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	<title>Virtual Journal Club &#187; Am J Gastroenterol</title>
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	<link>http://beckerinfo.net/JClub</link>
	<description>Division of Hospital Medicine Virtual Journal Club</description>
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		<title>A comparative evaluation of radiologic and clinical scoring systems in the early prediction of severity in acute pancreatitis.</title>
		<link>http://beckerinfo.net/JClub/2012/05/23/a-comparative-evaluation-of-radiologic-and-clinical-scoring-systems-in-the-early-prediction-of-severity-in-acute-pancreatitis/</link>
		<comments>http://beckerinfo.net/JClub/2012/05/23/a-comparative-evaluation-of-radiologic-and-clinical-scoring-systems-in-the-early-prediction-of-severity-in-acute-pancreatitis/#comments</comments>
		<pubDate>Wed, 23 May 2012 17:01:44 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=f8178e9cd277647ef8b191da6cf80fe6</guid>
		<description><![CDATA[A comparative evaluation of radiologic and clinical scoring systems in the early predicti...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>A comparative evaluation of radiologic and clinical scoring systems in the early prediction of severity in acute pancreatitis.</b></p>
        <p>Am J Gastroenterol. 2012 Apr;107(4):612-9</p>
        <p>Authors:  Bollen TL, Singh VK, Maurer R, Repas K, van Es HW, Banks PA, Mortele KJ</p>
        <p>Abstract<br/>
        OBJECTIVES: The early identification of clinically severe acute pancreatitis (AP) is critical for the triage and treatment of patients. The aim of this study was to compare the accuracy of computed tomography (CT) and clinical scoring systems for predicting the severity of AP on admission.<br/>
        METHODS: Demographic, clinical, and laboratory data of all consecutive patients with a primary diagnosis of AP during a two-and-half-year period was prospectively collected for this study. A retrospective analysis of the abdominal CT data was performed. Seven CT scoring systems (CT severity index (CTSI), modified CT severity index (MCTSI), pancreatic size index (PSI), extrapancreatic score (EP), ''extrapancreatic inflammation on CT'' score (EPIC), ''mesenteric oedema and peritoneal fluid'' score (MOP), and Balthazar grade) as well as two clinical scoring systems: Acute Physiology, Age, and Chronic Health Evaluation (APACHE)-II and Bedside Index for Severity in AP (BISAP) were comparatively evaluated with regard to their ability to predict the severity of AP on admission (first 24 h of hospitalization). Clinically severe AP was defined as one or more of the following: mortality, persistent organ failure and/or the presence of local pancreatic complications that require intervention. All CT scans were reviewed in consensus by two radiologists, each blinded to patient outcome. The accuracy of each imaging and clinical scoring system for predicting the severity of AP was assessed using receiver operating curve analysis.<br/>
        RESULTS: Of 346 consecutive episodes of AP, there were 159 (46%) episodes in 150 patients (84 men, 66 women; mean age, 54 years; age range, 21-91 years) who were evaluated with a contrast-enhanced CT scan (n = 131 episodes) or an unenhanced CT scan (n = 28 episodes) on the first day of admission. Clinically severe AP was diagnosed in 29/159 (18%) episodes; 9 (6%) patients died. Overall, the Balthazar grading system (any CT technique) and CTSI (contrast-enhanced CT only) demonstrated the highest accuracy among the CT scoring systems for predicting severity, but this was not statistically significant. There were no statistically significant differences between the predictive accuracies of CT and clinical scoring systems.<br/>
        CONCLUSIONS: The predictive accuracy of CT scoring systems for severity of AP is similar to clinical scoring systems. Hence, a CT on admission solely for severity assessment in AP is not recommended.<br/></p><p>PMID: 22186977 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		</item>
		<item>
		<title>Natural History Following the First Attack of Acute Pancreatitis.</title>
		<link>http://beckerinfo.net/JClub/2012/05/23/natural-history-following-the-first-attack-of-acute-pancreatitis/</link>
		<comments>http://beckerinfo.net/JClub/2012/05/23/natural-history-following-the-first-attack-of-acute-pancreatitis/#comments</comments>
		<pubDate>Wed, 23 May 2012 17:01:43 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=28171e76e432e7e070f1a413abfc2477</guid>
		<description><![CDATA[Natural History Following the First Attack of Acute Pancreatitis.
