Effect of carvedilol on portal hypertension depends on the degree of endothelial activation and inflammatory changes
Language English Country Great Britain, England Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
17101577
DOI
10.1080/00365520600780403
PII: K40V83771116M665
Knihovny.cz E-resources
- MeSH
- Adrenergic beta-Antagonists therapeutic use MeSH
- Biomarkers blood MeSH
- Endothelium, Vascular physiopathology MeSH
- E-Selectin blood MeSH
- Liver Cirrhosis physiopathology MeSH
- Carbazoles therapeutic use MeSH
- Carvedilol MeSH
- Middle Aged MeSH
- Humans MeSH
- Intercellular Adhesion Molecule-1 blood MeSH
- Hypertension, Portal drug therapy physiopathology MeSH
- Propanolamines therapeutic use MeSH
- Tumor Necrosis Factor-alpha blood MeSH
- Hepatic Veins physiopathology MeSH
- Venous Pressure physiology MeSH
- Inflammation physiopathology MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Adrenergic beta-Antagonists MeSH
- Biomarkers MeSH
- E-Selectin MeSH
- Carbazoles MeSH
- Carvedilol MeSH
- Intercellular Adhesion Molecule-1 MeSH
- Propanolamines MeSH
- Tumor Necrosis Factor-alpha MeSH
OBJECTIVE: Bleeding from esophageal varices is a major complication of liver cirrhosis. Non-selective beta-blockers exert an influence on the functional part of portal hypertension, thereby reducing the risk of bleeding. Direct measurement of this functional part is not possible; nevertheless, pro-inflammatory markers as well as parameters of endothelial dysfunction might serve as surrogate markers. The aim of study was to assess the correlation between the therapeutic efficacy of carvedilol and markers of endothelial dysfunction and systemic inflammation in patients with liver cirrhosis and portal hypertension. MATERIAL AND METHODS: Thirty-six patients with cirrhosis and portal hypertension were given carvedilol, 25 mg q.i.d. for 30 days. Hepatic venous pressure gradient (HVPG) and biochemical determinations were performed prior to and after the treatment. Eight healthy individuals served as controls for comparison of biochemical markers. RESULTS: In the whole group of cirrhotic patients, HVPG decreased from 17.7+/-3.8 to 14.9+/-4.8 mmHg (p<0.001). Complete response was seen in 15 patients (42%). Baseline serum levels of E-selectin were significantly higher in responders than in non-responders (119.8+/-70.6 versus 52.6+/-25.7 ng/ml; p=0.023) and in controls (28.8+/-22.2 ng/ml; p=0.004). Furthermore, baseline TNF-alpha levels were significantly higher in responders than in non-responders (22.8+/-15.7 versus 7+/-8.9; p=0.047) and in controls (5.5+/-5.9 pg/ml; p=0.005). Serum levels of ICAM-1 showed the same trend (4360+/-2870 versus 2861+/-1577 versus 651+/-196 ng/ml), although differences did not reach statistical significance. CONCLUSIONS: Markers of systemic inflammation and endothelial dysfunction seem to predict the hypotensive effect of carvedilol on portal hypertension in patients with liver cirrhosis and may be useful in the assessment of the efficacy of the therapy.
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