic liver disease. Conclusion Platelet research in liver disease is a growing area of investigation and could provide new pathophysiological insights.

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Section: Platelet Functionmentioning

confidence: 79%

Section: Platelet Functionmentioning

confidence: 99%

Review article: blood platelet number and function in chronic liver disease and cirrhosis

Witters

Freson

Verslype

et al. 2008

Aliment Pharmacol Ther

155

134

View full text Add to dashboard Cite

show abstract

“…Moreover, in previous studies, the presence of a vascular fragment was necessary to put in evidence the effect of ASA at ULD on platelet aggregation [5,6] . It should be noted that Kunihiro et al [18] found differences in platelet aggregation from blood samples obtained from systemic and portal circulation in cirrhotic patients complicated with hepatocellular carcinoma, and they attributed those differences to intraportal PGI 2 . For the above cited elements, we could conclude that platelet aggregation ex vivo induced by ADP and in vivo laser induction thrombus formation may not behave in an identical way.…”

Section: Discussionmentioning

confidence: 99%

Platelet Aggregation in Portal Hypertension and Its Modification by Ultra-Low Doses of Aspirin

Eizayaga

Aguejouf²,

Belon³

et al. 2005

Pathophysiol Haemos Thromb

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Aspirin (ASA) is widely accepted as antithrombotic drug, but several reports point out that its use in ultra-low doses (ULD) has prothrombotic properties. In this study, we evaluate the effect of portal hypertension in rats on platelet aggregation in an in vivo arterial thrombosis model induced by a laser beam. Portal hypertension was produced by calibrated stenosis of the portal vein. ASA in ULD was injected to both control and portal hypertensive groups. Platelet aggregation induced by ADP, prothrombin time, activated partial thromboplastin time, fibrinogen and induced hemorrhagic time test were also performed. Portal hypertensive rats showed a diminished number of emboli and duration of embolization in the laser procedure and an increase in induced hemorrhagic time. These changes were reverted by one injection of ASA at ULD. This observation could be of importance for primary prevention or the treatment of recurrence in upper digestive tract hemorrhage in portal hypertensive patients.

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“…[191] In fact, differences exist between the peripheral and splanchnic circulation, with higher platelet activation and aggregation in the portal circulation. [192][193][194] Clinically speaking, these mechanisms could be relevant in the portal circulation where lipopolysaccharide-induced platelet activation and other site-specific alterations of hemostasis [71] may contribute to the development of PVT. [195] Historically, BT was increased in 40% of cirrhosis, [165] and the bleeding phenotype observed in these patients was linked to impaired platelet aggregation [7] based on experiments using LTA.…”

Section: The Evolving Concept Of Platelet Dysfunction In Patients Wit...mentioning

confidence: 99%

The evolving knowledge on primary hemostasis in patients with cirrhosis: A comprehensive review

et al. 2023

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Patients with cirrhosis develop complex alterations in primary hemostasis that include both hypocoagulable and hypercoagulable features. This includes thrombocytopenia, multiple alterations of platelet function, and increased plasma levels of von Willebrand factor. Contrary to the historical view that platelet dysfunction in cirrhosis might be responsible for an increased bleeding tendency, the current theory posits a rebalanced hemostasis in patients with cirrhosis. Severe thrombocytopenia is not indicative of the bleeding risk in patients undergoing invasive procedures and does not dictate per se the need for pre-procedural prophylaxis. A more comprehensive and individualized risk assessment should combine hemostatic impairment, the severity of decompensation and systemic inflammation, and the presence of additional factors that may impair platelet function, such as acute kidney injury and bacterial infections. Although there are multiple, complex alterations of platelet function in cirrhosis, their net effect is not yet fully understood. More investigations evaluating the association between alterations of platelet function and bleeding/thrombosis may improve risk stratification in patients with decompensated cirrhosis. Besides hemostasis, the assessment of von Willebrand factor Ag and ADP-induced, whole-blood platelet aggregation normalized by platelet count (VITRO score and PLT ratio) are promising biomarkers to predict the risk of hepatic decompensation and survival in both compensated and decompensated patients. Further investigations into the in vivo interplay between platelets, circulating blood elements, and endothelial cells may help advance our understanding of cirrhotic coagulopathy. Here, we review the complex changes in platelets and primary hemostasis in cirrhosis and their potential clinical implications.

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Platelet aggregation and coagulation and fibrinolysis parameters in both portal and systemic circulations in patients with cirrhosis and hepatocellular carcinoma

Cited by 5 publications

References 17 publications

Review article: blood platelet number and function in chronic liver disease and cirrhosis

Review article: blood platelet number and function in chronic liver disease and cirrhosis

Platelet Aggregation in Portal Hypertension and Its Modification by Ultra-Low Doses of Aspirin

The evolving knowledge on primary hemostasis in patients with cirrhosis: A comprehensive review

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