Colorectal cancer(CRC)is the third most commonly diagnosed cancer in the world.The incidence and mortality show wide geographical variations.Screening is recommended to reduce both incidence and ...mortality.However,there are significant differences among studies in implementation strategies and detection.This review aimed to present the results and strategies of different screening programs worldwide.We reviewed the literature on national and international screening programs published in Pub Med,on web pages,and in clinical guidelines.CRC Screening programs are currently underway in most European countries,Canada,specific regions in North and South America,Asia,and Oceania.The most extensive screening strategies were based on fecal occult blood testing,and more recently,the fecal immunochemical test(FIT).Participation in screening has varied greatly among different programs.The Netherlands showed the highest participation rate(68.2%)and some areas of Canada showed the lowest(16%).Participation rates were highest among women and in programs that used the FIT test.Men exhibited the greatest number of positive results.The FIT test has been the most widely used screening program worldwide.The advent of this test has increased participation rates and the detection of positive results.
Peptic ulcer disease Lanas, Angel, Prof; Chan, Francis K L, MD
The Lancet (British edition),
08/2017, Volume:
390, Issue:
10094
Journal Article
Peer reviewed
Summary The rapidly declining prevalence of Helicobacter pylori infection and widespread use of potent anti-secretory drugs means peptic ulcer disease has become substantially less prevalent than it ...was two decades ago. Management has, however, become more challenging than ever because of the threat of increasing antimicrobial resistance worldwide and widespread use of complex anti-thrombotic therapy in the ageing population. Peptic ulcers not associated with H pylori infection or the use of non-steroidal anti-inflammatory drugs are now also imposing substantial diagnostic and therapeutic challenges. This Seminar aims to provide a balanced overview of the latest advances in the pathogenetic mechanisms of peptic ulcers, guidelines on therapies targeting H pylori infection, approaches to treatment of peptic ulcer complications associated with anti-inflammatory analgesics and anti-thrombotic agents, and the unmet needs in terms of our knowledge and management of this increasingly challenging condition.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
Nonsteroidal anti-inflammatory drugs (NSAIDs) can damage the gastrointestinal tract, causing widespread morbidity and mortality. Although mechanisms of damage involve the activities of ...prostaglandin-endoperoxide synthase 1 (PTGS1 or cyclooxygenase COX 1) and PTGS1 (COX2), other factors are involved. We review the mechanisms of gastrointestinal damage induction by NSAIDs via COX-mediated and COX-independent processes. NSAIDs interact with phospholipids and uncouple mitochondrial oxidative phosphorylation, which initiates biochemical changes that impair function of the gastrointestinal barrier. The resulting increase in intestinal permeability leads to low-grade inflammation. NSAID inhibition of COX enzymes, along with luminal aggressors, results in erosions and ulcers, with potential complications of bleeding, protein loss, stricture formation, and perforation. We propose a model for NSAID-induced damage to the gastrointestinal tract that includes these complex, interacting, and inter-dependent factors. This model highlights the obstacles for the development of safer NSAIDs.
Introduction: 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.
Aspirin was commercialized more than a 100 years ago. Today, this compound is still widely prescribed, and new mechanisms of action and indications are being tested. Inhibition of cyclooxygenase ...(COX)-1 and COX-2 by aspirin or its related compounds, nonsteroidal antiinflammatory drugs (NSAIDs), has been associated with both adverse and beneficial effects in the gastrointestinal (GI) tract. Inhibition of COX-1 has been linked to GI adverse effects. Adverse effects of NSAIDs and aspirin in the upper GI tract include esophagitis, peptic ulcer, peptic ulcer complications, and death. Effective preventive therapies are available that have been associated with a progressive decline in the rate of hospitalization due to upper GI complications. NSAIDs and aspirin can also damage the small bowel and the colon. NSAID enteropathy is frequent and in most cases subclinical (increased mucosal permeability, inflammation, erosion, ulcer). However, more serious clinical outcomes such as anemia, bleeding, perforation, obstruction, diverticulitis, and deaths have also been described. Prevention therapy of NSAID damage to the lower GI tract is not well defined. Inhibition of COX-2 by NSAIDs, coxibs, or aspirin seems to provide beneficial effects to the GI tract. Observational studies show that these compounds reduce the risk of both upper and lower GI cancers. Randomized controlled trials have shown that aspirin and coxibs reduce the recurrence rate of colonic polyps, and long-term cohort studies have shown that aspirin reduces the risk of colon cancer time and dose dependently. New studies will have to define the appropriate population that may benefit with these therapies.
