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Blood and plasma 5-hydroxytryptamine levels in patients with cirrhosis

โœ Scribed by Patrice Beaudry; Antoine Hadengue; Jacques Callebert; Christophe Gaudin; Hany Soliman; Richard Moreau; Jean Marie Launay; Dr. Didier Lebrec


Publisher
John Wiley and Sons
Year
1994
Tongue
English
Weight
420 KB
Volume
20
Category
Article
ISSN
0270-9139

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โœฆ Synopsis


Serotoninergic mechanisms are thought to play a role in portal hypertension. Because this biomine is metabolized by the liver, peripheral blood and plasma levels of 5-hydroxytryptamine and 5-hydroxyindole acetic acid (the main metabolite of 5-hydroxytryptamine) were measured in 30 patients with cirrhosis. Whole-blood 5-hydroxytryptamine levels were significantly lower in patients with cirrhosis (158 2 28 nM) than in age-matched controls (332 & 19 nM), and no correlation was found between these levels and the se- verity of cirrhosis. Unconjugated plasma 5-hydroxytryptamine levels, an indication of the active form of 5-hydroxytryptamine, were significantly higher in patients with cirrhosis than in controls (6.8 & 1.7 nM and 3.4 & 0.5 nM, respectively), and in patients with cirrhosis these levels were higher in Pugh grade A than in Pugh grade C patients. Conjugated-plasma 5-hydroxytryptamine levels were not significantly different between patients with cirrhosis (32.2 & 8.1 nmol/L) and controls (16.4 & 1.4 nmol/L). Plasma 5-hydroxyindole acetic acid was significantly lower in patients with cirrhosis than in controls (1.5 f 0.1 nmoln and 2.3 & 0.1 nmol/L, respectively). In conclusion, this study shows that serotoninergic mechanisms are altered in patients with cirrhosis. (HEPATOLOGY 1994;20:800-803.)

Several clinical and experimental studies have shown that ketanserin and ritanserin, two antagonists of 5-HT, receptors, reduce portal pressure in patients and animals with portal hypertension (1-7). It has also been shown t h a t the isolated mesenteric vein in portal hypertensive rats was more reactive t o 5-HT than veins from sham-operated rats (1). These different studies suggest that serotonergic mechanisms may play a role in portal hypertension. The mechanisms of these effects remain, however, to be explained. Moreover, because


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