        Am J Gastroente...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Natural History Following the First Attack of Acute Pancreatitis.</b></p>
        <p>Am J Gastroenterol. 2012 May 22;</p>
        <p>Authors:  Yadav D, O'Connell M, Papachristou GI</p>
        <p>Abstract<br/>
        OBJECTIVES:Data on natural history following a sentinel attack of acute pancreatitis (AP) are limited. The objective of this study was to determine the risk of recurrent AP (RAP) and subsequent chronic pancreatitis (CP) diagnosis after the first attack of AP.METHODS:Using the Pennsylvania Health Care Cost Containment Council (PHC4) data set, we identified all unique White and Black Allegheny County residents who received a first-time primary inpatient discharge diagnosis of AP from 1996 through 2005. AP etiology was determined using associated diagnoses codes. We also checked whether any of these patients were readmitted for AP and/or received inpatient CP diagnosis until third quarter of 2007.RESULTS:In all, 7,456 unique residents (mean age 58±20?years, 45% male, 80% White) with incident AP admission were identified. Common etiologies included biliary (28%), alcohol (19%), and idiopathic (36%). Compared with other causes, alcoholic AP patients were significantly younger and more likely to be male and Black. Among survivors (98.1%) and those without pancreatic cancer, follow-up (median 40 months, interquartile range 18, 69) was available for 84% of patients. Readmission for primary or any AP was recorded for 22 and 29%; subsequent primary or any CP diagnosis was assigned to 6 and 12.8%, respectively. Significant independent predictors for RAP were alcohol etiology and tobacco abuse and for CP were RAP and tobacco abuse. RAP risk in biliary AP increased with the duration between AP and cholecystectomy.CONCLUSIONS:Readmissions following a sentinel attack of AP are common. Progression to CP is infrequent and usually occurs in the setting of RAP, alcohol, and smoking. Cholectstectomy should be considered as soon as feasible after an attack of biliary AP. Natural history of CP may be altered through early behavioral intervention.Am J Gastroenterol advance online publication, 22 May 2012; doi:10.1038/ajg.2012.126.<br/></p><p>PMID: 22613906 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Prospective Evaluation of Subjects With Chronic Asymptomatic Pancreatic Hyperenzymemia.</title>
		<link>http://beckerinfo.net/JClub/2012/05/16/prospective-evaluation-of-subjects-with-chronic-asymptomatic-pancreatic-hyperenzymemia/</link>
		<comments>http://beckerinfo.net/JClub/2012/05/16/prospective-evaluation-of-subjects-with-chronic-asymptomatic-pancreatic-hyperenzymemia/#comments</comments>
		<pubDate>Wed, 16 May 2012 18:32:35 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=ca675748b6e251a270feb7a62fd73bad</guid>
		<description><![CDATA[Prospective Evaluation of Subjects With Chronic Asymptomatic Pancreatic Hyperenzymemia.
 ...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Prospective Evaluation of Subjects With Chronic Asymptomatic Pancreatic Hyperenzymemia.</b></p>
        <p>Am J Gastroenterol. 2012 May 15;</p>
        <p>Authors:  Amodio A, Manfredi R, Katsotourchi AM, Gabbrielli A, Benini L, Mucelli RP, Vantini I, Frulloni L</p>
        <p>Abstract<br/>
        OBJECTIVES:Chronic asymptomatic pancreatic hyperenzymemia (CAPH) has been described since 1996 as a benign disease. Recent studies described pathological findings at magnetic resonance cholangiopancreatography with secretin stimulation (s-MRCP) in more than half of the CAPH subjects. The aim of this study was to investigate the frequency and clinical relevance of s-MRCP findings in patients with CAPH.METHODS:Subjects prospectively enrolled from January 2005 to December 2010 underwent s-MRCP and biochemical tests routinely performed.RESULTS:Data relative to 160 subjects (94 males, 66 females, age 49.6±13.6 years) were analyzed. In all, 51 (32%) subjects had hyperamylasemia, 9 (6%) hyperlipasemia, and 100 (62%) an increase in both enzyme levels. The time between the first increased dosage of serum pancreatic enzymes and our observation was 3.3±3.9 years (range: 1-15). Familial pancreatic hyperenzymemia was observed in 26 out of 133 subjects (19.5%). Anatomic abnormalities of the pancreatic duct system at s-MRCP were found in 24 out of 160 subjects (15%). Pathological MRCP findings were present in 44 subjects (27.5%) before and in 80 subjects (50%) after secretin administration (P&lt;0.0001). Five subjects (3.1%) underwent surgery, 3 for pancreatic endocrine tumor, 1 for pancreatic adenocarcinoma, and 1 for intraductal papillary-mucinous neoplasia (IPMN) involving the main pancreatic duct, and 18 patients (11.3%) needed a follow-up (17 for IPMN and 1 for endocrine tumor).CONCLUSIONS:Alterations of the pancreatic duct system at s-MRCP in subjects with CAPH can be observed in 50% of the subjects and are clinically relevant in 14.4% of cases.Am J Gastroenterol advance online publication, 15 May 2012; doi:10.1038/ajg.2012.125.<br/></p><p>PMID: 22584217 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>Development of ascites in compensated cirrhosis with severe portal hypertension treated with ?-blockers.</title>
