Beta-Blockers to Prevent Gastroesophageal Varices in Patients with Cirrhosis

Groszmann, Roberto J.; García–Tsao, Guadalupe; Bosch, Jaime; Grace, Norman D.; Burroughs, Andrew K.; Planas, Ramón; Escorsell, Àngels; García-Pagán, Juan Carlos; Patch, David; Matloff, Daniel S.; Gao, Hong; Makuch, Robert W.

doi:10.1056/nejmoa044456

Cited by 892 publications

(723 citation statements)

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“…Our findings support the current empirical recommendation that patients with PVT without varices need to be submitted to follow-up screening endoscopies. Indeed, the observed incidence of EVs in our study is almost identical to that found in the prospective timolol study (17) and only slightly lower than the 5%, 17%, and 28% at 1, 2, and 3 years, respectively, reported in patients with cirrhosis by Merli et al (18) Although ours was not a prospective study, in our cohort of patients the median interval time between baseline and follow-up endoscopies was 17.6 months, lower than the 2-year to 3-year interval recommended to assess variceal development in patients with compensated cirrhosis. (5) There are scarce data on the probability of variceal growth in patients with PVT.…”

Section: Discussionsupporting

confidence: 90%

“…Follow-up endoscopy was not performed due to follow-up time <2 years in five patients and for unknown reasons in four. Median elapsed time was 27 months (range 9-218) months, the time/endoscopy index was 11 (range 5-83) months, and the median number of endoscopies performed was two (range [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19].…”

Section: Ev Growthmentioning

confidence: 99%

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Natural history and management of esophagogastric varices in chronic noncirrhotic, nontumoral portal vein thrombosis

et al. 2016

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In patients with chronic noncirrhotic, nontumoral portal vein thrombosis (PVT), the usually recommended strategy for endoscopic screening and management of varices is the same as in cirrhosis. However, the efficacy of this policy in patients with PVT is unknown. We assessed the course of gastroesophageal varices in a large cohort of patients with chronic PVT. Patients prospectively registered in two referral centers for vascular liver disorders were eligible for the study. Endpoints were development and growth of varices and the incidence and outcome of portal hypertensionrelated bleeding. Included were 178 patients with chronic PVT. Median follow-up was 49 (1-598) months. Variceal bleeding was the initial manifestation in 27 (15%) patients. Initial endoscopy in the remaining 151 patients showed no varices in 52 (34%), small esophageal varices in 28 (19%), large esophageal varices (LEVs) in 60 (40%), and gastric varices without LEVs in 11 (7%). Ascites and splenomegaly were independent predictors for the presence of varices. In patients without varices, the probability of developing them was 2%, 22%, and 22% at 1, 3, and 5 years, respectively. In those with small esophageal varices, growth to LEVs was observed in 13%, 40%, and 54% at 1, 3, and 5 years, respectively. In patients with LEVs on primary prophylaxis, probability of bleeding was 9%, 20%, and 32% at 1, 3, and 5 years, respectively. Nine (5%) patients died after a median 51 (8-280) months, only one due to variceal bleeding. Conclusions: The course of varices in chronic noncirrhotic, nontumoral PVT appears to be similar to that in cirrhosis; using the same therapeutic approach as for cirrhosis is associated with a low risk of bleeding and death. (HEPATOLOGY 2016;63:1640-1650 C hronic noncirrhotic, nontumoral portal vein thrombosis (PVT) is a rare vascular disorder of the liver, with variceal bleeding being its main manifestation. (1,2) Indeed, several retrospective cohort studies have shown a high prevalence of esophageal varices (EVs) at the time of chronic PVT diagnosis. (3,4) Due to the low incidence and prevalence of PVT, specific studies aimed at determining adequate strategies for endoscopic screening and management of varices are scarce and small-sized. Consequently, the 2015 Baveno VI Consensus suggested applying to patients with PVT the same recommendations validated for patients with cirrhosis and portal hypertension, i.e., to perform a baseline endoscopy at diagnosis of PVT and subsequent endoscopies at 2-year or 3-year intervals in patients with no EVs or small EVs (SEVs) at baseline, to use beta-blockers or endoscopic band ligation (EBL) as a primary prophylaxis, and to Abbreviations: EBL, endoscopic band ligation; EV, esophageal varix; GOV, gastroesophageal varix; GV, gastric varix; IGV, isolated gastric varix; LEV, large esophageal varix; NSBB, nonselective beta-blocker; PVT, portal vein thrombosis; SEV, small esophageal varix.

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Section: Discussionsupporting

confidence: 90%

Section: Ev Growthmentioning

confidence: 99%

Natural history and management of esophagogastric varices in chronic noncirrhotic, nontumoral portal vein thrombosis

et al. 2016

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“…15 HVPG Ͼ10 mmHg predicts the development of complications of HCV cirrhosis. 16 HVPG has been put forward as a test that would reflect progression during both precirrhotic and cirrhotic stages of HCV liver disease and be an end point in antiviral therapy, irrespective of antiviral response. 17 Fibrosis associated with recurrent HCV infection after liver transplantation (LT).…”

