Les collections pancréatiques symptomatiques au contenu au moins en partie solide sont habituellement drainées échoendoscopiquement par des prothèses plastiques. Des séances de débridement endoscopique des résidus solides peuvent éventuellement être associées. Des complications hémorragiques et perforatives ont été décrites mais restent rares. Plusieurs auteurs ont rapporté leur expérience de prothèses métalliques complètement couverte dans cette indication avec une efficacité certaine et des complications hémorragiques peu fréquentes mais potentiellement graves. La prothèse Hot Axios récemment disponible a été conçue d'une part pour faciliter la pose et d'autre part pour assurer une étanchéité entre la collection drainée et l'estomac ou le duodénum en apposant les parois de ces cavités. Nous rapportons ici notre expérience initiale de l'utilisation de cette prothèse.

Perforation of the colon during colonoscopy is still one of the most severe complications of this technique and occurs with a frequency of between 0.12% and 0.2% of cases after diagnostic colonoscopy and in up to 3% of patients after therapeutic colonoscopy. The site of perforation is usually the sigmoid colon. The gold standard for treatment of this complication is surgery to be performed as rapidly as possible: a simple suture and peritoneal cleaning, with limited resection and anastomosis or colostomy only in case of confirmed fecal peritonitis. However, interventional endoscopy has made progress, in particular endoscopic suturing and Natural Orifice Transluminal Endocopic Surgery (NOTES) has been developed. There are several reports of endoscopically sutured perforated colons, most less than 10 mm. We report our experience of two colonic perforations which were at least 10 mm treated by endoscopic suturing with hemoclips: a perforated sigmoid diverticulum during simple colonoscopy in the first case and a large polypectomy by endoscopic mucosal resection of the ascending colon in the second. (C) 2009 Elsevier Masson SAS. All rights reserved.

Les buts de cette étude étaient d’évaluer la faisabilité et l’efficacité à long terme de la mise en place d’endoprothèses métalliques ou plastiques pour des sténoses recto-coliques malignes ou bénignes dans la ≪vraie vie≫.

SIRS, We have read with interest the review article by Jenkins & Berein regarding the use of somatostatin and its long-acting analogue, octreotide, in the treatment of pancreatic diseases.’ We acknowledge their point that much evidence in this field is equivocal, especially with regard to the use of these agents in acute pancreatitis and post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis. Many of the difficulties associated with the use of somatostatin and octreotide in these conditions relates to poor definition of the aetiology and pathology of acute pancreatitis. McKay et al. in their review of the field have noted that individual investigators have defined acute pancreatitis in an idiosyncratic manner, leading to a great deal of inter-study variability and general confusion as to the role of somatostatin and octreotide as treatment measures.2 This is highlighted in the aborted study by Sternlieb et aL3 to which Jenkins & Berein refer and which was halted after an apparent increase in post-ERCP complications in a group of patients treated with octreotide. This study was analysed by us at the time4 and was the subject of a long methodological analysis in the volume of the American Journal of Gastroenterology in which the original study a~pea red .~ Once again the problem of defining pancreatitis is at the crux of the confusion here, as Sternlieb and his colleagues employed a liberal definition of post-ERCP pancreatitis. In order to explain the apparent difference between octreotide and somatostatin in the treatment of acute and EKCP-induced pancreatitis, Jenkins & Berein refer to the paper by Binmoeller et al., which deals with the effect of octreotide on the human sphincter of OddL6 To our knowledge this is the only published work relating to this subject, and it found that octreotide increases sphincter of Oddi tone and contractile frequency. In the absence of corroborative evidence these results must stand alone, however we feel that a number of caveats should be entered before using the study’s findings to support Jenkins & Berein’s rather broad hypothesis. In the absence of strong information from human studies, it is usual to look to animal data for clues. However, in the case of the sphincter of Oddi, a major problem arises as it is well recognized that the activity of the sphincter demonstrates a great deal of inter-species variability, thus preventing direct clinical correlation. Moreover, data from animal studies of the effect of somatostatin on sphincter of Oddi function are contradictory, with some reporting stimulation’ while others report inhibition of the sphincter.* We would like to highlight one publication regarding the effect of somatostatin itself on the human sphincter of Oddi. Warzee et al. studied sphincter of Oddi activity in 29 patients, 15 min after the administration of somatostatin (250 pg bolus i.v., then 250 pg/h inf~s ion) .~ After a delay of approximately 4 min, phasic activity (6-10 min) began in the sphincter of Oddi, again lasting for a period of approximately 4 min. This evidence seems to contradict Jenkins & Berein’s contention that octreotide and somatostatin have entirely different activities at the sphincter of Oddi. Given the authors’ hypothesis that treatment with octreotide increases sphincter of Oddi tone and thus causes an increased risk of retention of enzymes, this raises the question of clinical data to support this hypothesis. We believe there are none, as even in large trials such as Binmoeller et al. (245 patients), octreotide treatment is not associated with a higher incidence of pancreatitis than control subjects.1° The most likely reason for this lies in the strong antisecretory effects of octreotide on exocrine pancreas. Numerous studies have detailed the inhibitory effect of octreotide on pancreatic enzyme and fluid secretion both in animals and humans. In 1992, Kemmer et al. reported in this journal that octreotide (even at doses as low as 5 pg/h i.v.) strongly inhibited secretin and ceruletide-stimulated pancreatic enzyme and bicarbonate secreti0n.l’ These findings are in agreement with the work of Gullo and colleagues, who demonstrated (in six healthy volunteers) that octreotide (12.5-50 pg s.c.) significantly inhibited cerulein-stimulated pancreatic enzyme synthesis (as measured by pancreatic amino acid uptake).12 The thrust of these studies is that octreotide can inhibit the production and release of fluid, and more importantly enzymes, from the pancreas. As retention and intracellular activation of pancreatic secretions is thought to be responsible for increased ductal pressure and autodigestion of the gland’s parenchyma, the action of octreotide is likely to