		<link>http://beckerinfo.net/JClub/2012/04/28/development-of-ascites-in-compensated-cirrhosis-with-severe-portal-hypertension-treated-with-%ce%b2-blockers/</link>
		<comments>http://beckerinfo.net/JClub/2012/04/28/development-of-ascites-in-compensated-cirrhosis-with-severe-portal-hypertension-treated-with-%ce%b2-blockers/#comments</comments>
		<pubDate>Sat, 28 Apr 2012 10:00:30 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=8e1f9477aec674d82ff6549496bdfaae</guid>
		<description><![CDATA[Development of ascites in compensated cirrhosis with severe portal hypertension treated w...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Development of ascites in compensated cirrhosis with severe portal hypertension treated with ?-blockers.</b></p>
        <p>Am J Gastroenterol. 2012 Mar;107(3):418-27</p>
        <p>Authors:  Hernández-Gea V, Aracil C, Colomo A, Garupera I, Poca M, Torras X, Miñana J, Guarner C, Villanueva C</p>
        <p>Abstract<br/>
        OBJECTIVES: In compensated cirrhosis, a threshold value of hepatic venous pressure gradient (HVPG) ?10?mm?Hg is required for the development of decompensation. However, whether the treatment of portal hypertension (PHT) can prevent the transition into development of ascites once this level has been reached is unclear. Our aim was to assess the relationship between changes in HVPG induced by ?-blockers and development of ascites in compensated cirrhosis with severe PHT.<br/>
        METHODS: Eighty-three patients without any previous decompensation of cirrhosis, with large esophageal varices and HVPG ?12?mm?Hg were included. After baseline hemodynamic measurements nadolol was administered and a second hemodynamic study was repeated 1-3 months later.<br/>
        RESULTS: During 53±30 months of follow-up, decompensation occurred in 52 patients (62%) and in 81% of them ascites was the first manifestation. Using receiver operating characteristic curve analysis a decrease in HVPG ?10% was the best cutoff to predict ascites. As compared with nonresponders, patients with an HVPG decrease ?10% had a lower probability of developing ascites (19% vs. 57% at 3 years, P&lt;0.001), refractory ascites (P=0.007), and hepatorenal syndrome (P=0.027). By Cox regression analysis hemodynamic nonresponse was the best predictor of ascites. By stepwise logistic regression, development of ascites was independently associated with nonresponse, whereas refractory ascites, hepatorenal syndrome, and spontaneous bacterial peritonitis were not.<br/>
        CONCLUSIONS: In patients with compensated cirrhosis and large varices treated with ?-blockers, an HVPG decrease ?10% significantly reduces the risk of developing ascitic decompensation and other related complications such as refractory ascites or hepatorenal syndrome.<br/></p><p>PMID: 22334252 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Pancreas divisum is not a cause of pancreatitis by itself but acts as a partner of genetic mutations.</title>
		<link>http://beckerinfo.net/JClub/2012/04/12/pancreas-divisum-is-not-a-cause-of-pancreatitis-by-itself-but-acts-as-a-partner-of-genetic-mutations/</link>
		<comments>http://beckerinfo.net/JClub/2012/04/12/pancreas-divisum-is-not-a-cause-of-pancreatitis-by-itself-but-acts-as-a-partner-of-genetic-mutations/#comments</comments>
		<pubDate>Thu, 12 Apr 2012 20:00:36 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=4a31ecc57a6b1b2485756554701bc599</guid>
		<description><![CDATA[Pancreas divisum is not a cause of pancreatitis by itself but acts as a partner of geneti...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Pancreas divisum is not a cause of pancreatitis by itself but acts as a partner of genetic mutations.</b></p>
        <p>Am J Gastroenterol. 2012 Feb;107(2):311-7</p>
        <p>Authors:  Bertin C, Pelletier AL, Vullierme MP, Bienvenu T, Rebours V, Hentic O, Maire F, Hammel P, Vilgrain V, Ruszniewski P, Lévy P</p>
        <p>Abstract<br/>
        OBJECTIVES: The role of pancreas divisum (PD) as a cause of acute recurrent or chronic pancreatitis (AR/CP) is still a matter of debate.<br/>
