Diverticular disease of the colon (DDC) includes a spectrum of conditions from asymptomatic diverticulosis to symptomatic uncomplicated diverticulosis, segmental colitis associated with diverticulosis, and acute diverticulitis without or with complications that may have serious consequences. Clinical and scientific interest in DDC is increasing because of the rising incidence of all conditions within the DDC spectrum, a better, although still limited understanding of the pathogenic mechanisms involved; the increasing socioeconomic burden; and the new therapeutic options being tested. The goals of treatment in DDC are symptom and inflammation relief and preventing disease progression or recurrence. The basis for preventing disease progression remains a high-fiber diet and physical exercise, although evidence is poor. Other current strategies do not meet expectations or lack a solid mechanistic foundation; these strategies include modulation of gut microbiota or dysbiosis with rifaximin or probiotics, or using mesalazine for low-grade inflammation in uncomplicated symptomatic diverticulosis. Most acute diverticulitis is uncomplicated, and the trend is to avoid hospitalization and unnecessary antibiotic therapy, but patients with comorbidities, sepsis, or immunodeficiency should receive broad spectrum and appropriate antibiotics. Complicated acute diverticulitis may require interventional radiology or surgery, although the best surgical approach (open versus laparoscopic) remains a matter of discussion. Prevention of acute diverticulitis recurrence remains undefined, as do therapeutic strategies. Mesalazine with or without probiotics has failed to prevent diverticulitis recurrence, whereas new studies are needed to validate preliminary positive results with rifaximin. Surgery is another option, but the number of acute events cannot guide this indication. We need to identify risk factors and disease progression or recurrence mechanisms to implement appropriate preventive strategies.
Gastrointestinal bleeding (GIB) is a major problem in patients on oral anticoagulation therapy. This issue has become even more pressing since the introduction of direct oral anticoagulants (DOACs) in 2009. Areas covered: Here we review current evidence related to GIB associated with oral anticoagulants, focusing on randomized controlled trials, meta-analyses, and post-marketing observational studies. Dabigatran 150 mg twice daily and rivaroxaban 20 mg once daily increase the risk of GIB compared to warfarin. The risk increase with edoxaban is dose-dependent, while apixaban shows apparently, no increased risk. We summarize what is known about GIB risk factors for individual anticoagulants, the location of GIB in patients taking these compounds, and prevention strategies that lower the risk of GIB. Expert opinion: Recently there has been an important shift in the clinical presentation of GIB. Specifically, upper GIB has decreased with the decreased incidence of peptic ulcers due to the broad use of proton pump inhibitors and the decreased prevalence of H. pylori infections. In contrast, the incidence of lower GIB has increased, due in part to colonic diverticular bleeding and angiodysplasia in the elderly. In this population, the addition of oral anticoagulation therapy, especially DOACs, seems to increase the risk of lower GIB.
Bioactive peptides secreted by probiotic Bifidobacterium longum (peptide B7) and opportunistic pathogen Bacteroides fragilis (peptide B12) modulate the intestinal cytokine milieu in health. Here, we characterized their capacity to modulate both the mucosal cytokine production and the phenotype of circulating antigen presenting cells (APCs) in active inflammatory bowel disease (IBD). The IBD mucosa produced higher levels of pro-inflammatory cytokines referred to healthy controls (HCs). Peptides B7 and B12, however, did not ameliorate the mucosal cytokine milieu in IBD. Human circulating APCs (B-cells, monocytes, plasmacytoid dendritic cells (pDCs), and conventional dendritic cells (cDCs)) were characterized by flow cytometry in presence/absence of the peptides. Circulating B-cells, monocytes, and cDCs from IBD patients were more activated than those from HCs. Peptide B7, but not B12, decreased CCR2 expression on all APC subsets from HC, but not IBD patients. Moreover, both peptides tend to further increase their pro-inflammatory profile in IBD. In summary, IBD patients display mucosal and circulating APC pro-inflammatory properties. Peptide B7 immunomodulatory capacity elicited over circulating APCs from HC, but not IBD patients, suggests the presence of disrupted modulatory mechanisms for this peptide in IBD. Future studies should address the effect of bacteria-derived immunomodulatory peptides in non-inflamed (quiescent) IBD patients.
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