Sylvie Evrard

Self-expanding plastic stents for benign esophageal lesions

BACKGROUND A benign condition is a relative contraindication to the use of self-expanding metallic stents, because these devices usually are not retrievable. The self-expanding plastic stent is removable and induces less tissue hyperplasia. This study prospectively evaluated the use of a self-expanding plastic stent to treat benign esophageal conditions. METHODS Over 4 years, 21 patients underwent self-expanding plastic stent placement for various benign esophageal disorders, including refractory peptic (n = 2), caustic (n = 3), post-radiotherapy (n = 3), and anastomotic (n = 4) stenoses; hyperplastic (n = 5) stenosis within a previously implanted metallic stent; and anastomotic leak (n = 4) after esophagectomy. The self-expanding plastic stent was removed from all patients. Patients were followed for at least 8 months after stent removal. RESULTS Implantation was successful in all cases. Temporary self-expanding plastic stent placement was curative in 17/21 patients, especially those with caustic and hyperplastic strictures and anastomotic fistula, all of which were treated successfully without re-intervention. Median follow-up was 21 months (range 8-39 months) after stent removal. Moreover, by inducing tissue ischemia, self-expanding plastic stent allowed delayed removal of metallic stents. Only one severe complication (tracheal compression) was encountered, and this resolved after stent removal. CONCLUSIONS A range of benign stenosing disorders of the esophagus can be treated safely with a self-expanding plastic stent. Because the long-term results were highly favorable, self-expanding plastic stent placement could be used as the initial treatment for various conditions. Self-expanding plastic stent insertion within an esophageal self-expanding metallic stent allowed removal of the latter, theoretically unretrievable, stent.

Enteral nutrition with or without N-acetylcysteine in the treatment of severe acute alcoholic hepatitis: a randomized multicenter controlled trial.

BACKGROUND & AIMS Severe acute alcoholic hepatitis is associated with a high mortality rate. Oxidative stress is involved in the pathogenesis of acute alcoholic hepatitis. Previous findings had also suggested that enteral nutritional support might increase survival in patients with severe acute alcoholic hepatitis. Therefore, the aim of the present study was to evaluate the efficacy of N-acetylcysteine in combination with adequate nutritional support in patients with severe acute alcoholic hepatitis. METHODS Patients with biopsy-proven acute alcoholic hepatitis and mDF ≥32 were randomized to receive N-acetylcysteine intravenously or a placebo perfusion along with adequate nutritional support for 14 days. The primary endpoint was 6-month survival; secondary endpoints were biological parameter evolution and infection rate. RESULTS Fifty-two patients were randomized in the study (28 into the N-acetylcysteine arm, 24 into the control arm), and among them, five were excluded from the analysis for protocol violation. The two groups did not differ in baseline characteristics. Survival rates at 1 and 6 months in N-acetylcysteine and control groups were 70.2 vs. 83.8% (p=0.26) and 62.4 vs. 67.1% (p=0.60), respectively. Early biological changes, documented infection rate at 1 month, and incidence of hepatorenal syndrome did not differ between the two groups. CONCLUSIONS In this study, high doses of intravenous N-acetylcysteine therapy for 14 days conferred neither survival benefits nor early biological improvement in severe acute alcoholic hepatitis patients with adequate nutritional support. However, these results must be viewed with caution, since the study suffered from a lack of power.

The predictive value of FIB‐4 versus FibroTest, APRI, FibroIndex and Forns index to noninvasively estimate fibrosis in hepatitis C and nonhepatitis C liver diseases