        METHODS: The aims of this study were to evaluate the frequency of PD diagnosed using magnetic resonance cholangiopancreatography (MRCP) in patients with AR/CP of unknown origin (n=40) after careful exclusion of all known causes and to test the hypothesis of an interaction between anatomical (PD) and functional genetic anomalies (SPINK1, PRSS1, or CFTR gene mutations or polymorphisms (n=19, 25, and 30, respectively)) that could result in AR/CP. Patients with alcohol-induced pancreatitis (n=29) and subjects who had MRCP for a nonpancreatic disease (n=45) served as controls.<br/>
        RESULTS: PD frequency was 7% in subjects without pancreatic disease, 7% in patients with alcohol-induced pancreatitis, and 5, 16, 16, and 47% in those with idiopathic, and PRSS1-, SPINK1-, and CFTR-associated pancreatitis, respectively (P&lt;0.0001). There was no significant difference between idiopathic pancreatitis and the two control groups. The frequency of PD was higher in patients with CFTR gene-associated pancreatitis as compared with those with idiopathic and alcoholic pancreatitis (P&lt;0.0001) and with those with SPINK1 and PRSS1 gene-associated pancreatitis (P&lt;0.02).<br/>
        CONCLUSIONS: The frequency of PD was not different in patients with idiopathic pancreatitis as compared with controls, demonstrating that PD by itself is not a cause of pancreatitis. PD frequency was higher in patients with genetic pancreatitis, especially in those with CFTR mutations or polymorphisms, suggesting a cumulative effect of these two cofactors.<br/></p><p>PMID: 22158025 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>Saccharomyces boulardii for the Prevention of Antibiotic-Associated Diarrhea in Adult Hospitalized Patients: A Single-Center, Randomized, Double-Blind, Placebo-Controlled Trial.</title>
		<link>http://beckerinfo.net/JClub/2012/04/05/saccharomyces-boulardii-for-the-prevention-of-antibiotic-associated-diarrhea-in-adult-hospitalized-patients-a-single-center-randomized-double-blind-placebo-controlled-trial/</link>
		<comments>http://beckerinfo.net/JClub/2012/04/05/saccharomyces-boulardii-for-the-prevention-of-antibiotic-associated-diarrhea-in-adult-hospitalized-patients-a-single-center-randomized-double-blind-placebo-controlled-trial/#comments</comments>
		<pubDate>Thu, 05 Apr 2012 21:31:10 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=a1eedc36242653fa08c7f529d5e7e40f</guid>
		<description><![CDATA[Saccharomyces boulardii for the Prevention of Antibiotic-Associated Diarrhea in Adult Hos...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Saccharomyces boulardii for the Prevention of Antibiotic-Associated Diarrhea in Adult Hospitalized Patients: A Single-Center, Randomized, Double-Blind, Placebo-Controlled Trial.</b></p>
        <p>Am J Gastroenterol. 2012 Apr 3;</p>
        <p>Authors:  Pozzoni P, Riva A, Bellatorre AG, Amigoni M, Redaelli E, Ronchetti A, Stefani M, Tironi R, Molteni EE, Conte D, Casazza G, Colli A</p>
        <p>Abstract<br/>
        OBJECTIVES:Antibiotic-associated diarrhea (AAD) and Clostridium difficile-associated diarrhea (CDAD) are common complications of antibiotic use. Probiotics were effective in preventing AAD and CDAD in several randomized controlled trials. This study was aimed at testing the effect of Saccharomyces boulardii on the occurrence of AAD and CDAD in hospitalized patients.METHODS:A single-center, randomized, double-blind, placebo-controlled, parallel-group trial was performed. Patients being prescribed antibiotics or on antibiotic therapy for &lt;48?h were eligible. Exclusion criteria were ongoing diarrhea, recent assumption of probiotics, lack of informed consent, inability to ingest capsules, and severe pancreatitis. Patients received a capsule containing S. boulardii or an indistinguishable placebo twice daily within 48?h of beginning antibiotic therapy, continued treatment for 7 days after antibiotic withdrawal, and were followed for 12 weeks after ending antibiotic treatment.RESULTS:Of 562 consecutive eligible patients, 275 patients aged 79.2±9.8 years (134 on placebo) were randomized and 204 aged 78.4±10.0 years (98 on placebo) completed the follow-up. AAD developed in 13.3% (13/98) of the patients receiving placebo and in 15.1% (16/106) of those receiving S. boulardii (odds ratio for S. boulardii vs. placebo, 1.16; 95% confidence interval (CI), 0.53-2.56). Five cases of CDAD occurred, 2 in the placebo group (2.0%) and 3 in the probiotic group (2.8%; odds ratio for S. boulardii vs. placebo, 1.40; 95% CI, 0.23-8.55). There was no difference in mortality rates (12.7% vs. 15.6%, P=0.60).CONCLUSIONS:In elderly hospitalized patients, S. boulardii was not effective in preventing the development of AAD.Am J Gastroenterol advance online publication, 3 April 2012; doi:10.1038/ajg.2012.56.<br/></p><p>PMID: 22472744 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>Editorial: Beta-blockers and the prevention of decompensation in cirrhosis: worth the trouble.</title>
