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      Comparison of the effect of midodrine versus octreotide on hemodynamic status in cirrhotic patients with ascites


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          In cirrhotic patients peripheral vasodilatation may decrease renal blood flow and subsequently raises plasma renin activity. Octreotide with several mechanisms causes peripheral arterial vasoconstriction. Midodrine is an alpha agonist and acts as a peripheral vasoconstrictor; therefore it may reduce plasma renin activity and improve renal function. In this study the effects of these two agents were compared on cirrhotic patients to determine their ability to reduce plasma renin activity and increase GFR.


          This study was a randomized clinical trial and was performed in Al-Zahra hospital in 2008-2009; 34 patients with CHILD C cirrhosis enrolled in this study. They were randomly divided into two groups. First group were treated by 3 days of subcutaneous octreotide 50 μg tid (n = 17). For the second group oral midodrine 7.5 mg tid was administrated for 3 days. Plasma renin activity, blood pressure, glomerular filtration rate, and body weight were measured and compared before and after therapy in both groups.


          In both groups, plasma rennin activity decreased significantly after treatment. The present study showed that both midodrine and octreotide can reduce plasma renin activity but midodrine can reduce PRA and increase GFR more potently than octreotide.


          Midodrine has a favorable hemodynamic effect in nonazotemic cirrhotic patients by decreasing plasma renin activity and increasing GFR.

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          Reversal of type 1 hepatorenal syndrome with the administration of midodrine and octreotide.

          The aim of the study was to verify the effects of the administration of an inhibitor of the release of endogenous vasodilators together with a vasoconstrictor agent in patients with hepatorenal syndrome (HRS). This new medical perspective was compared with a traditional medical approach for HRS, such as the infusion of nonpressor doses of dopamine to produce renal vasodilation. Thirteen patients with type 1 HRS were enrolled in the study. Five of them were treated with the oral administration of midodrine and the parenteral administration of octreotide. In addition, the patients received 50 to 100 mL of 20% human albumin solution daily for 20 days. Midodrine and octreotide were dosed to obtain a stable increase of at least 15 mm Hg of mean arterial pressure. Eight patients were treated with the intravenous administration of nonpressor doses of dopamine (2-4 micrograms/kg/min) and the same daily amount of albumin. After 20 days of treatment with midodrine and octreotide, an impressive improvement in renal plasma flow (RPF), glomerular filtration rate, and urinary sodium excretion was observed in patients. This was accompanied by a significant reduction in plasma renin activity, plasma vasopressin, and plasma glucagon. No side effects were observed. Three patients were discharged from the hospital. One of them successfully underwent liver transplantation. One of the two remaining patients is still alive after 472 days with a preserved renal function, and the other died from terminal liver failure after 76 days. One of the two patients who were not discharged from the hospital successfully underwent liver transplantation, and the other died from pneumonia after 29 days. Seven out of eight patients who were treated with dopamine experienced a progressive deterioration in renal function and died during the first 12 days. Only one patient recovered renal function and underwent liver transplantation. In conclusion, the long-term administration of midodrine and octreotide seems to be an effective and safe treatment of type 1 HRS in patients with cirrhosis.
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            Peripheral arterial vasodilation hypothesis: a proposal for the initiation of renal sodium and water retention in cirrhosis.

            Renal sodium and water retention and plasma volume expansion have been shown to precede ascites formation in experimental cirrhosis. The classical "underfilling" theory, in which ascites formation causes hypovolemia and initiates secondary renal sodium and water retention, thus seems unlikely. While the occurrence of primary renal sodium and water retention and plasma volume expansion prior to ascites formation favors the "overflow" hypothesis, the stimulation of the renin-angiotensin-aldosterone system, vasopressin release and sympathetic nervous system associated with cirrhosis is not consonant with primary volume expansion. In this present article, the "Peripheral Arterial Vasodilation Hypothesis" is proposed as the initiator of sodium and water retention in cirrhosis. Peripheral arterial vasodilation is one of the earliest observations in the cirrhotic patient and experimental animals with cirrhosis. Arterial vasodilators and arteriovenous fistula are other examples in which renal sodium and water retention occur secondary to a decreased filling of the arterial vascular tree. An increase in cardiac output and hormonal stimulation are common features of cirrhosis, arteriovenous fistula and drug-induced peripheral arterial vasodilation. However, a predilection for the retained sodium and water to transudate into the abdominal cavity occurs with cirrhosis because of the presence of portal hypertension. The Peripheral Arterial Vasodilation Hypothesis also explains the continuum from compensated to decompensated cirrhosis to the hepatorenal syndrome.
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              Effects of noradrenalin and albumin in patients with type I hepatorenal syndrome: a pilot study.

              Treatment of hepatorenal syndromes (HRSs) is currently based on vasopressin analogs. The aim of this pilot study was to evaluate the efficacy and safety of noradrenalin (NA) in the treatment of type 1 HRS. Between 1998 and 2000, 12 consecutive patients with type 1 HRS (7 men, 5 women; mean age, 54 +/- 11 years; mean Child-Pugh score, 11.3 +/- 1.7) were treated with intravenous NA (0.5-3 mg/h), in combination with intravenous albumin and furosemide. NA was given for 10 +/- 3 days, at a mean dose of 0.8 +/- 0.3 mg/h. Reversal of HRS was observed in 10 of 12 patients (83%; 95% confidence interval, 52%-98%) after a median of 7 days (range, 5-10 days). Serum creatinine levels fell from 358 +/- 161 to 145 +/- 78 micromol/L (P <.001), creatinine clearance rose from 13 +/- 9 to 40 +/- 15 mL/min (P =.003), and urinary sodium output increased from 8 +/- 14 to 52 +/- 72 mEq/d (P =.002). Changes in renal function under NA treatment were associated with an increase in mean arterial pressure (MAP; 65 +/- 7 to 73 +/- 9 mm Hg, P =.01) and a marked reduction in active renin (565 +/- 989 to 164 +/- 196 ng/L, P =.001) and aldosterone plasma concentrations (1,945 +/- 1,931 to 924 +/- 730 ng/mL, P =.02). There was one episode of reversible myocardial hypokinesia (in a patient on 1.5 mg/h NA) that did not recur after a dose reduction. In conclusion, NA combined with albumin and furosemide appears effective and safe for the treatment of type 1 HRS.

                Author and article information

                J Res Med Sci
                Journal of Research in Medical Sciences : The Official Journal of Isfahan University of Medical Sciences
                Medknow Publications & Media Pvt Ltd (India )
                January 2011
                : 16
                : 1
                : 87-93
                [a ]Assistant Professor of Gastroenterology and Hepatology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
                [b ]Resident of Internal Medicine, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
                [c ]Researcher, Poursina Hakim Research Center, Isfahan, Iran
                [d ]Associate Professor of Gastroenterology and Hepatology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
                Author notes
                [* ]Corresponding Author shavakhi@ 123456med.mui.ac.ir
                Copyright: © Journal of Research in Medical Sciences

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                : 14 May 2010
                : 22 June 2010
                Original Article

                renin,liver cirrhosis,octreotide,plasma,midodrine
                renin, liver cirrhosis, octreotide, plasma, midodrine


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