UNLABELLED To evaluate the diagnostic efficiency of the magnetic resonance cholangiography (MRC) in the detection of main bile duct stones in a set of 102 patients. METHODOLOGY Criteria of inclusion were: Clinic and biological suspicion of biliary stones obstruction with exams of first intention no contributive. We used the turbo spin echo sequences with thick slices in single shot mode and fine slides with reconstruction in 3D by a computer. Exams of reference were the endoscopic retrograde cholangiography (76.47%), an intraoperative cholangiography (20.59%) and a per-cutaneous cholangiography (2.94%). RESULTS Stones of the main bile duct have been diagnosed at thirty-five patient (35.7%); we had 3 positive forgeries and 6 negative forgeries of the MRC. The sensitivity was 82,9%, the specificity of 95,5%, the positive predictive value and the negative predictive value were, respectively, of 90,6% and 91,4%. The observant variance test was excellent (kappa = 0.83). Mistakes of diagnosis of the MRC were bound to: stones less than 3 mms with a bile duct no dilated, malignant stenosis, structural details as the presence of a duodenal diverticula's or severe duodenitis and a certain difficulty to see the sphincter complex. CONCLUSION Performances of the CIRM was good, and only in very particular cases, it was the origin of confusions.

Objectives The aim of this study was to determine the value of serum fibrosis markers for the diagnosis of oesophageal varices in alcoholic patients. Methods Fifty-four sets of clinical and biochemical data, including serum markers of fibrosis, obtained from 146 heavy alcohol drinkers (106 men, 40 women; mean age 49.2±9.0 years) without any history of variceal bleeding were analysed. Gastroscopy and liver biopsy were performed in all patients. Multivariate analysis was performed to identify the markers best correlated with oesophageal varices. Results Fifty-nine patients (40.4%) had severe fibrosis (3+) and 48 (32.9%) had oesophageal varices (all grades considered together). In multivariate analysis, a prothrombin index below 60%, alkaline phosphatase activity over 110 IU/l, and hyaluronate over 100 g/l were the best markers for the prediction of oesophageal varices. The diagnostic accuracy for medium to large oesophageal varices using these three factors was 86%. Eight patients (16.7%) with oesophageal varices presented no or moderate fibrosis (F<3): one patient (12.5%) had an alkaline phosphatase level >110 IU/l. However, all eight of these patients had small oesophageal varices. Conclusions These three non-invasive markers correctly predict the presence or absence of medium to large oesophageal varices in 86% of alcoholic patients.