		<link>http://beckerinfo.net/JClub/2012/03/09/editorial-beta-blockers-and-the-prevention-of-decompensation-in-cirrhosis-worth-the-trouble/</link>
		<comments>http://beckerinfo.net/JClub/2012/03/09/editorial-beta-blockers-and-the-prevention-of-decompensation-in-cirrhosis-worth-the-trouble/#comments</comments>
		<pubDate>Fri, 09 Mar 2012 06:03:26 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=a633d6471c4831bf8a16f36fc4ac12cb</guid>
		<description><![CDATA[Editorial: Beta-blockers and the prevention of decompensation in cirrhosis: worth the tro...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Editorial: Beta-blockers and the prevention of decompensation in cirrhosis: worth the trouble.</b></p>
        <p>Am J Gastroenterol. 2012 Mar;107(3):428-30</p>
        <p>Authors:  Northup PG, Henry ZH</p>
        <p>Abstract<br/>
        Non-selective beta-blockers have been a cornerstone of therapy for prevention of esophageal variceal bleeding in cirrhosis patients for more than two decades. When lowering the hepatic vein portal pressure gradient (HVPG) below 12?mm?Hg or decreasing the pressure by 20% from baseline, these drugs are of proven benefit in reducing variceal bleeding and improving survival in this patient population. The recent work by Hendández-Gea et al., suggests that initiation of the beta-blocker nadolol in cirrhosis patients with high-risk varices can delay or prevent the first occurrence of clinically evident ascites. This finding comes with some caveats, however. The beneficial effect was only seen in patients who had an improvement by 10% or more from baseline HVPG pressure (only 51% of the treated patients in this study). This class of medications has some risk and tolerance issues, and many patients do not respond, even when the heart rate is optimally decreased. Despite this, the use of beta-blockers may be beneficial in the primary prevention of the formation of ascites and further decompensation of cirrhosis.<br/></p><p>PMID: 22388023 [PubMed - in process]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>Management of delayed postpolypectomy bleeding: a decision analysis.</title>
		<link>http://beckerinfo.net/JClub/2012/03/09/management-of-delayed-postpolypectomy-bleeding-a-decision-analysis/</link>
		<comments>http://beckerinfo.net/JClub/2012/03/09/management-of-delayed-postpolypectomy-bleeding-a-decision-analysis/#comments</comments>
		<pubDate>Fri, 09 Mar 2012 06:03:26 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=dd92423dd993ebbb38ac39b051b04015</guid>
		<description><![CDATA[Management of delayed postpolypectomy bleeding: a decision analysis.
        Am J Gastroe...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Management of delayed postpolypectomy bleeding: a decision analysis.</b></p>
        <p>Am J Gastroenterol. 2012 Mar;107(3):339-42</p>
        <p>Authors:  Sonnenberg A</p>
        <p>Abstract<br/>
        Objectives:The benefit of repeat colonoscopy in managing delayed postpolypectomy bleeding is unknown. This study aimed to assess the outcome of repeat colonoscopy to achieve hemostasis.Methods:Endoscopic management of postpolypectomy bleeding is modeled as a decision tree, measuring the expected overall fraction of patients who benefit from therapeutic hemostasis and the number of patients needed to treat (NNT) in order to achieve one beneficial hemostasis.Results:A repeat colonoscopy to identify and treat postpolypectomy bleeding is beneficial in about 22% of patients, corresponding to an NNT of 4.5 patients. The outcome of the model is sensitive to assumptions underlying the fractions of patients who need treatment and would benefit from successful endoscopic hemostasis. Varying these probabilities over a broad range changes the fraction of patients benefiting from endoscopy between 3% and 33% and the NNT between 28 and 3 patients, respectively.Conclusions:The expected outcome of repeat colonoscopy justifies the endoscopic attempts at therapeutic hemostasis. The results also suggest that in many patients expectant management aimed at spontaneous resolution of the bleeding remains a valid option.<br/></p><p>PMID: 22388016 [PubMed - in process]</p></body>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>Editorial: drug-induced acute pancreatitis: uncommon or commonplace?</title>
		<link>http://beckerinfo.net/JClub/2012/02/18/editorial-drug-induced-acute-pancreatitis-uncommon-or-commonplace/</link>
		<comments>http://beckerinfo.net/JClub/2012/02/18/editorial-drug-induced-acute-pancreatitis-uncommon-or-commonplace/#comments</comments>
		<pubDate>Sat, 18 Feb 2012 12:02:45 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=44c4d0c7036b201434c483e5d6e3aa18</guid>
		<description><![CDATA[Editorial: drug-induced acute pancreatitis: uncommon or commonplace?
