In Vitro Inhibition of Platelet Aggregation by Bile Salts

Baele, G; Beke, R; Barbier, F

doi:10.1055/s-0038-1650084

Cited by 14 publications

(9 citation statements)

References 7 publications

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“…Bile salts can also exert a negative effect. In vitro aggregation studies show an inhibitory effect of bile salts on platelet aggregation and serotonin release induced by ADP or collagen 88 . Only chenodeoxycholic acid is an aggregation‐inducing bile salt 88 .…”

Section: Platelet Functionmentioning

confidence: 99%

“…In vitro aggregation studies show an inhibitory effect of bile salts on platelet aggregation and serotonin release induced by ADP or collagen 88 . Only chenodeoxycholic acid is an aggregation‐inducing bile salt 88 . In vivo studies in rat models associated with elevated bile acids (bile duct ligation and cholic acid feeding) show a clear inhibitory effect on ADP‐epinephrine induced aggregation 89 …”

Section: Platelet Functionmentioning

confidence: 99%

See 1 more Smart Citation

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: 99%

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

“…In diets containing cholesterol and cholic acid (CA), increased thrombin and adenosine diphosphate (ADP)-induced platelet aggregation and an acceleration of the platelet-rich plasma clotting time were found (McGregor et al, 1980 ). Other authors, however, observed that sodium salts of some bile acids, such as cholic acid, showed a clear inhibitory effect on platelet aggregation by ADP, while the sodium salt of chenodeoxycholic acid (CDA) was an inducer of platelet aggregation (Baele et al, 1980 ). In other experiments, deoxycholic acid inhibited platelet aggregation and ADP secretion in platelets activated with either collagen or thrombin (Tan et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Bile Acids Do Not Contribute to the Altered Calcium Homeostasis of Platelets from Rats with Biliary Cirrhosis

et al. 2017

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Previously, we have found that intracellular calcium homeostasis is altered in platelets from an experimental model of liver cirrhosis, the bile-duct ligated (BDL) rat; these alterations are compatible with the existence of a hypercoagulable state and related to an enhanced intracellular calcium release evoked by thrombin and an increased amount of calcium stored in the intracellular organelles. In the present study we have investigated the role of bile acids in those alterations of the BDL cirrhotic model. Cholic acid (CA) or deoxycholic acid (DCA) did not change P-selectin expression or platelet aggregation in any group but elevated baseline platelet calcium levels. Incubation with both bile acids reduced calcium release after stimulation with thrombin in the absence of extracellular calcium. Pretreatment with CA but not with DCA reduced significantly thrombin-induced calcium entry in all three experimental groups. The capacitative calcium entry was also significantly lower in platelets pretreated with both bile acids. The simultaneous addition of thapsigargin and ionomycin to estimate the total amount of calcium in platelet internal stores was decreased by pretreatment with both CA and DCA, although these changes were significantly different in the control rats only with CA and in the BDL platelets with DCA. These results indicate that CA and DCA reduce calcium movements in platelets of control and BDL animals, thus suggesting that bile acids do not participate in the alterations observed in the BDL cirrotic model.

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“…Maintenance of platelet counts within normal limits depends on the ability of bone marrow to increase production, which is reflected in the proportion of young elements in the circulation. Although thrombocytopoiesis is under the direct effect of thrombopoietin, a growth factor synthesized mainly by the liver and the kidney, and whose serum levels decrease in advanced cirrhosis and portal hypertension, its titers do not correlate directly with medullary platelets synthesis (8). This apparent discordance results from the fact that the removal of thrombopoietin from the circulation is made through its internalization in megakaryocytes and platelets, including those which are pooled in the spleen (9).…”

Section: Discussionmentioning

confidence: 99%

The risk of bleeding and encephalopathy in surgical patients with liver cirrhosis

Banu¹,

Salvatore²,

Merlo³

et al. 2019

JMMS

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Liver cirrhosis is a disease with an increasing incidence. Surgical procedures in patients with cirrhosis are also increasing, due to a longer life expectancy in these patients and also to the improvement of therapeutic and diagnostic resources.Digestive hemorrhage in the cirrhotic patient requires emergency medical intervention (intensive therapy, endoscopic or even surgical approaches), being at the same time a factor that precipitates episodes of encephalopathy, i.e. the conventional complication of cirrhosis. Hepatic encephalopathy represents one of the most severe clinical events of cirrhosis, being associated with high morbidity and mortality. The causes of hepatic encephalopathy are briefly presented in this paper. Therapeutic approaches currently available consist in the administration of non-absorbable disaccharides such as lactulose and non-absorbable antibiotics such as rifaximin. New therapeutic perspectives are under evaluation, e.g. ammonia scavengers and the modulation of gut microbiota.Clotting disorders in patients with liver cirrhosis are more severe as the disease progresses and involves complex mechanisms, as presented in this review. The correction of possible disorders of hemostasis should be promptly made as a sine qua non condition prior to surgery.

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In Vitro Inhibition of Platelet Aggregation by Bile Salts

Cited by 14 publications

References 7 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

Bile Acids Do Not Contribute to the Altered Calcium Homeostasis of Platelets from Rats with Biliary Cirrhosis

The risk of bleeding and encephalopathy in surgical patients with liver cirrhosis

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