Low-grade dysplasia in Barrett's esophagus has a high risk of progression

Lim, C. H.; Treanor, Darren; Dixon, M. F.; Axon, A. T. R.

doi:10.1055/s-2007-966592

Cited by 93 publications

(65 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…If physicians are unable to accurately identify which patients with LGD will go on to develop HGD or EAC, surely intervention should be an option that is considered? Although most deaths are not cancer-related, a significant number of patients with LGD develop esophageal cancer [38] , which in itself is associated with significant morbidity and burden to both the patient and the healthcare system.…”

Section: Esophageal Adenocarcinomamentioning

confidence: 99%

Low grade dysplasia in Barrett’s esophagus: Should we worry?

Jagadesham

2014

WJGP

View full text Add to dashboard Cite

The optimal management for low-grade dysplasia (LGD) in Barrett's esophagus is unclear. In this article the importance of LGD is discussed, including the significant risk of progression to esophageal adenocarcinoma. Endoscopic surveillance is a management option but is plagued by sampling error and issues of suboptimal endoscopy. Furthermore endoscopic surveillance has not been demonstrated to be cost-effective or to reduce cancer mortality. The emergence of endoluminal therapy over the past decade has resulted in a paradigm shift in the management of LGD. Ablative therapy, including radiofrequency ablation, has demonstrated promising results in the management of LGD with regards to safety, cost-effectiveness, durability and reduction in cancer risk. It is, however, vital that a shareddecision making process occurs between the physician and the patient as to the preferred management of LGD. As such the management of LGD should be "individualised." Core tip: Low-grade dysplasia (LGD) in Barrett's esophagus (BE) is an important entity and poses a significant risk of progression to esophageal adenocarcinoma. With the emergence of endoluminal therapy over the past decade there has been a paradigm shift in the management of LGD. Ablative therapy, such as radiofrequency ablation, has demonstrated promising results in the management of LGD with regards to safety, costeffectiveness, durability and reduction in cancer risk. It is, however, critical that management should be through a shared-decision making process and "individualised". It is our belief that physicians should "worry " about LGD in BE.Jagadesham VP, Kelty CJ. Low grade dysplasia in Barrett's esophagus: Should we worry? World J Gastrointest Pathophysiol 2014; 5(2): 91-99 Available from:

show abstract

Section: Esophageal Adenocarcinomamentioning

confidence: 99%

Low grade dysplasia in Barrett’s esophagus: Should we worry?

Jagadesham

2014

WJGP

View full text Add to dashboard Cite

show abstract

“…As mentioned earlier, the definition of dysplasia is fraught with difficulties and without a well-defined uniform natural history compounded by widely varying risk estimates for progression to cancer of 0.6-1.6% [Lim et al 2007;Sharma et al 2006b;Dulai et al 2005;Shaheen et al 2000]. Therefore, it is difficult to be definite about ablative therapy in this group at this time although it in the future it can be considered as a therapeutic option especially if the high-risk population of progressors could be identified.…”

Section: Low-grade Dysplastic Barrett's Oesophagusmentioning

confidence: 99%

“…The reasons include poor interobserver correlation (reactive changes due to oesophagitis versus LGD), biopsy sampling error and regression of LGD as a result of immunosurveillance [Sharma et al 2004[Sharma et al , 2006bRajendra and Robertson, 2010]. Some authorities have estimated the incidence of OA in LGD to be between 1.7% and 14.6% per annum [Fleischer et al 2010] based on meta-analysis [Wani et al 2009] and individual studies [Skacel et al 2000;Gatenby et al 2009;Lim et al 2007;Veith, 2007]. Nevertheless, in a large multicentre study conducted by one of the authors (PS) revealed that the incidence of OA among patients with Barrett's LGD was even lower at 0.6% per year [Sharma et al 2006b].…”

Section: Introductionmentioning

confidence: 99%

Management of Barrett’s oesophagus and intramucosal oesophageal cancer: a review of recent development

Rajendra

2012

Therap Adv Gastroenterol

View full text Add to dashboard Cite

Barrett’s oesophagus is the most important and recognizable precursor lesion for oesophageal adenocarcinoma, which is the one of the fastest growing cancers in the Western World. The incidence of oesophageal adenocarcinoma has increased 600% in the United States between 1975 and 2001 and is thought to represent a real increase in burden rather than a result of histologic or anatomical misclassification or overdiagnosis. Thus, the cancer risk in Barrett’s oesophagus has to be managed and involves prevention (surveillance endoscopy), treating underlying gastroesophageal reflux disease (medically and or surgically) and endoscopic therapy to remove diseased epithelium in appropriate patient subgroups. In the last decade, new developments in imaging and molecular markers as well as an armamentarium of novel and effective endoscopic eradication therapy has become available to the endoscopist to combat this exponential rise in oesophageal adenocarcinoma. Paradoxically, the cancer risk in Barrett’s oesophagus gets progressively downgraded which raises fundamental questions about our understanding of the known and unknown risk factors and molecular aberrations that are involved in the Barrett’s metaplasia–dysplasia–carcinoma sequence. Future research has to be directed at these areas to fine tune our screening and surveillance programs to identify more accurately the high-risk group of progressors to oesophageal adenocarcinoma who would benefit most from endoscopic therapy.