Proton pump inhibitors(PPIs) represent a milestone in the treatment of acid-related diseases, and are the mainstay in preventing upper gastrointestinal bleeding in high-risk patients treated with ...nonsteroidal antiinflammatory drugs(NSAIDs) or low-dose aspirin. However, this beneficial effect does not extend to the lower gastrointestinal tract. PPIs do not prevent NSAID or aspirin-associated lower gastrointestinal bleeding(LGB). PPIs may increase both small bowel injury related to NSAIDs and low-dose aspirin treatment and the risk of LGB. Recent studies suggested that altering intestinal microbiota by PPIs may be involved in the pathogenesis of NSAID-enteropathy. An increase in LGB hospitalization rates may occur more frequently in older patients with more comorbidities and are associated with high hospital resource utilization, longer hospitalization, and increased mortality. Preventive strategies for NSAID and aspirin-associated gastrointestinal bleeding should be directed toward preventing both upper and lower gastrointestinal damage. Future research should be directed toward identifying patients at low-risk for gastrointestinal events associated with the use of NSAIDs or aspirin to avoid inappropriate PPI prescribing. Alternatively, the efficacy of new pharmacologic strategies should be evaluated in high-risk groups, with the aim of reducing the risk of both upper and lower gastrointestinal bleeding in these patients.
Non-steroidal anti-inflammatory drugs (NSAIDs) are one of the most widely prescribed medication in the world. Their main benefit derives from their anti-inflammatory and analgesic effect, but the use ...of these agents is not innocuous since they mainly increase the risk of gastrointestinal (GI) and cardiovascular complications compared with non-NSAID users. NSAIDs injures the upper and lower gut by depleting COX-1 derived prostaglandins and causing topical injury to the mucosa. The risk of upper GI complications varies, depending on the presence of one or more risk factors. Among them, the three main risk factors are prior history of peptic ulcer, the single most important risk factor, age, the most common, and concomitant aspirin use, due to their GI and cardiovascular implications. Those individuals at-risk should be considered for alternatives to NSAID therapy and modifications of risk factors. If NSAID therapy is required, patients at risk will need prevention strategies including co-therapy of NSAID with gastroprotectants (PPI or misoprostol) or the prescription of COX-2 selective inhibitors. The probable introduction of NO-NSAIDs in the market in the near future may open a new therapeutic option for patients with hypertension who need NSAIDs.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Refractory peptic ulcer is now a rare disease since most peptic ulcers heal with appropriate treatment with proton pump inhibitors (PPIs) and/or Helicobacter pylori eradication.
The most frequent ...cause of apparent refractoriness is lack of adherence to treatment. Persistence of H. pylori infection, use or abuse (often surreptitious) of high dose non-steroidal anti-inflammatory drugs (NSAIDs) or aspirin (ASA) are the two major causes of true refractory ulcers. There is a growing number of peptic ulcers which are not linked to either NSAIDs or H. pylori infection. Refractoriness in these ulcers can be linked to gastric acid hypersecretion, rapid PPI metabolization, ischemia, chemo-radiotherapy, immune diseases, more rarely to other drugs or be fully idiopathic. Treatment of the cause of the ulcer, if known, is essential. This review is based on pertinent publications retrieved by a selective search in PubMed, with particular attention to refractory peptic ulcer.
High-dose PPI or the new potassium competitive acid blocker or the combination of PPIs with misoprostol can be recommended in these cases. Other more experimental treatments such the topical application of platelet-rich plasma or mesenchymal stem cells have also been suggested. Surgery is the last option, but there is no guarantee of success, especially in NSAID or ASA abusers.
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.
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