        Am J Gastroe...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Editorial: drug-induced acute pancreatitis: uncommon or commonplace?</b></p>
        <p>Am J Gastroenterol. 2011 Dec;106(12):2189-91</p>
        <p>Authors:  Grendell JH</p>
        <p>Abstract<br/>
        Many drugs have been implicated as causing acute pancreatitis (AP), mainly based on the recurrence of pancreatitis following rechallenge with a drug that the patient had been taking at the time of an initial episode of AP. However, estimates of the relative frequency with which drugs cause AP vary widely. This is largely because many patients may be taking a number of drugs, may have co-morbidities such as gallstone disease or hypertriglyceridemia, or may be consuming large amounts of alcohol, making it difficult to determine what actually is the primary cause of an episode of AP. Large, rigorously designed epidemdiological studies are needed to better define the frequency with which the drugs in general cause AP and the specific risk of pancreatitis associated with any individual drug.<br/></p><p>PMID: 22138943 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		<title>Editorial: Not So Nosocomial Anymore: The Growing Threat of Community-Acquired Clostridium difficile.</title>
		<link>http://beckerinfo.net/JClub/2012/01/06/editorial-not-so-nosocomial-anymore-the-growing-threat-of-community-acquired-clostridium-difficile/</link>
		<comments>http://beckerinfo.net/JClub/2012/01/06/editorial-not-so-nosocomial-anymore-the-growing-threat-of-community-acquired-clostridium-difficile/#comments</comments>
		<pubDate>Fri, 06 Jan 2012 17:34:55 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=95a2289367a63d97c573f30a506608a2</guid>
		<description><![CDATA[Editorial: Not So Nosocomial Anymore: The Growing Threat of Community-Acquired Clostridiu...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Editorial: Not So Nosocomial Anymore: The Growing Threat of Community-Acquired Clostridium difficile.</b></p>
        <p>Am J Gastroenterol. 2012 Jan;107(1):96-8</p>
        <p>Authors:  Leffler DA, Lamont JT</p>
        <p>Abstract<br/>
        Clostridium difficile infection is widely accepted to be the leading cause of nosocomial infection-related morbidity and mortality, outpacing both antibiotic-resistant staphylococcus and enterococcus. The existence and prevalence of community-acquired Clostridium difficile infection, on the other hand, is much less well appreciated. Growing evidence now suggests that community-acquired Clostridium difficile infection may account for more than a third of Clostridium difficile-associated diarrhea overall. Similar to nosocomial Clostridium difficile infection, community-acquired cases appear to be increasing in incidence, and although associated mortality is lower than in nosocomial cases, morbidity including hospitalization and recurrence are high. Further, traditional risk factors for Clostridium difficile infection including antibiotic exposure appear to be less important in community-acquired cases and common routes of exposure and infection in the community are yet to be elucidated. In this issue of the American Journal of Gastroenterology, Khanna et al. provide important epidemiological data on the growing threat of community-acquired Clostridium difficile infection.<br/></p><p>PMID: 22218031 [PubMed - in process]</p></body>]]></content:encoded>
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		<title>Editorial: fluid resuscitation in acute pancreatitis: striking the right balance.</title>
		<link>http://beckerinfo.net/JClub/2011/12/14/editorial-fluid-resuscitation-in-acute-pancreatitis-striking-the-right-balance/</link>
		<comments>http://beckerinfo.net/JClub/2011/12/14/editorial-fluid-resuscitation-in-acute-pancreatitis-striking-the-right-balance/#comments</comments>
		<pubDate>Wed, 14 Dec 2011 11:32:58 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=ab49e6858640637109a7705aba0e8e2b</guid>
		<description><![CDATA[Editorial: fluid resuscitation in acute pancreatitis: striking the right balance.
       ...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Editorial: fluid resuscitation in acute pancreatitis: striking the right balance.</b></p>
        <p>Am J Gastroenterol. 2011 Oct;106(10):1851-2</p>
        <p>Authors:  Wu BU</p>
        <p>Abstract<br/>
        Fluid resuscitation is a key component of the early management of acute pancreatitis. Current clinical practice guidelines recommend aggressive fluid resuscitation despite limited prospective data. In this month's issue of the American Journal of Gastroenterology, de-Madaria et al. present findings from a prospective cohort study that evaluate the relationship between early resuscitation parameters and several important outcome measures. Their findings challenge several of our long held beliefs regarding the benefits of vigorous fluid resuscitation in the early phase of acute pancreatitis. Findings from this study along with several others now suggest that a more tailored approach to resuscitation is needed.<br/></p><p>PMID: 21979206 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		<title>Influence of fluid therapy on the prognosis of acute pancreatitis: a prospective cohort study.</title>
		<link>http://beckerinfo.net/JClub/2011/12/14/influence-of-fluid-therapy-on-the-prognosis-of-acute-pancreatitis-a-prospective-cohort-study/</link>
		<comments>http://beckerinfo.net/JClub/2011/12/14/influence-of-fluid-therapy-on-the-prognosis-of-acute-pancreatitis-a-prospective-cohort-study/#comments</comments>
		<pubDate>Wed, 14 Dec 2011 11:32:58 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=6fcc6a6bc38a10e49485f603f4d5626f</guid>
		<description><![CDATA[Influence of fluid therapy on the prognosis of acute pancreatitis: a prospective cohort s...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Influence of fluid therapy on the prognosis of acute pancreatitis: a prospective cohort study.</b></p>
