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      The role of propranolol in congestive gastropathy of portal hypertension

      , , ,
      Hepatology
      Wiley

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          Abstract

          Heavy diffuse bleeding from congested gastric mucosa (congestive gastropathy) was treated by propranolol (dose = 24 to 480 mg per day) in 14 consecutive patients with portal hypertension. Thirteen patients (93%) stopped bleeding within 3 days. Gastric mucosal cherry red spots (a sign of severe gastropathy) were unchanged in 5 patients, became less obvious in 4 and appearances returned to normal in 5. Propranolol was discontinued electively in seven patients after 2 to 6 months; four of these patients rebled from the same lesion and stopped bleeding when propranolol was recommenced. No patient has rebled from congestive gastropathy while receiving propranolol during follow-up of 12 to 42 (median = 23) months. A further 24 patients with nonbleeding congestive gastropathy received 160 mg long-acting propranolol per day in a double-blind placebo controlled cross-over trial. Twenty-two patients completed the study; in nine patients, endoscopic grading of congestive gastropathy improved after propranolol compared to three after placebo (p less than 0.05). Although the mechanism of action is not understood, propranolol appears to have a clinically significant role in the management of nonvariceal gastric bleeding in portal hypertension.

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          Most cited references12

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          Gastric lesions in portal hypertension: inflammatory gastritis or congestive gastropathy?

          This paper reports the incidence and natural history of macroscopic gastritis in a series of 127 consecutive patients with portal hypertension of various aetiologies. Gastritis was observed endoscopically in 65 patients (51%) and was of two main types. Twenty eight patients had severe or persistent gastritis which caused clinically significant bleeding on 80 occasions and accounted for 25% of the bleeds from all sources. The remainder had mild gastritis. The presence of gastritis seemed to be independent of the severity of liver disease or the degree of rise of wedged hepatic venous pressure and there was no difference in age, sex, or drugs prescribed in patients with or without gastritis. The mean follow up period and the mean number of sclerotherapy treatments was significantly greater (p less than 0.005) in patients with gastritis. Full thickness gastric biopsies in seven surgical patients and 11 autopsy specimens showed dilated and tortuous submucosal veins. Endoscopic biopsies in 14 patients showed vascular ectasia in the mucosal layer which was in excess of the degree of inflammatory infiltrate. Gastritis occurred in patients with portal hypertension of all common aetiologies and the clinical and pathological evidence supports the contention that it reflects a congested gastric mucosa and should be renamed congestive gastropathy. As injection sclerotherapy improves survival from variceal bleeding congestive gastropathy may become more common. The response to conventional ('anti-erosive') therapy is poor and measures aimed at reducing the gastric portal pressure may be the only effective means of treating this condition.
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            Propranolol--a medical treatment for portal hypertension?

            Continuous, oral administration of propranolol at doses which reduced the heart-rate by 25% produced a sustained decrease in portal venous pressure in cirrhotic patients with portal hypertension. This effect of propranolol might be useful in preventing recurrent bleeding due to ruptured oesophageal varices in patients with portal hypertension.
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              The General rules for recording endoscopic findings on esophageal varices

              K Inokuchi (1980)
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                Author and article information

                Journal
                Hepatology
                Hepatology
                Wiley
                02709139
                15273350
                May 1987
                May 1987
                : 7
                : 3
                : 437-441
                Article
                10.1002/hep.1840070304
                3552921
                4fd45dda-1122-47f7-8db2-df3834be5993
                © 1987

                http://doi.wiley.com/10.1002/tdm_license_1.1

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