Background: No study on bioclinical criteria predicting a biliary origin for acute pancreatitis has included endosonography as a reference examination. Re-examination of bioclinical parameters deserves consideration in the era where other causes are known (e.g. hereditary, autoimmune). Aim and Methods: To determine the performance of bioclinical markers in predicting a biliary origin of acute pancreatitis where the diagnosis of biliary lithiasis was established or ruled out using endosonography. Only patients with a first acute episode of pancreatitis were included. Results: 213 patients (male: 55%; median age: 56 years) were prospectively included in 14 centres. Causes of acute pancreatitis were: biliary (62%), alcoholic (25%), other (13%). Delay between symptom-onset and admission was <48 h in 80%. Endosonography was the sole method establishing the diagnosis of biliary pancreatitis in 15% of patients. At univariate analysis, age, female sex, declared alcohol consumption, elevated aspartate and alanine transaminases on admission, gammaglutamyl transferase, alkaline phosphatase, total bilirubin, lipase, mean corpuscular volume were predictive of a biliary origin. Only age (p < 0.0001), sex (p < 0.0008) and alanine transaminase (p < 0.0004) remained significant at multivariate analysis. At age 50, the respective sensitivity and specificity were 73 and 65%. With an elevated alanine transaminase at 2 times the upper limit of normal range, the respective sensitivity and specificity were 74 and 84%. The probability of a biliary origin of acute pancreatitis could be estimated by the following formula: = 1/1 + exp(4.6967 − 0.0656 × age + 1.1208 × sex − 0.6909 × alanine transaminase). Conclusion: When endosonography is performed to confirm or exclude a biliary origin of acute pancreatitis, age, sex and alanine transaminase at admission are the only factors predictive of a biliary cause.

Senile systemic amyloidosis (SSA) is characterized by infiltration of amyloid transthyretin fibrils in the myocardium.SSA occurs mainly (but not always) in elderly men.SSA leads to hypertrophic and/or restrictive cardiomyopathy complicated by conduction disturbances, atrial arrhythmia and systemic embolization (stroke…). That is why SSA needs a special care and to be diagnosed.Cardiac SSA diagnosis needs to exclude two other forms of cardiac amyloidosis: AL amyloidosis (light chain) and hereditary transthyretin amyloidosis (genetic testing).Scintigraphic 99mTc-DPD heart retention is observed in cardiac amyloidosis. DPD heart retention is more frequent in cardiac transthyretin amyloidosis than in cardiac AL amyloidosis.Specific treatments of cardiac TTR amyloidosis are in development.Les amyloses séniles systémiques sont liées principalement aux dépôts intramyocardiques extracellulaires de fibrilles amyloïdes constituées de transthyrétine sauvage.Les amyloses séniles systémiques touchent principalement les hommes âgés.L’atteinte cardiaque est prédominante et est responsable d’insuffisance cardiaque, de troubles de la conduction et d’embolies systémiques. Les amyloses séniles nécessitent donc une prise en charge cardiologique spécifique.Deux diagnostics différentiels doivent être systématiquement éliminés du fait d’une prise en charge et d’un traitement spécifiques : l’amylose AL (chimiothérapie) et l’amylose héréditaire à transthyrétine (conseil génétique, prise en charge familiale). L’examen clinique, l’échocardiographie et l’IRM ne permettent pas de distinguer ces différentes formes d’amylose.Une fixation myocardique à la scintigraphie DPD ou HMDP (traceurs osseux) est plus fréquente et intense dans les amylose à transthyrétine (sénile ou héréditaire) que dans les amyloses AL.Des traitements spécifiques de l’amylose à transthyrétine sont en cours d’évaluation.

