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Background Endoscopic mucosal resection (EMR) is an established technique for treating large laterally spreading type (LST) lesions ≥20 mm. The aim of our study was to compare the use of argon plasma (APC) versus snare-tip coagulation on the recurrence rate of large LST lesions. Methods All patients with large LST lesions resected by EMR between January 2006 and December 2014 were enrolled. After piecemeal resection, patients underwent either APC or snare-tip coagulation of the rim of the resection area and any residual adenomatous tissue. Follow up included colonoscopy and biopsies. Medical records, including characteristics of patients and polyps, complications and recurrence were retrieved and collected. Results One hundred one patients were included in the final analysis. They were divided into the APC group (n=50) and the snare-tip coagulation group (n=51). The 2 groups were similar concerning patients’ characteristics, size of polyps and histology. Post-polypectomy coagulation syndrome was observed in 8 patients (7.9%) (APC group: n=5 and snare tip group: n=3). EMR-related bleeding occurred in 9 patients (8.9%) (APC group: n=4 and snare tip group: n=5). Total recurrence rate was 14.85% (16% and 13.7% in APC and snare-tip groups, respectively, P=0.34). Conclusion The effectiveness of snare-tip coagulation is comparable with that of APC with respect to recurrence rate after resection of large LST lesions. It thus represents a cost-effective alternative to APC.

Background:Observational studies have shown an increased risk of upper gastrointestinal bleeding in users of selective serotonin receptor inhibitors (SSRIs). We retrospectively investigated the impact of SSRIs, alone or combined with aspirin (ASA) or nonsteroidal anti-inflammatory drugs (NSAIDs), on the incidence of post-endoscopic sphincterotomy (post-ES) bleeding.Methods:A total of 3058 patients were included. Of these, 457 patients received SSRIs, alone or plus ASA or NSAIDs, until the day of ES (SSRIs group), while 2659 patients (non SSRIs group) had never been on SSRIs (n=1925), though some had been on ASA (n=613) or NSAIDS (n=121). Patient assessment included indication for endoscopic retrograde cholangiopancreatography (ERCP), comorbid diseases, detailed drug history before and after ES, procedural details, and risk factors for post-ES bleeding. Primary outcome was defined as the incidence, type and severity of post-ES bleeding.Results:There was no statistical difference in age, sex, indication for ERCP, comorbid diseases, technical characteristics or results of therapeutic ERCP between the 2 groups. The incidence of post-ES bleeding was 3.9% in the SSRIs group and 3% in the non SSRIs group, a difference not statistically significant (P=0.754). Likewise, there was no difference in type (P=0.145) or severity of bleeding (P=0.754) between the 2 groups. Multivariate analysis showed the precut technique as the only independent risk factor for post ES hemorrhage (odds ratio 2.56, 95% confidence interval 1.23-3.63; P=0.001).Conclusion:This study found that SSRIs, alone or combined with ASA or NSAIDs, had no influence on the incidence or the severity of post-ES bleeding.

In their prospective clinical trial, Schulz et al. concluded that the amount of ammonia produced by Helicobacter pylori infection (Hp-I) does not influence ammonia serum levels and is not associated with an increased prevalence of minimal hepatic encephalopathy (MHE) in patients with liver cirrhosis (LC). Therefore, an additional benefit of Hp eradication in the treatment of HE in LC patients is unlikely to occur [1].Apart from ammonia, recent considerations [2, 3] postulated that Hp may be involved in the pathophysiology of the post-HE persistent cognitive impairment in cirrhotic patients, related with sequelae such as falls, fractures or motor vehicle accidents, by several additional mechanisms. Helicobacter pylori may be involved in the pathophysiology of the cirrhosis-related cognitive impairment by releasing proinflammatory and vasoactive substances, involved, through blood-brain-barrier (BBB) disruption, in a number of vascular disorders including mild cognitive impairment (MCI), a prodromal phase of Alzheimer' s disease (AD), which can lead to long-term neurologic deficits [4][5][6].Specifically, inflammatory mediators (e.g., cytokines and chemokines induced by Hp-I) and oxidative stress have been implicated in inducing BBB disruption. Helicobacter pylori could indirectly affect the brain through the release of numerous cytokines such as the tumor necrosis factor (TNF)-alpha, acting at a distance; TNF-alpha is involved in BBB disruption through a mechanism involving matrix metalloproteinases upregulation. In addition, the Hp-induced cytotoxin VacA exhibits chemotactic activities to the bone marrow-derived mast cells (BMDMCs) and induces BMDMCs to produce proinflammatory cytokines which disturb the BBB [7, 8]. Mast cell degranulation is able to secrete these potent mediators which could orchestrate neuroinflammation and affect the BBB integrity, thereby playing a role in neuropathies. The "cross-talk" between mast cells, lymphocytes, neurons and LETTERS TO THE EDITORglia constitutes a neuroimmune axis implicated in a range of neurodegenerative diseases with an inflammatory and/or autoimmune component [8]. Blood-brain-barrier disruption could play an important role in promoting the entry of immune cells (autoreactive effector CD4+ and CD8+ T cells) infiltrations and pathogens into the brain resulting in brain pathologies. In this regard, activated monocytes (possibly infected with Hp due to defective autophagy resulting in Hp replication in autophagic vesicles) might also enter the brain due to BBB disruption (Trojan horse theory), contributing to cirrhosis-related brain pathologies [2, 5, 9].Helicobacter pylori may be further involved in the pathophysiology of the cirrhosis-related cognitive impairment by promoting platelet-leukocyte aggregation proposed to play pathophysiologic roles in MCI, AD and liver fibrosis; producing reactive oxygen metabolites involved in AD pathophysiology and complications of cirrhosis; causing the development of cross mimicry between endothelial and Hp antigens; increasing homo...

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