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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We conducted a prospective randomized trial of propranolol for the prevention of recurrent variceal bleeding in 48 patients with cirrhosis of the liver. During a follow-up period of up to 21 months, 12 of 26 patients in the propranolol group and 11 of 22 in the control group had rebleeding from esophageal varices. There was no significant difference in rebleeding between the two groups. This contrasts with a previous report of the efficacy of propranolol in preventing recurrent gastrointestinal bleeding in alcoholic cirrhosis. The difference in results may be due to the inclusion in our study of patients with other causes of cirrhosis and more severe liver disease. Propranolol may not be indicated for the prophylaxis of variceal rebleeding in such patients, and we advocate that its use be limited at present to controlled clinical trials.
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PMID:Controlled trial of propranolol for the prevention of recurrent variceal hemorrhage in patients with cirrhosis. 636 53

Propranolol hydrochloride is reported to lower portal pressure and inhibit renin secretion in patients with chronic liver disease, actions that might lessen the tendency to ascites formation. We compared the effect of diuretics with that of the same dose of diuretics plus propranolol on natriuresis, urine output, and daily weight loss in 13 hospitalized patients with stable chronic liver disease, sodium retention, and ascites. The propranolol hydrochloride dose was 20 to 160 mg four times a day, titrated to reduce resting pulse by 25% or systolic BP 10 mm Hg. Diuretics given were furosemide, 80 to 160 mg, and triamterene, 100 or 200 mg/day. Periods of time when each regimen was received ranged from one to four days. Creatinine excretion documented complete urine collections. Compared with diuretics alone, diuretics plus propranolol substantially reduced resting pulse, systolic BP, and urine sodium excretion, although not creatinine clearance. This antinatriuretic effect may limit the proposed usefulness of propranolol for prevention of variceal bleeding in patients with cirrhosis and ascites.
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PMID:Propranolol in the treatment of cirrhotic ascites. 647 94

Forty-one patients with hepatic cirrhosis of alcoholic etiology and esophageal varices were subjected to endoscopic sclerotherapy. Four patients were treated during the intervals between hemorrhages; thirty after their first hemorrhage and 7 prophylactically. Propranolol was administered to 5 patients, in doses of 60-80 mg daily. The survival rate for a period of 5 to 16 months was 83%. No complications attributable to the procedure were observed.
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PMID:Injection sclerotherapy of esophageal varices. 698 Jan 14

Chronic liver disease is well known to be associated with pulmonary abnormalities. Hypoxemia, clubbing, cyanosis and hyperventilation are common. The hypoxemia in cirrhotic patients has several causes: diffuse shunts due to intrapulmonary arteriolar vasodilatation, impaired hypoxic vasoconstriction, impaired matching of ventilation to perfusion, pleural effusions and diaphragmatic dysfunction. Because of gravity, shifting of blood to the dilated precapillary beds of the lung bases results in an increased hypoxemic dyspnea when the patient is in the upright position, also known as orthodeoxia and platypnea. It has only been described in 5% of the cirrhotic patients and has not been described in a Belgian refereed journal (Medline literature search 1983-Aug 1993). It should be considered in the initial differential diagnosis of hypoxemia in patients with liver cirrhosis and dyspnea. Measuring arterial blood gases in the lying and upright position can prevent further invasive investigations, and whole body nuclide scan with technetium-99m macroaggregated albumin can confirm the diagnosis. Standard therapy with spironolactone (Aldactone) can worsen the condition and we found no additional benefit of beta-antagonists (propranolol/Inderal) in the reduction of the shunt fraction, probably because the main reason for the shunting is precapillary vasodilatation. Since there are no anatomical porto-pulmonary shunts, surgery is also inappropriate. The only therapy consists of oxygen supplements and low dose diuretics in patients with edema.
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PMID:Orthodeoxia and platypnea in liver cirrhosis: effects of propranolol. 751 28