Background: Pain relapse after oral refeeding occurs in 21% of the patients with acute pancreatitis, and in 35% of those with CT Balthazar's score greater than or equal toD [Gut 1997; 40: 262]. Somatostatin analogues may decrease the pain relapse rate by inhibiting exocrine pancreatic secretion. Aims, Patients and Methods: To assess the frequency of pain relapse in patients with acute necrotizing pancreatitis after treatment with one intramuscular injection of lanreotide 30 mg on the day before refeeding. The refeeding procedure was standardized and progressive. Results: greater than or equal to3 patients were included in 4 centres. Acute pancreatitis was alcoholic (n = 11), biliary ( n = 7), other ( n = 5). Twelve patients had 63 Ranson's criteria. Balthazar's score ( 1985) was D or E in 7 and 16 patients, respectively. Median duration of pain and of interruption of oral feeding were 11 (3-23) and 16 (5-34) days, respectively. Median hospital stay was 22 (9-41) days. Only 1 patient (4.3%) had pain occurring 3 days after refeeding. Conclusion: Pain relapse occurred in 4.3% of patients pretreated with the somatostatin analogue lanreotide, and this figure is lower than the expected 35% rate which was previously reported without preventive treatment. This suggests that one intramuscular injection of lanreotide 30 mg on the day before refeeding could decrease pain relapse in patients with acute necrotizing pancreatitis, but has to be confirmed in a phase III study. Copyright (C) 2004 S. Karger AG, Basel and IAP.

outcome and MRI severity score.Results: Thirty-nine patients (23 males, 16 females), with a median age of 47 years (range:15-86) were studied during a 21-month period.AP was considered of biliary etiology in 19 patients (48.7%).Ranson score was > or = to 3 for 18 patients (46%).A strong correlation was demonstrated between CTSI and MRSI on admission (r = 0.863, p or = to 3 (respectively p=0.058 and p=0.002) and a MRSI > or = to 3 (respectively p=0.003 and p=0.001).S-MRCP detected early pancreatic duct leakage in three patients (7.6%)~ who required further endoscopic drainages procedures.Conclusions: MRI is a reliable method for staging AP severity and it has prognostic value for clinical outcome It can also reveal pancreatic duct rupture, which can occur early in the course of AP Furthermore, S-MRCP can detect pancreatic duct irregularity and abnormal duodenal filling, which are associated with severe AP.

Background and aims: Fatigue is a frequent and disabling symptom reported by patients with chronic hepatitis C (CHC). Its mechanism is poorly understood. Recent attention has focused on the role of leptin and energy expenditure in CHC. Our aims were to analyse fatigue in CHC and to determine its relationship with disease activity, resting energy expenditure (REE), circulating leptin, and tumour necrosis factor α (TNF-α). Methods: Seventy eight CHC patients, 22 healthy controls, and 13 primary biliary cirrhosis (PBC) patients underwent measurements of REE, body composition, leptin, and TNF-α. All subjects completed the fatigue impact scale (FIS) questionnaire. A liver biopsy and viral load measurements were performed in all patients. Results: Thirty eight of 78 CHC patients considered fatigue the worst or initial symptom of their disease. The fatigue score of patients was significantly higher than that of controls (53.2 (40.1) v 17.7 (16.9); p<0.0001) and was more pronounced in females (p=0.003). Leptin was increased significantly in CHC patients compared with controls (15.4 (20.7) v 6.4 (4.1) ng/ml; p<0.05). In CHC patients, the fatigue score correlated significantly with leptin corrected for fat mass (r=0.30, p=0.01). This correlation increased when the physical domain of fatigue was included (r=0.39, p=0.0009). Furthermore, a similar positive correlation was found in PBC patients (r=0.56, p=0.04). No correlation was found between fatigue and age, REE, liver function tests, viral load, or the METAVIR score in CHC patients. Conclusions: Fatigue is present in CHC patients and is more pronounced in females. The FIS questionnaire is clinically relevant and may be useful for future therapeutic trials aimed at reducing fatigue. Fatigue may be partly mediated by leptin.