Noninvasive indirect biochemical markers of liver fibrosis have gained popularity, but hepatologists are now facing the difficult dilemma of choosing among the 20 fibrosis markers that are now available.1 Stanislas Pol’s group2 claim that FIB-4, initially developed in a human immunodeficiency virus (HIV)-hepatitis C virus (HCV) coinfected population, is a simple, inexpensive, and readily available marker which is reliable for predicting fibrosis in HCV monoinfected patients. It combines platelets, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and age as measurement factors. However, they did not present comparative area under the receiver operating characteristic curves (AUROCs) with other inexpensive, simple, and readily available scores such as APRI (aspartate aminotransferase-to-platelet ratio index), Forns index, FibroIndex, and FibroTest, which have been widely validated in the HCV3-5 and non-HCV population.6-8 They do not provide data for other liver diseases besides HCV and, finally, they do not give data related to the value of FIB-4 for the prediction of significant (Metavir F2-4 or Brunt S2-4) fibrosis, another important issue for the clinician because this is the cut-off above which progression of fibrosis occurs and medical treatment is needed. We sought to compare, independently from the promoters, the diagnostic accuracy using AUROCs of the 5 biochemical scores in our HCV population (n 152) and our global series (n 290) of patients with chronic liver disease including also hepatitis B virus (n 16), alcoholic (n 54), nonalcoholic (n 38), and other (n 23) diseases. The prevalence of significant fibrosis (F2-4 or S2-4), advanced fibrosis (F3-4 or S3-4), and cirrhosis (F4 or S4), evaluated histologically using the METAVIR (in the HCV, HBV, and other populations) or the BRUNT classification (in alcoholic and nonalcoholic liver disease) was 77%, 23%, and 12% and 77%, 34%, and 21%, respectively, in the HCV series and the global series. This compares to 36%, 17%, and 7% in Pol’s HCV series. Comparing the performance of the 5 tests in our HCV and global series for the diagnosis of significant fibrosis, advanced fibrosis, and cirrhosis (Table 1), FibroTest and FIB-4 have equal excellent diagnostic power, FibroIndex being the least accurate. Table 1 and Fig. 1 show a trend for FibroTest to have better AUROCs, even if they are not statistically significant. In the global series, the Forns index is less accurate than FibroTest and FIB-4 for the diagnosis of cirrhosis and APRI also has less discriminative power than FibroTest and FIB-4 for the diagnosis of significant fibrosis, advanced fibrosis, and cirrhosis. Thus, the results of our study reinforce the last recommendations9 of the HAS (Haute Autorité de la Santé) in France, which equally ranked the following methods for the diagnosis of liver cirrhosis: liver biopsy, Fibroscan, and FibroTest. Our data are in accordance with those of Pol’s group2 and confirm, in a HCV series where the prevalence of advanced fibrosis is similar, that FIB-4 is an alternative to FibroTest albeit with less expense for 3 clinically pertinent issues: the noninvasive diagnosis

An inhibitor of interleukin-6 trans-signalling, sgp130, contributes to impaired acute phase response in human chronic liver disease

In chronic liver disease, high circulating interleukin (IL)‐6 contrasts with a poor acute phase response. We evaluated the impact of liver and circulating IL‐6‐receptor (IL‐6R) forms on IL‐6 bioactivity in chronic liver disease. IL‐6, soluble IL‐6‐receptor and sgp130 levels were assayed in plasma from 45 patients with alcoholic liver disease, 84 with hepatitis C virus (HCV) infection undergoing transjugular liver biopsies and 15 healthy subjects. IL‐6R mRNA was quantified on liver extracts from 54 patients with alcoholic liver disease with or without cirrhosis and 18 HCV‐infected patients. The effect of gp130–Fc on fibrinogen secretion induced by IL‐6 trans‐signalling was evaluated on hepatocyte cultures. Levels of plasma IL‐6 and sgp130, but not soluble IL‐6R, increased with the stage of chronic liver disease, and correlated significantly with disease severity. Alcoholic liver disease patients had higher plasma IL‐6 levels than hepatitis C, but lower liver IL‐6R expression. In alcoholic and HCV‐related liver diseases, liver IL‐6R expression decreased with advanced fibrosis stage. In vitro, on hepatocytes, gp130–Fc blunted the acute phase response while soluble IL‐6R enhanced IL‐6 stimulation. In advanced chronic liver disease, high plasma IL‐6 is associated with low liver IL‐6R expression. This situation enables high plasma sgp130 to act as a major negative regulator of liver IL‐6 trans‐signalling, as demonstrated functionally here on hepatocytes. This might explain the poor acute phase response induced by IL‐6 in chronic liver disease.

