Irritable bowel syndrome (IBS) is a prevalent functional gastrointestinal disorder characterized by chronic abdominal pain and altered bowel habits. It can be subclassified in different subtypes according to the main clinical manifestation: constipation, diarrhea, mixed, and unclassified. Over the past decade, the role of gut microbiota in IBS has garnered significant attention in the scientific community. Emerging research spotlights the intricate involvement of microbiota dysbiosis in IBS pathogenesis. Studies have demonstrated reduced microbial diversity and stability and specific microbial alterations for each disease subgroup. Microbiota-targeted treatments, such as antibiotics, probiotics, prebiotics, synbiotics, fecal microbiota transplantation, and even diet, offer exciting prospects for managing IBS. However, definitive conclusions are hindered by the heterogeneity of these studies. Further research should focus on elucidating the mechanisms, developing microbiome-based diagnostics, and enabling personalized therapies tailored to an individual’s microbiome profile. This review takes a deep dive into the microscopic world inhabiting our guts, and its implications for IBS. Our aim is to elucidate the complex interplay between gut microbiota and each IBS subtype, exploring novel microbiota-targeted treatments and providing a comprehensive overview of the current state of knowledge.

Low-grade intestinal inflammation plays a key role in the pathophysiology of irritable bowel syndrome (IBS), and this role is likely to be multifactorial. The aim of this review was to summarize the evidence on the spectrum of mucosal inflammation in IBS, highlighting the relationship of this inflammation to the pathophysiology of IBS and its connection to clinical practice. We carried out a bibliographic search in Medline and the Cochrane Library for the period of January 1966 to December 2014, focusing on publications describing an interaction between inflammation and IBS. Several evidences demonstrate microscopic and molecular abnormalities in IBS patients. Understanding the mechanisms underlying low-grade inflammation in IBS may help to design clinical trials to test the efficacy and safety of drugs that target this pathophysiologic mechanism.

Acute variceal bleeding (AVB) is a potentially fatal complication of clinically significant portal hypertension and is one of the most common causes of acute upper gastrointestinal bleeding. Thus, esophagogastric varices represent a major economic and population health issue. Patients with advanced chronic liver disease typically undergo an upper endoscopy to screen for esophagogastric varices. However, upper endoscopy is not recommended for patients with liver stiffness < 20 KPa and platelet count > 150 × 10⁹/L as there is a low probability of high-risk varices. Patients with high-risk varices should receive primary prophylaxis with either nonselective beta-blockers or endoscopic band ligation. In cases of AVB, patients should receive upper endoscopy within 12 h after resuscitation and hemodynamic stability, whereas endoscopy should be performed as soon as possible if patients are unstable. In cases of suspected variceal bleeding, starting vasoactive therapy as soon as possible in combination with endoscopic treatment is recommended. On the other hand, in cases of uncontrolled bleeding, balloon tamponade or self-expandable metal stents can be used as a bridge to more definitive therapy such as transjugular intrahepatic portosystemic shunt. This article aims to offer a comprehensive review of recommendations from international guidelines as well as recent updates on the management of esophagogastric varices.

Introduction: About 30–40% of patients with acute severe ulcerative colitis (UC) fail to respond\ud 23 to intensive intravenous (iv) corticosteroid treatment. Iv cyclosporine and infliximab are an ef-\ud 24 fective rescue therapy in steroid-refractory UC patients but up to now it is still unclear which is\ud Q225 the best therapeutic choice in this setting of patients.\ud 26 Methods: We reviewed our series of severe steroid-refractory colitis admitted consecutively in\ud 27 our referral center since 1994 comparing two historical cohort treated with cyclosporine or\ud 28 infliximab. Iv cyclosporine was administered at the dosage of 2 mg/kg and infliximab at the dos-\ud 29 age of 5 mg/kg. The main outcome was the colectomy rate at 3 months, 12 months and at the\ud 30 end of the follow-up.\ud 31 Results: A total of 65 patients were included: 35 in the cyclosporine group and 30 in the inflix-\ud 32 imab one. After 3 months from the acute episode the colectomy rate was: 28.5% (10/35) in the\ud 33 cyclosporine group and 17% (5/30) in the infliximab group (p=0.25). At 12 months the rate of\ud 34 colectomy increased to 48% in the cyclosporine group versus 17% in the infliximab group\ud 35 (p=0.007, OR 4.7; 95% CI: 1.47–15.16). The 1–2–3 year cumulative colectomy rates were 48%,\ud 36 54%, and 57% in the cyclosporine group, and 17%, 23%, and 27% in the infliximab group. At the\ud 37 end of the follow-up the colectomy rate was: 60% in the cyclosporine group and 30% in the inflix-\ud 38 imab group (p=0.04, HR 2.2; 95% CI: 1.11–4.86). High level of C reactive protein (p=0.04, OR\ud 39 2.9; 95% CI: 1.18–8.28), extensive disease (p=0.01, OR 5.5; 95% CI: 1.57–19.01) and no azathi-\ud 40 oprine treatment after the rescue therapy (pb0.001, OR 8.7; 95% CI: 2.49–30.12) were related\ud 41 to the risk of colectomy

New therapeutic perspectives in irritable bowel syndrome: Targeting low-grade inflammation, immuno-neuroendocrine axis, motility, secretion and beyond