A 69-year-old female was admitted to our hospital because of leg edema, proteinuria (2.1 g/day), and gross hematuria. She had non-alcoholic liver cirrhosis of unknown etiology. Esophageal varices also were found. Examination of the renal biopsy specimen revealed mesangial proliferative glomerulonephritis with IgA deposits. Propranolol was administered orally to reduce portal hypertension, resulting in a progressive decrease in urinary microalbumin excretion. This case suggests that portal hypertension is involved in the pathogenesis of IgA nephropathy in liver cirrhosis.
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PMID:IgA nephropathy associated with portal hypertension in liver cirrhosis due to non-alcoholic and non-A, non-B, non-C hepatitis. 780 17

This study examined the hemodynamic effects of selective beta 2-adrenergic blockade (ICI 118,551, 100 micrograms/kg intravenous (i.v.)), selective beta 1-blockade (atenolol, 2 mg i.v.) and nonselective beta-blockade (propranolol, 2 mg i.v.) in conscious rats with cirrhosis. Pressure and blood flow measurements (radioactive microsphere method) were performed before and following drug administration. ICI 118,551 significantly decreased portal tributary blood flow (21%), portal pressure (4%) and cardiac index (12%). Portal tributary blood flow decreases were significantly more marked than changes in cardiac index. Atenolol significantly decreased portal tributary blood flow (27%), portal pressure (15%), cardiac index (17%) and arterial pressure (7%). Propranolol significantly decreased portal tributary blood flow (37%), portal pressure (17%), cardiac index (30%), and arterial pressure (9%). Portal tributary blood flow decreases due to ICI 118,551, but not those due to atenolol, were significantly less marked than the decreases caused by propranolol. ICI 118,551- and atenolol-induced cardiac index decreases were significantly less marked than propranolol-induced decreases. In conclusion, in rats with cirrhosis, selective beta 2-blockade reduces portal pressure and portal tributary blood flow mainly by a direct effect on splanchnic vessels. This portal hypotensive action, however, was slight. Propranolol decreases portal tributary blood flow by the combination, but not the summation, of its beta 1- and beta 2-blocking effects.
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PMID:Hemodynamic responses to selective blockade of beta 2- and beta 1-adrenoceptors in conscious rats with cirrhosis. 789 Aug 94

Propranolol can reduce portal hypertension, therefore is recommended in prevention of variceal bleeding in patients with liver cirrhosis. However, in certain patients with cirrhosis portal hypotensive effect of propranolol cannot be obtained, and the reason of this finding is unknown. In 28 patients with cirrhosis the effect of seven days administration of propranolol on collateral blood flow from inferior mesenteric vein was examined by means of per-rectal portal scintigraphy. Portosystemic shunt index was significantly reduced by propranolol by 17.4 +/- 4.8%. This reduction was observed in cirrhotics classified to A and B, but not C Child-Pugh. These data suggest that propranolol increases vascular resistance in portosystemic circulation which depends on severity of liver failure. This mechanism opposes reduction of portal pressure.
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PMID:[Per-rectal scintigraphy of the portal system with pertechnetate TC-99M: effect of propranolol on portosystemic collateral circulation in patients with cirrhosis. Part II]. 797 73

To alleviate the risk of variceal bleeding, the portal pressure gradient--usually evaluated as the hepatic venous pressure gradient (HVPG)--must be reduced to < or = 12 mmHg. Although beta-blocking agents are accepted therapy for preventing first or subsequent bleeding episodes, propranolol therapy decreases final HVPG to < or = 12 mmHg in only 12% of patients, while only 24% of patients have a > or = 20% reduction in HVPG and nearly 40% show no reduction in HVPG. This has stimulated research on alternative or additional treatments. Nitrates such as isosorbide dinitrate reduce portal pressure by decreasing resistance to portal and collateral blood flow and by promoting reflex splanchnic vasoconstriction. However, while nitrates are effective in the acute situation, tolerance leading to refractoriness develops over the long term unless they are combined with diuretics or other agents in the treatment of portal hypertension. Propranolol and isosorbide-5-mononitrate combined cause a substantially greater reduction in HVPG than monotherapy with either drug in both acute and long-term use. Presumably concomitant isosorbide-5-mononitrate administration opposes the increase in portal resistance induced by propranolol. Spironolactone, which has been shown to lower HVPG in patients with cirrhosis, produces a reduction in plasma volume that attenuates the increased cardiac output associated with cirrhosis and triggers vasoactive mechanisms that decrease splanchnic blood flow. Potentially, spironolactone may maintain and enhance the decrease in portal pressure achieved by nitrates or propranolol. Triple therapy with a beta-blocker, a nitrate and spironolactone may be feasible.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New approaches in the pharmacologic treatment of portal hypertension. 809 42

