Drug treatment for bleeding oesophageal varices

Citation
L. Dagher et al., Drug treatment for bleeding oesophageal varices, BEST PR RES, 14(3), 2000, pp. 365-390
Citations number
169
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
BEST PRACTICE & RESEARCH IN CLINICAL GASTROENTEROLOGY
ISSN journal
15216918 → ACNP
Volume
14
Issue
3
Year of publication
2000
Pages
365 - 390
Database
ISI
SICI code
1521-6918(200006)14:3<365:DTFBOV>2.0.ZU;2-I
Abstract
At the time of diagnosis of cirrhosis, varices are present in about 60% of decompensated and 30% of compensated patients. The risk factors for the fir st episode of variceal bleeding in cirrhotic patients are the severity of l iver dysfunction, a large size of the varices and the presence of endoscopi c red colour signs, but only a third of patients who suffer variceal haemor rhage demonstrate the above risk factors. The only treatment that does nor require sophisticated equipment or the skills of a specialist, and is immed iately available, is vasoactive drug therapy. Hence, drug therapy should be considered to be the initial treatment of choice and can be administered w hile the patient is transferred to hospital, as has been done in one recent study, Moreover, drug therapy is no longer considered to be only a' stop-g ap' therapy until definitive endoscopic therapy is performed. Several recen t trials have reported an efficacy similar to that of emergency sclerothera py in the control of variceal bleeding. Furthermore, recent evidence sugges ts that those patients with high variceal or portal pressure are likely to continue to bleed or re-bleed early, implying that prolonged therapy loweri ng the portal pressure over several days may be the optimal treatment. Phar macological treatment with beta-blockers is safe, effective and the standar d long-term treatment for the prevention of recurrence of variceal bleeding . The combination of beta-blockers with isosorbide-5-mononitrate needs furt her testing in randomized controlled trials. The use of haemodynamic target s for the reduction of the HVPG response needs further study, and surrogate markers of the pressure response need evaluation. Ligation has recently be en compared with beta-blockers for primary prophylaxis, but there is as yet no good evidence to recommend banding for primary prophylaxis if beta-bloc kers can be given.