Present and future of prophylactic antibiotics for severe acute pancreatitis.
Wor…

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Current treatment of ulcerative colitis.
World J Gastroenterol. 2011 Jul 21;17(2…

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Three initial diets for management of mild acute pancreatitis: A meta-analysis.
W…

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Infected pancreatic necrosis: Not necessarily a late event in acute pancreatitis.
World J Gastroenterol. 2011 Jul 21;17(27):3173-6
Authors: Petrov MS, Chong V, Windsor JA
Abstract
It is widely believed that inf…

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Diagnostics in inflammatory bowel disease: Ultrasound.
World J Gastroenterol. 2011 Jul 21;17(27):3192-7
Authors: Strobel D, Goertz RS, Bernatik T
Abstract
Diagnosis of chronic inflammatory bowel diseases (IBD) …

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Current treatment of ulcerative colitis.
World J Gastroenterol. 2011 Jul 21;17(27):3204-12
Authors: Meier J, Sturm A
Abstract
Ulcerative colitis (UC) is a chronic disease featuring recurrent inflammation of the…

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Severe alcoholic hepatitis: Glucocorticoid saves lives and transplantation is promising.
World J Gastroenterol. 2011 May 21;17(19):2454
Authors: Braillon A
Glucocorticosteroids have been used as the only treatment for …

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Epidemiological trends and geographic variation in hospital admissions for diverticulitis in the United States.
World J Gastroenterol. 2011 Mar 28;17(12):1600-5
Authors: Nguyen GC, Sam J, Anand N
To characterize the in…

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Diagnosis and therapy of ascites in liver cirrhosis.
World J Gastroenterol. 2011 Mar 14;17(10):1237-48
Authors: Biecker E
Ascites is one of the major complications of liver cirrhosis and is associated with a poor progn…

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Proton pump inhibitors as a risk factor for recurrence of Clostridium-difficile-associated diarrhea.

World J Gastroenterol. 2010 Jul 28;16(28):3573-7

Authors: Kim JW, Lee KL, Jeong JB, Kim BG, Shin S, Kim JS, Jung HC, Song IS

To investigate the risk factors for Clostridium-difficile-associated diarrhea (CDAD) recurrence, and its relationship with proton pump inhibitors (PPIs).

PMID: 20653067 [PubMed - indexed for MEDLINE]

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Benefit of combination ?-blocker and endoscopic treatment to prevent variceal rebleeding: A meta-analysis.

World J Gastroenterol. 2010 Dec 21;16(47):5982-92

Authors: Funakoshi N, Ségalas-Largey F, Duny Y, Oberti F, Valats JC, Bismuth M, Daurès JP, Blanc P

To determine whether the association of ?-blockers with endoscopic treatment is superior to endoscopic treatment alone for the secondary prophylaxis of oesophageal variceal bleeding.

PMID: 21157975 [PubMed - in process]

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PPIs are not associated with a lower incidence of portal-hypertension-related bleeding in cirrhosis.

World J Gastroenterol. 2010 Dec 14;16(46):5869-5873

Authors: Garcia-Saenz-de-Sicilia M, Sanchez-Avila F, Chavez-Tapia NC, Lopez-Arce G, Garcia-Osogobio S, Ruiz-Cordero R, Tellez-Avila FI

AIM: To determine if proton pump inhibitor use in cirrhotic patients with endoscopic findings of portal hypertension is associated with a lower frequency of gastrointestinal bleeding. METHODS: Patients with cirrhosis and endoscopic findings related to portal hypertension, receiving or not receiving proton pump inhibitor (PPI) therapy, were included retrospectively. We assigned patients to two groups: group 1 patients underwent PPI therapy and group 2 patients did not undergo PPI therapy. RESULTS: One hundred and five patients with a median age of 58 (26-87) years were included, 57 (54.3%) of which were women. Esophageal varices were found in 82 (78%) patients, portal hypertensive gastropathy in 72 (68.6%) patients, and gastric varices in 15 (14.3%) patients. PPI therapy was used in 45.5% of patients (n = 48). Seventeen (16.1%) patients presented with upper gastrointestinal bleeding; in 14/17 (82.3%) patients, bleeding was secondary to esophageal varices, and in 3/17 patients bleeding was attributed to portal hypertensive gastropathy. Bleeding related to portal hypertension according to PPI therapy occurred in 18.7% (n = 9) of group 1 and in 14% (n = of group 2 (odds ratio: 0.83, 95% confidence interval: 0.5-1.3, P = 0.51). CONCLUSION: Portal hypertension bleeding is not associated with PPI use. These findings do not support the prescription of PPIs in patients with chronic liver disease with no currently accepted indication.

PMID: 21155009 [PubMed - as supplied by publisher]

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Non-steroidal anti-inflammatory drugs: What is the actual risk of liver damage?

