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Ultra-low-dose aspirin might decrease bleeding severity in portal hypertension
October 10, 2007In rats with portal hypertension, ultra-low-dose aspirin has shown a normalizing effect of platelet-endothelial cell alterations and bleeding time. Further, this effect is mediated by Cyclooxygenase 2 inhibition.
This study, performed by a team led by Professor C. Doutremepuich, is described in a research article to be published in the October 14 issue of the World Journal of Gastroenterology.
Portal hypertension is a major complication of chronic liver disease, and bleeding is one of its most severe problems, leading often to death. Currently no treatment is used to modify the altered platelet activity observed in this pathology.
Ultra-low-dose aspirin has a prothrombotic effect that is the opposite of that observed with usual doses for the prevention of stroke or heart attack. The antithrombotic properties of low-dose aspirin are achieved by the inhibition of COX 1 in platelets. Aspirin is the most widely used antithrombotic agent. Previous research in rats has shown that the prothrombotic properties of ultra-low-dose aspirin are not mediated by platelets but by endothelial cells, and as such they have the potential of reversing the platelet-endothelial cell interaction alterations observed in portal hypertension.
In the view of the authors, to date no clear explanation has existed to elucidate the effect of such a small dose of aspirin, and no mechanism has been found to explain this contradictory action.
The prothrombotic effects of COX 2 inhibitors became evident in 2004 when one of the most widely accepted non-steroidal anti-inflammatory drugs was withdrawn from the market because of concerns about increased risk of heart attack and stroke associated with long-term, high-dosage use. Only aspirin has been demonstrated to have a prothrombotic effect at a very low dose.
In an elegant study design, including a model of in vivo Laser induced thrombosis in rats, bleeding time and prostanoid dosing, this research was performed by doctors from the Laboratory of Haematology of the Faculty of Pharmacy at the University of Bordeaux 2, France, Laboratoires Boiron and from the CEBBAD, Universidad Maimonides, Buenos Aires, Argentina.
Further research should explain the consequences of COX 2 inhibition produced by ultra-low doses of aspirin.
World Journal of Gastroenterology
Ultra-low-dose aspirin has a prothrombotic effect that is the opposite of that observed with usual doses for the prevention of stroke or heart attack. The antithrombotic properties of low-dose aspirin are achieved by the inhibition of COX 1 in platelets. Aspirin is the most widely used antithrombotic agent. Previous research in rats has shown that the prothrombotic properties of ultra-low-dose aspirin are not mediated by platelets but by endothelial cells, and as such they have the potential of reversing the platelet-endothelial cell interaction alterations observed in portal hypertension.
In the view of the authors, to date no clear explanation has existed to elucidate the effect of such a small dose of aspirin, and no mechanism has been found to explain this contradictory action.
The prothrombotic effects of COX 2 inhibitors became evident in 2004 when one of the most widely accepted non-steroidal anti-inflammatory drugs was withdrawn from the market because of concerns about increased risk of heart attack and stroke associated with long-term, high-dosage use. Only aspirin has been demonstrated to have a prothrombotic effect at a very low dose.
In an elegant study design, including a model of in vivo Laser induced thrombosis in rats, bleeding time and prostanoid dosing, this research was performed by doctors from the Laboratory of Haematology of the Faculty of Pharmacy at the University of Bordeaux 2, France, Laboratoires Boiron and from the CEBBAD, Universidad Maimonides, Buenos Aires, Argentina.
Further research should explain the consequences of COX 2 inhibition produced by ultra-low doses of aspirin.
World Journal of Gastroenterology
Study shows positive findings in treating patients with advanced hepatitis C
The hepatitis C therapy peginterferon alfa-2b, when given as low-dose maintenance therapy, can prevent disease progression in certain patients who failed previous interferon-based hepatitis C therapies and have advanced liver disease, according to findings from a large, four-year study presented today at the 43rd annual meeting of the European Association for the Study of the Liver (EASL).
Optimal systemic and splanchnic hemodynamic state after living-donor liver transplantation
Almost all adult recipients who undergo LDLT develop liver cirrhosis with long-term portal hypertension. Portal hypertension results in vascular dilatation and collateral pathways. Thus, various alterations in systemic hemodynamics and splanchnic circulation occur, and adult recipients often present characteristic hemodynamics before LDLT.
Can liver cirrhosis be partially cured?
The diffusion of hepatitis C virus infection worldwide is astonishing. Liver cirrhosis is present in at least 10-20% of these infected patients, with highly increasing health care and emotional costs.
New Mayo Clinic MRI technology enables noninvasive liver diagnoses
Two recent Mayo Clinic studies have found that magnetic resonance elastography (MRE), a new imaging technique invented at Mayo Clinic, is an accurate tool for non-invasive diagnosis of liver diseases.
Researchers uncover mechanisms leading to portal hypertension
A physician-scientist at UT Southwestern Medical Center and his research team have identified mechanisms causing a potentially deadly type of hypertension that results from liver damage-findings that could lead to its prevention.
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