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J Hepatol. 1997 Apr;26(4):816-25.

Octreotide long-term treatment in patients with portal hypertension: persistent inhibition of postprandial glucagon response without major changes in renal function.

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Institute of Internal Medicine, University of Milan, Italy.



Octreotide acutely decreases splanchnic blood flow and postprandial portal pressure in patients with portal hypertension. Inhibition of glucagon release parallels the hemodynamic changes. We studied the hormonal and renal effects of long-term treatment with octreotide (100 microg s.c., t.i.d., immediately before meals, for 2 weeks) in 12 patients with cirrhosis and portal hypertension.


Postprandial blood levels of glucagon, insulin and glucose, and renal function tests were monitored in a study where patients acted as their own controls. Eleven patients completed the study, octreotide being discontinued in one patient who developed jaundice after 6 days of therapy.


Long-term treatment did not cause any change in fasting hormonal levels measured 12 h after the last injection of octreotide. However, pre-prandial injection of octreotide induced a marked fall in blood glucagon (163+/-49 pg/ml, after 20 min, vs. 254+/-71 pg/ml, basal; p<0.01), thus preventing the postprandial response occurring without treatment (322+/-102 pg/ml, 30 min-peak, vs. 249+/-77 pg/ml, basal; p<0.03). Inhibition of postprandial glucagon was maintained after 2 weeks of therapy (159+/-33 pg/ml, after 20 min, vs. 237+/-54 pg/ml, basal; p<0.01). Octreotide abolished the insulin postprandial response with no major change in glycemic control. Treatment had no long-term effect on renal plasma flow (effective renal plasma flow: 596+/-79 ml/min, baseline, vs. 609+/-71 ml/min, at 2 weeks; p>0.5), glomerular filtration rate (glomerular filtration rate: 99+/-11 vs. 99+/-12 ml/min; p>0.5), blood urea and creatinine, whereas it induced a mild decrease in plasma electrolyte levels (p<0.02).


Long-term octreotide treatment persistently suppresses the postprandial glucagon response of patients with portal hypertension without causing deterioration in their renal function.

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