        <p>Am J Gastroenterol. 2011 Oct;106(10):1843-50</p>
        <p>Authors:  de-Madaria E, Soler-Sala G, Sánchez-Payá J, Lopez-Font I, Martínez J, Gómez-Escolar L, Sempere L, Sánchez-Fortún C, Pérez-Mateo M</p>
        <p>Abstract<br/>
        OBJECTIVES: Although aggressive fluid therapy during the first days of hospitalization is recommended by most guidelines and reviews on acute pancreatitis (AP), this recommendation is not supported by any direct evidence. We aimed to evaluate the association between the amount of fluid administered during the initial 24 h of hospitalization and the incidence of organ failure (OF), local complications, and mortality.<br/>
        METHODS: This was a prospective cohort study. We included consecutive adult patients admitted with AP. Local complications and OF were defined according to the Atlanta Classification. Persistent OF was defined as OF of &gt;48-h duration. Patients were divided into three groups according to the amount of fluid administered during the initial 24 h: group A: &lt;3.1 l (less than the first quartile), group B: 3.1-4.1 l (between the first and third quartiles), and group C: &gt;4.1 l (more than the third quartile).<br/>
        RESULTS: A total of 247 patients were analyzed. Administration of &gt;4.1 l during the initial 24 h was significantly and independently associated with persistent OF, acute collections, respiratory insufficiency, and renal insufficiency. Administration of &lt;3.1 l during the initial 24 h was not associated with OF, local complications, or mortality. Patients who received between 3.1 and 4.1 l during the initial 24 h had an excellent outcome.<br/>
        CONCLUSIONS: In our study, administration of a small amount of fluid during the initial 24 h was not associated with a poor outcome. The need for a great amount of fluid during the initial 24 h was associated with a poor outcome; therefore, this group of patients must be carefully monitored.<br/></p><p>PMID: 21876561 [PubMed - indexed for MEDLINE]</p></body>]]></content:encoded>
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		<title>The Epidemiology of Community-Acquired Clostridium difficile Infection: A Population-Based Study.</title>
		<link>http://beckerinfo.net/JClub/2011/11/24/the-epidemiology-of-community-acquired-clostridium-difficile-infection-a-population-based-study/</link>
		<comments>http://beckerinfo.net/JClub/2011/11/24/the-epidemiology-of-community-acquired-clostridium-difficile-infection-a-population-based-study/#comments</comments>
		<pubDate>Thu, 24 Nov 2011 17:30:14 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=f04ff9ba776f44ef9efb23b42f658b62</guid>
		<description><![CDATA[The Epidemiology of Community-Acquired Clostridium difficile Infection: A Population-Base...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>The Epidemiology of Community-Acquired Clostridium difficile Infection: A Population-Based Study.</b></p>
        <p>Am J Gastroenterol. 2011 Nov 22;</p>
        <p>Authors:  Khanna S, Pardi DS, Aronson SL, Kammer PP, Orenstein R, St Sauver JL, Harmsen WS, Zinsmeister AR</p>
        <p>Abstract<br/>
        OBJECTIVES:Clostridium difficile infection (CDI) is a common hospital-acquired infection with increasing incidence, severity, recurrence, and associated morbidity and mortality. There are emerging data on the occurrence of CDI in nonhospitalized patients. However, there is a relative lack of community-based CDI studies, as most of the existing studies are hospital based, potentially influencing the results by referral or hospitalization bias by missing cases of community-acquired CDI.METHODS:To better understand the epidemiology of community-acquired C. difficile infection, a population-based study was conducted in Olmsted County, Minnesota, using the resources of the Rochester Epidemiology Project. Data regarding severity, treatment response, and outcomes were compared in community-acquired vs. hospital-acquired cohorts, and changes in these parameters, as well as in incidence, were assessed over the study period.RESULTS:Community-acquired CDI cases accounted for 41% of 385 definite CDI cases. The incidence of both community-acquired and hospital-acquired CDI increased significantly over the study period. Compared with those with hospital-acquired infection, patients with community-acquired infection were younger (median age 50 years compared with 72 years), more likely to be female (76% vs. 60%), had lower comorbidity scores, and were less likely to have severe infection (20% vs. 31%) or have been exposed to antibiotics (78% vs. 94%). There were no differences in the rates of complicated or recurrent infection in patients with community-acquired compared with hospital-acquired infection.CONCLUSIONS:In this population-based cohort, a significant proportion of cases of CDI occurred in the community. These patients were younger and had less severe infection than those with hospital-acquired infection. Thus, reports of CDI in hospitalized patients likely underestimate the burden of disease and overestimate severity.Am J Gastroenterol advance online publication, 22 November 2011; doi:10.1038/ajg.2011.398.<br/></p><p>PMID: 22108454 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
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		<title>The Risk of Peptic Ulcer Bleeding Mortality in Relation to Hospital Admission on Holidays: A Cohort Study on 8,222 Cases of Peptic Ulcer Bleeding.</title>
		<link>http://beckerinfo.net/JClub/2011/11/24/the-risk-of-peptic-ulcer-bleeding-mortality-in-relation-to-hospital-admission-on-holidays-a-cohort-study-on-8222-cases-of-peptic-ulcer-bleeding/</link>