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confidence: 99%

Hepatic venous pressure gradient to assess fibrosis and its progression after liver transplantation for HCV cirrhosis

et al. 2007

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Progression of fibrosis following recurrent hepatitis C virus (HCV) infection is frequent after liver transplantation (LT).Histology remains the gold standard to assess fibrosis, but the value of hepatic venous pressure gradient (HVPG) is being explored. We evaluated patients with recurrent HCV infection after LT to assess whether HVPG correlates with liver histology, particularly fibrosis. A total of 90 consecutive patients underwent 170 HVPG measurements concomitant with transjugular liver biopsy (TJB), with 31.5 (range, 6-156) months of follow up. Median biopsy length was 22 mm and total portal tract count was 12 (complete 6, partial 6). Median HVPG was 4 mmHg: 38% of patients Ն6 mmHg (portal hypertension, PHT), 13% Ն10 mmHg. HVPG correlated with Ishak stage (r ϭ 0.73, P Ͻ 0.001) for mild (0-3) and severe fibrosis (4-6), and grade score (r ϭ 0.47, P Ͻ 0.001), but neither correlated with interval from LT nor biopsy length. HVPG was Ն10 mmHg in 15 patients: 12 had stage 5 or 6, and 3 severe portal expansion. HVPG was repeated in 49, between 7 and 60 months with weak correlation to fibrosis score (r ϭ 0.30, P ϭ 0.045). A total of 12 patients with HVPG Ն6 mmHg had fibrosis score Յ3, while 8 patients had normal HVPG but fibrosis stage Ն4. These discrepancies were mostly associated with specific histological features such as perisinusoidal fibrosis rather than errors in measuring HVPG. In 29 with HVPG Ͻ6 mmHg at 1 yr, none decompensated compared to 4 of 13 (31%) with PHT. In conclusion, HVPG correlates with fibrosis and its progression, due to recurrent HCV infection, assessed in TJB. Liver Transpl 13:1305Transpl 13: -1311Transpl 13: , 2007 The severity of portal hypertension (PHT) correlates with the severity of liver disease and cirrhosis, both functionally and histologically 1 and also with the Model for End-Stage Liver Disease, 2 such that it has independent prognostic value separate from clinical and laboratory assessment. 2,3 Hepatic vein catheterisation 4 was modified by Groszmann et al. 5 using a balloon catheter. The measurement of hepatic venous pressure gradient (HVPG) (the difference between wedge hepatic venous pressure [WHVP] Ϫ free hepatic venous pressure) is reproducible 6 and is the preferred technique for evaluating PHT, correlating 1:1 with the direct measurement of portal vein pressure in patients with sinusoidal and postsinusoidal causes of cirrhosis, 7,8 particularly alcoholic and viral-related cirrhosis. Normally HVPG ranges from 1 to 5 mmHg; pressures Ն6 mmHg indicate PHT. 6 WHVP increases with progression of chronic hepatitis and PHT, before histologically detectable cirrhosis. 9 A gradient Ͼ5 mmHg was always associated with significant changes in liver biopsy in 1 study, although a normal gradient did not completely rule out cirrhosis, 10 suggesting that WHVP could provide supplementary information to liver biopsy, with a higher predictive value for assessing stage and activity of chronic liver disease, than routine biochemical tests. 10 Other studies have correlated HVPG both with severit...

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“…In accordance to previous studies, a UGIE every 2 years is considered sufficient for patients without varices [7]. Patients with small varices develop large varices at a rate of 5-12% per year [13,19]. Decompensated cirrhosis (Child-Turcotte-Pugh B and C), alcohol etiology, or the presence of red signs at the time of baseline UGIE is associated with rapid progression from small to large varices and a more strict surveillance with UGIEs at 1-year intervals is recommended [19].…”

Section: Definitions Of Varices and Variceal Bleed Prophylaxismentioning

confidence: 59%

“…Quite often, early primary prophylaxis has been used for both groups of patients [13]. To clarify the matter, another term preprimary prophylaxis, which has been used by some investigators, was suggested.…”

Section: Definitions Of Varices and Variceal Bleed Prophylaxismentioning

confidence: 99%

Primary prophylaxis of gastroesophageal variceal bleeding: consensus recommendations of the Asian Pacific Association for the Study of the Liver

et al. 2008

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The Asian Pacific Association for the Study of the Liver (APASL) set up a Working Party on Portal Hypertension in 2002, with a mandate to develop consensus guidelines on various clinical aspects of portal hypertension relevant to disease patterns and clinical practice in the Asia-Pacific region. Variceal bleeding is a consequence of portal hypertension, which, in turn, is the major complication of liver cirrhosis. Primary prophylaxis to prevent the first bleed from varices is one of the most important strategies for reducing the mortality in cirrhotic patients. Experts predominantly from the Asia-Pacific region were requested to identify the different aspects of primary prophylaxis and develop the consensus guidelines. The APASL Working Party on Portal Hypertension evaluated the various therapies that have been used for the prevention of first variceal bleeding. A 2-day meeting was held on January 12 and 13, 2007, at New Delhi, India, to discuss and finalize the consensus statements. Only those statements that were unanimously approved by the experts were accepted. These statements were circulated to all the experts and were subsequently presented at the annual conference of the APASL at Kyoto, Japan, in March 2007.

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Beta-Blockers to Prevent Gastroesophageal Varices in Patients with Cirrhosis

Abstract: Nonselective beta-blockers are ineffective in preventing varices in unselected patients with cirrhosis and portal hypertension and are associated with an increased number of adverse events. (ClinicalTrials.gov number, NCT00006398.)

Cited by 892 publications

References 33 publications

Natural history and management of esophagogastric varices in chronic noncirrhotic, nontumoral portal vein thrombosis

Natural history and management of esophagogastric varices in chronic noncirrhotic, nontumoral portal vein thrombosis

Hepatic venous pressure gradient to assess fibrosis and its progression after liver transplantation for HCV cirrhosis

Primary prophylaxis of gastroesophageal variceal bleeding: consensus recommendations of the Asian Pacific Association for the Study of the Liver

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