Gastrointestinal polypoid lesions: a poorly known endoscopic feature of portal hypertension.

Aim To describe a poorly known endoscopic entity associated with portal hypertension, characterized by polypoid lesions either in the stomach or small intestine of patients with cirrhosis. Methods Between 2003 and 2012, patients with cirrhosis and portal hypertension underwent endoscopic workup of portal hypertension in our endoscopy unit. The clinical expression, endoscopic features of these lesions, and their pathological characteristics are described. Results A total of 1538 patients were included, among which 14 (0.9%) presented polypoid lesions; these patients had evidence of portal hypertension and had dilated capillaries in the lamina propria. Four patients presented with severe anaemia or melaena and required treatment. Propranolol was administered to three patients, and one patient needed a transjugular intrahepatic portosystemic shunt in order to control bleeding. For asymptomatic patients in whom polypoid lesions were resected, no recurrence of lesions was observed during follow-up gastroscopy (median 36 months, range 7–85 months). Conclusion Portal hypertension-associated gastric or small intestine polypoid lesions may be associated with a significant risk of bleeding and are responsive to adequate treatment of portal hypertension.

Chronic pancreatic alterations in AIDS patients

Patients with acquired immunodeficiency syndrome (AIDS) can develop biliary and pancreatic disorders, like sclerosing cholangitis and acute pancreatitis. Chronic pancreatic changes are rare and only poorly described. In this study, we report our endoscopic retrograde cholangiopancreatography (ERCP) findings in 20 patients with AIDS, focusing on pancreatographic changes. ERCP findings from 20 patients with advanced disease were analyzed. Patients with history of chronic alcoholism were ruled out. ERCP findings were correlated to the coexistence of an opportunistic infection and the taking of antiviral therapies. Bile duct and pancreatic duct abnormalities were observed in 11 (55%) of 20 and seven (37%) of 19 patients, respectively. Bile duct lesions were mainly sclerosing cholangitis, and chronic pancreatic alterations consisted of side-branch involvement (n = 4), multiple and diffuse strictures of the main duct (n = 1), and diffuse dilatation of the main pancreatic duct (n = 2). The presence of an opportunistic infection was correlated with sclerosing cholangitis but not with chronic pancreatic changes. Similarly, there was no association between the finding of an abnormal cholangiogram and the presence of pancreatic alterations. This population of patients with AIDS had a significant proportion (37%) of chronic pancreatic ductal changes, which do not seem to be related to morphologic alterations and/or opportunistic infections of the biliary tract.

Unexplained digestive bleeding in a cirrhotic patient

A 50 year old White man with cirrhosis due to hepatitis C virus (HCV) infection was admitted to our hospital for severe anaemia and intermittent melena. At admission, haemoglobin was …

504 INSULIN RESISTANCE CONFERS A HIGHER RISK OF PORTAL HYPERTENSION, CIRRHOSIS AND EARLY MORTALITY TO ALCOHOLIC LIVER DISEASE PATIENTS

504 INSULIN RESISTANCE CONFERS A HIGHER RISK OF PORTAL HYPERTENSION, CIRRHOSIS AND EARLY MORTALITY TO ALCOHOLIC LIVER DISEASE PATIENTS E. Trepo, D. Degre, A. Lemmers, T. Gustot, A. Gerkens, S. Evrard, R. Ouziel, P. Deltenre, M. Adler, J. Deviere, C. Moreno. Department Gastroenterology, Hepatopancreatology and Digestive Oncology, Erasme Hospital, Laboratory of Experimental Gastroenterology, Universite Libre de Bruxelles, Brussels, Hopital de Jolimont, Haine-Saint-Paul, Belgium E-mail: christophe.moreno@erasme.ulb.ac.be