Systemic and portal hemodynamic parameters were evaluated in eight cirrhotic patients in basal conditions and after food intake and placebo. Following seven days of oral propranolol administration, hemodynamic parameters were reevaluated in the fasting and postprandial states under similar conditions. Cardiac output and portal blood flow were measured by Doppler technique. Intraobserver variability of repeated measurements was less than 10%. Food intake caused a significant increase of portal blood flow (+28%, P < 0.05). No significant changes were observed in the other hemodynamic parameters studied. Propranolol at doses achieving effective beta blockade (84 +/- 14 mg/day) (mean +/- SD) reduced portal blood flow (-24%, P < 0.05). Food intake caused a significant increase in portal blood flow (+35%, P < 0.05) in propranolol treated patients. However, in absolute values, postprandial portal blood flow during propranolol treatment was significantly lower (986 +/- 402 ml/min) than that obtained after the initial food intake (1214 +/- 537 ml/min, P < 0.05). Placebo administration had no significant hemodynamic effects in either group. This study demonstrates that chronic propranolol administration could protect from portal hemodynamic changes following food intake. Doppler technique is a reliable technique to evaluate changes on portal and systemic hemodynamic parameters during a short period of time in patients with cirrhosis.
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PMID:Postprandial vascular response in patients with cirrhosis. Short-term effects of propranolol administration. 820 Feb 62

The purpose of this study was to investigate the possible value of continuous administration of propranolol in the prevention of recurrent upper gastrointestinal bleeding in patients with cirrhosis undergoing chronic endoscopic sclerotherapy. Among 239 patients admitted for acute variceal bleeding, 85 with cirrhosis were randomized to receive sclerotherapy either alone (40) or in combination with propranolol (45). Sclerotherapy was carried out with an intravariceal injection of 5% ethanolamine oleate through a fiberoptic endoscope. The procedure was performed every week, until the esophageal varices at the gastroesophageal junction were too small for any further injections. Varices were reinjected if they recurred. Propranolol was given orally twice a day until heart rate was reduced by 25% in the resting position. The mean follow-up period was 23.2 and 24.2 months for sclerotherapy and the sclerotherapy plus propranolol groups, respectively. During this period a significant (P = 0.001) reduction in the recurrence of esophageal varices was observed in patients treated with the combination of sclerotherapy plus propranolol compared with those treated with sclerotherapy alone. However, the time of rebleeding from any source or from esophageal varices did not differ significantly between the two groups. In the sclerotherapy group 21 patients rebled (35 bleeding episodes) compared with 14 (22 episodes) in the combination therapy group. Patients in the sclerotherapy group were more prone to bleed from gastric varices and congestive gastropathy than patients treated with the combination of sclerotherapy plus propranolol (P = 0.012). Twenty-five patients in the endoscopic sclerotherapy group developed complications attributed to sclerotherapy compared with 23 patients in the sclerotherapy plus propranolol group. Complications directly attributable to propranolol were observed in 11 patients. Three of these patients stopped taking the drug due to heart failure (1) and flapping tremor (2). Eight patients (17.8%) died in the latter group while the corresponding figure in the sclerotherapy group was nine (22.5%). It is concluded that the continuous administration of propranolol may reduce incidences of recurrent upper gastrointestinal hemorrhage from gastric sources in patients with cirrhosis undergoing chronic sclerotherapy.
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PMID:Propranolol in the prevention of recurrent upper gastrointestinal bleeding in patients with cirrhosis undergoing endoscopic sclerotherapy. A randomized controlled trial. 789 Sep 17


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