		<comments>http://beckerinfo.net/JClub/2011/11/24/the-risk-of-peptic-ulcer-bleeding-mortality-in-relation-to-hospital-admission-on-holidays-a-cohort-study-on-8222-cases-of-peptic-ulcer-bleeding/#comments</comments>
		<pubDate>Thu, 24 Nov 2011 17:30:14 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=426d5fd1bc06f1714facd99fe80dbbca</guid>
		<description><![CDATA[The Risk of Peptic Ulcer Bleeding Mortality in Relation to Hospital Admission on Holidays...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>The Risk of Peptic Ulcer Bleeding Mortality in Relation to Hospital Admission on Holidays: A Cohort Study on 8,222 Cases of Peptic Ulcer Bleeding.</b></p>
        <p>Am J Gastroenterol. 2011 Nov 22;</p>
        <p>Authors:  Tsoi KK, Chiu PW, Chan FK, Ching JY, Lau JY, Sung JJ</p>
        <p>Abstract<br/>
        OBJECTIVES:Urgent endoscopic intervention is important in the management of patients with peptic ulcer bleeding (PUB). Hospital admission on Sundays or on public holidays may be associated with an increased mortality. This study sets to investigate whether mortality among patients with PUB differs between holiday and weekday admissions, and also to investigate the association between mortality and the waiting time for endoscopy.METHODS:Patients with PUB admitted to the Prince of Wales Hospital from 1993 to 2005 were prospectively recruited in the data set. Mortality and cause of death were documented. Predicting variables included patient characteristics, waiting time for endoscopy, and holiday or weekday admissions. Bivariate analyses and multivariate logistic regression models were used to evaluate risk factors on 30-day mortality after endoscopy.RESULTS:A total of 8,222 patients with PUB were enrolled among which 1,573 (19.1%) were admitted on holidays. A total of 334 (4.1%) patients died within 30 days after hospital admission. There was no significant difference in mortality rate between holiday and weekday admissions (4.1 vs. 4.0%, P=0.876). Using logistic regression adjusted for age, hemodynamic shock, ulcer history, and severe comorbid illness, the waiting time for endoscopy was correlated with the risk of 30-day mortality (odds ratio (OR), 95% confidence interval (95% CI)=1.10, 1.06-1.14). Holiday admission has not increased the mortality risk (OR, 95% CI=1.07, 0.80-1.43).CONCLUSIONS:When therapeutic endoscopy can be offered within 1 day after admission for PUB, holiday admission will not adversely affect bleeding mortality.Am J Gastroenterol advance online publication, 22 November 2011; doi:10.1038/ajg.2011.409.<br/></p><p>PMID: 22108453 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
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		<title>Treatment of Hospitalized Adult Patients With Severe Ulcerative Colitis: Toronto Consensus Statements.</title>
		<link>http://beckerinfo.net/JClub/2011/11/24/treatment-of-hospitalized-adult-patients-with-severe-ulcerative-colitis-toronto-consensus-statements/</link>
		<comments>http://beckerinfo.net/JClub/2011/11/24/treatment-of-hospitalized-adult-patients-with-severe-ulcerative-colitis-toronto-consensus-statements/#comments</comments>
		<pubDate>Thu, 24 Nov 2011 17:30:14 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Gastroenterol]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=d8ef4a6506584c9205330b318b58d2ed</guid>
		<description><![CDATA[Treatment of Hospitalized Adult Patients With Severe Ulcerative Colitis: Toronto Consensu...]]></description>
			<content:encoded><![CDATA[<body><table><tr><td/></tr></table><p><b>Treatment of Hospitalized Adult Patients With Severe Ulcerative Colitis: Toronto Consensus Statements.</b></p>
        <p>Am J Gastroenterol. 2011 Nov 22;</p>
        <p>Authors:  Bitton A, Buie D, Enns R, Feagan BG, Jones JL, Marshall JK, Whittaker S, Griffiths AM, Panaccione R</p>
        <p>Abstract<br/>
        OBJECTIVES:The objective of this study was to provide updated explicit and relevant consensus statements for clinicians to refer to when managing hospitalized adult patients with acute severe ulcerative colitis (UC).METHODS:The Canadian Association of Gastroenterology consensus group of 23 voting participants developed a series of recommendation statements that addressed pertinent clinical questions. An iterative voting and feedback process was used to do this in conjunction with systematic literature reviews. These statements were brought to a formal consensus meeting held in Toronto, Ontario (March 2010), when each statement was discussed, reformulated, voted upon, and subsequently revised until group consensus (at least 80% agreement) was obtained. The modified GRADE (Grading of Recommendations Assessment, Development, and Evaluation) criteria were used to rate the strength of recommendations and the quality of evidence.RESULTS:As a result of the iterative process, consensus was reached on 21 statements addressing four themes (General considerations and nutritional issues, Steroid use and predictors of steroid failure, Cyclosporine and infliximab, and Surgical issues).CONCLUSIONS:Key recommendations for the treatment of hospitalized patients with severe UC include early escalation to second-line medical therapy with either infliximab or cyclosporine in individuals in whom parenteral steroids have failed after 72?h. These agents should be used in experienced centers where appropriate support is available. Sequential therapy with cyclosporine and infliximab is not recommended. Surgery is an option when first-line steroid therapy fails, and is indicated when second-line medical therapy fails and/or when complications arise during the hospitalization.Am J Gastroenterol advance online publication, 22 November 2011; doi:10.1038/ajg.2011.386.<br/></p><p>PMID: 22108451 [PubMed - as supplied by publisher]</p></body>]]></content:encoded>
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