show abstract

“…In the study of cost-effectivity in patients with BE, it was found that the rate of disease progression should be over 0.5% in order to make endoscopic surveillance at a frequency under 5 years (36). Although the annual progression rate of BE without dysplasia to HGD/EAC is demonstrated at different rates in studies, there is no study that shows it to be more than 0.5% (7,18,(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48). Considering the additional risk factors such as Prague M>3, male gender, Caucasian race, advanced age, smoking history, and central obesity, it is assumed that endoscopic surveillance should be made in BE patients who do not have dysplasia due to the low rate of progression at 3-5-year intervals by taking a decision particular to the patient's characteristics.…”

mentioning

confidence: 99%

“…The annual progression rate from LGD to HGD/EAC occurred in a wide range between 1.1% and 12.8% in different studies (7,8,(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50). Considering the annual progression rate, annual surveillance is recommended in BE with LGD.…”

mentioning

confidence: 99%

How should we describe, diagnose and observe the Barrett's esophagus?

Akın¹,

Aydın²

2017

Turk J Gastroenterol

View full text Add to dashboard Cite

A universal consensus on the definition Barrett's esophagus (BE) has not been achieved yet. Different definitions were made in the British Society of Gastroenterology (BSG) 2013 and American Gastroenterological Association (AGA) 2011 guidelines (1,2). With reference to the former, while the presence of any columnar epithelium between the gastroesophageal junction and squamocolumnar junction (fundic, cardiac, or specialized intestinal metaplasia (SIM)) is sufficient for the diagnosis of BE. The presence of SIM is required for the diagnosis, according to AGA 2011.There are some retrospective studies showing that cardiac-or fundic-type columnar epithelium is precancerous at the same rate with SIM (3,4). In addition, it was put forward in published histochemical and genetic studies that SIM and the other two columnar epithelia showed similar DNA abnormalities and the other columnar epithelia showed intestinal differentiation like SIM. A conclusion was made that the other columnar epithelia were a precursor lesion for SIM (5,6). However, population-based cohort studies with large numbers of patients have revealed that SIM-positive patients carry a much greater risk than SIM-negative patients in terms of the development of LGD, HGD, and esophagus adenocarcinoma (EAC) (7-9). While the annual progression rate to the EAC of SIM-positive patients was 0.24% in the analyses performed in this study, this rate was found to be 0.04% in SIM-negative patients. These results indicate that the presence of SIM is necessary for the diagnosis of BE.On the other hand, the definition of BE should be disassociated from the concept of irregular Z-lines. An ir- S26 ABSTRACT Barrett's esophagus (BE) is one of the major complications of gastroesophageal reflux disease (GERD) commonly encountered in gastroenterology clinics. A consensus has not been achieved yet with respect to the definition of BE in published guidelines. It is advised to use the Prague classification and not to use the definition of short and long segments for the endoscopic standardization of BE. Undertaking biopsies with white-light endoscopy from each of the 4 quadrants at 2-cm intervals is the standard method for the diagnosis of BE. Because of the ability to perform targeted biopsies, the available data indicate that advanced endoscopic techniques may reduce the number of biopsies needed for diagnoses. In the presence of severe esophagitis along with BE, the biopsies should be taken after 8 weeks of PPI therapy. The evidence values of the suggestions about the surveillance requirements and surveillance frequencies are low because the available data mostly rely on retrospective studies. We suggest that all the patients with BE should be referred to specialized centers for surveillance in Turkey. Considering the additional risk factors of the patient, endoscopy surveillance intervals of the patients with BE without dysplasia should be in a range of 3-5 years and annual surveillance should be made in BE with low-grade dysplasia. In the presence of BE with high-grade dysp...

show abstract

Low-grade dysplasia in Barrett's esophagus has a high risk of progression

Abstract: Patients diagnosed with LGD during surveillance of Barrett's esophagus are at a considerably increased risk of progressing to develop esophageal cancer over an 8-year period but most deaths are not cancer-related.

Cited by 93 publications

References 18 publications

Low grade dysplasia in Barrett’s esophagus: Should we worry?

Low grade dysplasia in Barrett’s esophagus: Should we worry?

Management of Barrett’s oesophagus and intramucosal oesophageal cancer: a review of recent development

How should we describe, diagnose and observe the Barrett's esophagus?

Contact Info

Product

Resources

About