The incidence of esophageal varices in cirrhosis

D’Amico, Gennaro; Pasta, Linda; Madonia, Salvatore; Tarantino, Ilaria; Mancuso, Andrea; Malizia, Giuseppe; Giannuoli, Gandolfo; Pagliaro, Luigi

doi:10.1016/s0016-5085(08)80011-x

Cited by 32 publications

(28 citation statements)

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“…This prevalence increases progressively in relation to the severity of liver damage. 4,5 The presence of EV is also a clear indicator of a certain stage of cirrhosis. 6 The development of EV in patients with cirrhosis occurs when the HVPG is greater than 10 mmHg, 3,7 with an incidence of approximately 5% per year and a yearly rate of progression to larger varices of 5% to 15%.…”

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confidence: 99%

Insulin resistance is a risk factor for esophageal varices in hepatitis C virus cirrhosis

et al. 2008

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P ortal hypertension (PH), defined by a hepatic venous pressure gradient (HVPG) greater than 6 mmHg, 1 is a common complication of cirrhosis. The presence and the development of esophageal varices (EV) is a clinical manifestation of PH, 2,3 with a prevalence that can range from 40% to 80% in patients with cirrhosis. This prevalence increases progressively in relation to the severity of liver damage. 4,5 The presence of EV is also a clear indicator of a certain stage of cirrhosis. 6 The development of EV in patients with cirrhosis occurs when the HVPG is greater than 10 mmHg, 3,7 with an incidence of approximately 5% per year and a yearly rate of progression to larger varices of 5% to 15%. 4,5,8 The clinical relevance of EV is linked to the risk of bleeding that occurs when HVPG is greater than 12 mmHg, 7-9 with a mortality rate that exceeds 20% within 6 weeks from the bleeding episode, despite aggressive treatment. 10 The Baveno IV 2005 Consensus Workshop 11 and the American Association for the Study of Liver Diseases 2007 single-topic symposium on portal hypertension 12 recommended that endoscopic screening for esophageal and gastric varices should always be performed when a diagnosis of cirrhosis is made. Upper endoscopy should be repeated at 2-year to 3-year intervals in patients without varices, and at 1-year to 2-year intervals in those with small varices, to evaluate their development or progression. 11,12 These guidelines might not be ideal for clinical

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confidence: 99%

Insulin resistance is a risk factor for esophageal varices in hepatitis C virus cirrhosis

et al. 2008

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“…[1][2][3] Primary prophylaxis with nonselective beta-blockers and endoscopic therapy with band ligation are effective in preventing variceal hemorrhage in patients with large varices. 1 Current guidelines recommend screening for gastroesophageal varices (GEV) with esophagogastroduodenoscopy (EGD) in all patients with cirrhosis and starting prophylactic therapy in those with medium to large varices. [4][5][6][7] In patients without varices, EGD is repeated in 2-3 years, whereas in patients with small varices, the recommendation is to repeat EGD in 1-2 years.…”

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confidence: 99%

Platelet count is not a predictor of the presence or development of gastroesophageal varices in cirrhosis

