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Reuters Health Information (2007-07-19): Long-acting octreotide improves portal hypertension in patients with cirrhosis


Long-acting octreotide improves portal hypertension in patients with cirrhosis

Last Updated: 2007-07-19 13:30:15 -0400 (Reuters Health)

NEW YORK (Reuters Health) - Long-acting octreotide improves portal hypertension throughout a 3-month course of treatment in patients with cirrhosis, according to a report in the July American Journal of Gastroenterology.

"In the treatment of portal hypertension, the aim is to decrease the hepatic venous pressure gradient (HVPG) by 20% or more, or to get under 12 mm Hg of HVPG," Dr. Laurent Spahr from University Hospital, Geneva, told Reuters Health. "In situations where this aim is very clinically important, long-term octreotide may be added to other vasoactive drugs (i.e., beta-blocker) to reduce portal hypertension as much as possible."

Dr. Spahr and associates investigated the effect of chronic treatment with octreotide on portal pressure, systemic hemodynamics, and biological markers in 18 carefully selected patients with cirrhosis and clinically significant portal hypertension.

Treatment with octreotide was associated with a significantly greater reduction in HVPG (26%) after 3 months, compared with placebo (4%), the authors report.

Six of 10 patients treated with octreotide experienced HVPG decreases greater than 20%, and these changes took place independent of systemic hemodynamic parameters.

Plasma VEGF decreased significantly in the octreotide group, but not in the placebo group, the researchers note. Plasma concentrations of nitrate/nitrite, urotensin II, and endothelin-I remained stable in both groups.

The changes in HVPG and plasma VEGF values during the 3-month study were significantly correlated.

Two patients developed spontaneous bacterial peritonitis during the study, but the other 16 patients remained clinically stable without modification in the degree of liver function.

"A new finding in this paper was the associated decrease in circulating VEGF, which suggest octreotide's hemodynamic effect is due to a reduced splanchnic hyperemia," Dr. Spahr said. "Whether the addition of a vasoconstrictor (like terlipressin) may potentiate the hemodynamic effect of long acting octreotide should be investigated."

"These findings should encourage further studies on long-term treatment with somatostatin analogs in larger groups of patients, and point to a sustained decrease in splanchnic hyperemia as a possible pharmacological mechanism of octreotide," the investigators write.

Am J Gastroenterol 2007;102:1397-1405.

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