World J Gastroenterol. 2010 Dec 7;16(45):5651-61

Authors: Bessone F

Non-steroidal anti-inflammatory drugs (NSAIDs) constitute a family of drugs, which taken as a group, represents one of the most frequently prescribed around the world. Thus, not surprisingly NSAIDs, along with anti-infectious agents, list on the top for causes of Drug-Induced Liver Injury (DILI). The incidence of liver disease induced by NSAIDs reported in clinical studies is fairly uniform ranging from 0.29/100 000 [95% confidence interval (CI): 0.17-051] to 9/100 000 (95% CI: 6-15). However, compared with these results, a higher risk of liver-related hospitalizations was reported (3-23 per 100 000 patients). NSAIDs exhibit a broad spectrum of liver damage ranging from asymptomatic, transient, hyper-transaminasemia to fulminant hepatic failure. However, under-reporting of asymptomatic, mild cases, as well as of those with transient liver-tests alteration, in conjunction with reports non-compliant with pharmacovigilance criteria to ascertain DILI and flawed epidemiological studies, jeopardize the chance to ascertain the actual risk of NSAIDs hepatotoxicity. Several NSAIDs, namely bromfenac, ibufenac and benoxaprofen, have been withdrawn from the market due to hepatotoxicity; others like nimesulide were never marketed in some countries and withdrawn in others. Indeed, the controversy concerning the actual risk of severe liver disease persists within NSAIDs research. The present work intends (1) to provide a critical analysis of the dissimilar results currently available in the literature concerning the epidemiology of NSAIDS hepatotoxicity; and (2) to review the risk of hepatotoxicity for each one of the most commonly employed compounds of the NSAIDs family, based on past and recently published data.

PMID: 21128314 [PubMed - in process]

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Predictors of rebleeding after initial hemostasis with epinephrine injection in high-risk ulcers.

World J Gastroenterol. 2010 Nov 21;16(43):5490-5495

Authors: Hu ML, Wu KL, Chiu KW, Chiu YC, Chou YP, Tai WC, Hu TH, Chiou SS, Chuah SK

AIM: To identify the predictors of rebleeding after initial hemostasis with epinephrine injection (EI) in patients with high-risk ulcers. METHODS: Recent studies have revealed that endoscopic thermocoagulation, or clips alone or combined with EI are superior to EI alone to arrest ulcer bleeding. However, the reality is that EI monotherapy is still common in clinical practice. From October 2006 to April 2008, high-risk ulcer patients in whom hemorrhage was stopped after EI monotherapy were studied using clinical, laboratory and endoscopic variables. The patients were divided into 2 groups: sustained hemostasis and rebleeding. RESULTS: A total of 175 patients (144, sustained hemostasis; 31, rebleeding) were enrolled. Univariate analysis revealed that older age (? 60 years), advanced American Society of Anesthesiology (ASA) status (category III, IV and V), shock, severe anemia (hemoglobin < 80 g/L), EI dose ? 12 mL and severe bleeding signs (SBS) including hematemesis or hematochezia were the factors which predicted rebleeding. However, only older age, severe anemia, high EI dose and SBS were independent predictors. Among 31 rebleeding patients, 10 (32.2%) underwent surgical hemostasis, 15 (48.4%) suffered from delayed hemostasis causing major complications and 13 (41.9%) died of these complications. CONCLUSION: Endoscopic EI monotherapy in patients with high-risk ulcers should be avoided. Initial hemostasis with thermocoagulation, clips or additional hemostasis after EI is mandatory for such patients to ensure better hemostatic status and to prevent subsequent rebleeding, surgery, morbidity and mortality.

PMID: 21086569 [PubMed - as supplied by publisher]

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Terlipressin and hepatorenal syndrome: What is important for nephrologists and hepatologists.

World J Gastroenterol. 2010 Nov 7;16(41):5139-47

Authors: Magan AA, Khalil AA, Ahmed MH

Hepatorenal syndrome (HRS) is a reversible form of functional renal failure that occurs with advanced hepatic cirrhosis and liver failure. Despite mounting research in HRS, its etiology and medical therapy has not been resolved. HRS encompasses 2 distinct types. Type 1 is characterized by the rapid development of renal failure that occurs within 2 wk and involves a doubling of initial serum creatinine. Type 2 has a more insidious onset and is often associated with ascites. Animal studies have shown that both forms, in particular type 1 HRS, are often precipitated by bacterial infections and circulatory changes. The prognosis for HRS remains very poor. Type 1 and 2 both have an expected survival time of 2 wk and 6 mo, respectively. Progression of liver cirrhosis and the resultant portal hypertension leads to the pooling of blood in the splanchnic vascular bed. The ensuing hyperdynamic circulation causes an ineffective circulatory volume which subsequently activates neurohormonal systems. Primarily the sympathetic nervous system and the renin angiotensin system are activated, which, in the early stages of HRS, maintain adequate circulation. Both advanced cirrhosis and prolonged activation of neurohormonal mechanisms result in fatal complications. Locally produced nitric oxide may have the potential to induce a deleterious vasodilatory effect on the splanchnic circulation. Currently medical therapy is aimed at reducing splanchnic vasodilation to resolve the ineffective circulation and maintain good renal perfusion pressure. Terlipressin, a vasopressin analogue, has shown potential benefit in the treatment of HRS. It prolongs both survival time and has the ability to reverse HRS in the majority of patients. In this review we aim to focus on the pathogenesis of HRS and its treatment with terlipressin vs other drugs.

PMID: 21049548 [PubMed - in process]

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