et al. 2007

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Current guidelines recommend esophagogastroduodenoscopy (EGD) in patients with cirrhosis to screen for gastroesophageal varices (GEV). Thrombocytopenia has been proposed as a noninvasive test to predict the presence of GEV. There is no agreement regarding a specific platelet count (PLT) that can reliably predict GEV. The present longitudinal study aims to (1) further investigate the relationship between varices and PLT at the time of endoscopy, (2) investigate whether changes in PLT from the baseline over time can predict the development of GEV, and (3) investigate whether changes in PLT correlate with the hepatic venous pressure gradient (HVPG). A secondary analysis was conducted for 213 subjects with compensated cirrhosis with portal hypertension but without GEV enrolled in a randomized, placebo-controlled, double-blind trial of a nonselective beta-blocker used to prevent GEV. PLTs were obtained every 3 months, and HVPG measurements and EGD were done annually. The PLTs were compared between subjects who did and did not develop GEV. In a median follow-up of 54.9 months, 84 patients developed GEV. PLT was greater than 150,000 in 15% of patients at the development of GEV. A receiver operating curve did not show any PLT with high sensitivity or specificity for the presence of GEV. Subjects with clinically insignificant portal hypertension (HVPG < 10 mm Hg) whose PLT remained greater than 100,000 had a 2-fold reduction in the occurrence of GEV (P ‫؍‬ 0.0374). A significant correlation was found between HVPG and PLT at the baseline, year 1, and year 5 (P < V ariceal hemorrhage is a leading cause of morbidity and mortality in cirrhosis. 1-3 Primary prophylaxis with nonselective beta-blockers and endoscopic therapy with band ligation are effective in preventing variceal hemorrhage in patients with large varices. 1 Current guidelines recommend screening for gastroesophageal varices (GEV) with esophagogastroduodenoscopy (EGD) in all patients with cirrhosis and starting prophylactic therapy in those with medium to large varices. [4][5][6][7] In patients without varices, EGD is repeated in 2-3 years, whereas in patients with small varices, the recommendation is to repeat EGD in 1-2 years. 2 Because of the cost and invasive nature of endoscopic screening, there is interest in developing a noninvasive predictor of the presence and development of GEV that would decrease the number of EGDs performed. The ideal noninvasive marker should be widely available at a reasonable cost, require minimal expertise, be reproducible, and be relatively unaffected by any other factors. A number of clinical, laboratory, and ultrasonographic variables have been considered. 8 However, the accuracy of these variables in predicting varices is currently inadequate to be recommended for clinical practice. 2 As varices are a direct consequence of portal hypertension, it is not surprising that the degree of portal hypertension determined by the hepatic venous pressure gradient (HVPG) has been found to be predictive of the

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Section: Prognostic Assessment In Primary Prophylaxismentioning

confidence: 99%

“…Gastroesophageal varices are present in approximately 50% of patients with cirrhosis [42]. Their presence correlates with the severity of liver disease: while only 40% of Child A patients have varices, they are present in 85% of Child C patients [42,43]. Variceal hemorrhage occurs at a yearly rate of 5%-15%, and the most important predictor of hemorrhage is the size of varices, with the highest risk of first hemorrhage (15% per year) occurring in patients with large varices [44].…”

Section: Prognostic Assessment In Primary Prophylaxismentioning

confidence: 99%

“…This technique is uncomfortable and invasive for patients and is costly and time-consuming, and it has been shown that there is interobserver variability as high as 30% for the detection of small esophageal varices. Moreover, since the point prevalence of medium/large varices is approximately 15%-25% [42], the majority of subjects undergoing screening endoscopy either do not have varices or have varices that do not require prophylactic therapy. Taking into account these issues, numerous non-invasive methods alternatives to endoscopy have been studied for determining the presence of varices, including biochemical and ultrasound methods, computed tomography (CT) scanning, video capsule endoscopy and spleen magnetic resonance imaging.…”

Section: Detection Of Varices and Prognostic Markers For Varicesmentioning

confidence: 99%

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Prognostic Markers in Patients with Cirrhosis and Portal Hypertension Who Have Not Bled

et al. 2011

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Abstract. Prognostic markers of compensated cirrhosis should mainly investigate factors involved with progression to decompensation because death in cirrhosis is related with decompensation. Portal hypertension plays a crucial role in the pathophysiology of most complications of cirrhosis. Accordingly, HVPG monitoring has strong prognostic value. An HVPG 10 mmHg determines a significantly higher risk of developing decompensation. Esophageal varices also can develop when the HVPG is 10 mmHg, although an HVPG 12 mmHg is required for variceal bleeding to occur. Monitoring the changes induced by the treatment of portal hypertension on HVPG, provides strong prognostic information. In compensated cirrhosis hemodynamic response is appropriate when the HVPG decreased to < 10 mmHg or by > 10% from baseline, because the incidence of complications such as bleeding or ascites significantly decrease when these targets are achieved. Whether serum markers, such as the FibroTest, they, may be valuable to predict decompensation should be established. Transient Elastography is a promising technique that has shown an excellent accuracy to detect severe portal hypertension. However, whether it can adequately determine clinically significant portal hypertension, and risk of developing varices and decompensation, should be established. Magnetic Resonance Elastography is also promising.

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The incidence of esophageal varices in cirrhosis

Cited by 32 publications

References 0 publications

Insulin resistance is a risk factor for esophageal varices in hepatitis C virus cirrhosis

Insulin resistance is a risk factor for esophageal varices in hepatitis C virus cirrhosis

Platelet count is not a predictor of the presence or development of gastroesophageal varices in cirrhosis

Prognostic Markers in Patients with Cirrhosis and Portal Hypertension Who Have Not Bled

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