Introduction

Superficial Barrett's adenocarcinoma (BAC) is a rare disease in Japan, and its clinicopathological characteristics are not well-defined. As a result, indications for endoscopic treatment have not been determined.

Aims & Methods

A histopathological study was performed to investigate whether there is a relationship between risk factors for lymph node metastasis and the mucin expression phenotypes of BAC. We conducted a retrospective analysis of a database comprising consecutive patients with superficial BAC treated by endoscopic or surgical resection. Immunohistochemical analysis was performed using the antibodies of MUC5AC, MUC6, MUC2, and CD10 to determine the classification of mucin expression phenotype.

Results

A total of 74 BAC lesions in 68 patients (54 males, median age 69 years) were identified. Mucin expression classification showed gastric (64%, complete gastric 24%, predominantly gastric 39%), intestinal (34%, complete intestinal 14%, predominantly intestinal 20%) or null (3%) phenotypes. Surgical treatment was performed in 30 patients, including additional treatment after ESD, and lymph node metastasis was observed in 4 patients (13%). Compared to the intestinal phenotype group, patients with gastric phenotype BAC had an almost significantly higher rate of lymphovascular invasion (38% vs 16%, P=0.06) and poorly differentiated component (23% vs 4%, P=0.09). All 4 lymph node metastasis-positive cases were in the gastric phenotype group (P=0.28).

Conclusion

Although our study did not show a direct relationship between the risk of lymph node metastasis and mucin expression phenotype of BAC, it did suggest BAC with gastric phenotype may be more likely to have lymphovascular invasion and poorly differentiated component. The endoscopic-specific findings of BAC with gastric phenotype are unknown. However, some specific endoscopic findings of gastric phenotype in gastric cancer are well-known, such as intralobular loop pattern or vessels within epithelial circle pattern. If we see such findings in BAC, due to a possible higher risk of lymphovascular invasion or poorly differentiated components, we should perform ESD rather than piecemeal EMR to obtain en-bloc tissue specimens for detailed pathological evaluation.

Disclosure

None

Introduction

Although the issue of post-colonoscopy colorectal cancer (PCCRC) has been widely discussed, the characteristics of overlooked Barrett's adenocarcinoma (BAC) remain unclear.

Aims & Methods

We aimed to identify the characteristics of BAC that were missed during screening gastroscopy. A retrospective review of 28 patients with superficial BAC who had undergone gastroscopy within three years prior to diagnosis was conducted. The patients were divided into two groups: “misdiagnosis of detection” (no images were appropriately taken of the area where the BAC was eventually diagnosed) and “misdiagnosis of malignancy” (the BAC was overlooked despite endoscopists having taken images of the location where the BAC eventually diagnosed).

Results

The study included 24 male patients with a mean age of 65. The interval months between endoscopy at diagnosis and the last endoscopy before diagnosis were less than 12 months (n=3, 11%), 12-23 months (n=23, 82%), and 24-36 months (n=2, 7%). Background Barrett’s esophagus was short-segment (SSBE, n=18, 64%) and long-segment (LSBE, n=10, 36%). The Paris classification of the lesions was 0-I (n=2, 7%), 0-IIa (n=13, 46%), 0-IIb (n=4, 14%), and 0-IIc (n=9, 32%). The median tumor size was 14.5mm (range 3-107). Tumor locations were located at 0-3 o’clock position (n=17, 61%), 3-6 (n= 5, 18%), 6-9 (n=2, 7%), 9-12 (n=3, 11%) and circumferential (n=1, 4%). Most cases were classified into “misdiagnosis of malignancy” (n=19, 68%). Comparing misdiagnosis of malignancy with misdiagnosis of detection groups, lesions located at the 0 to 3 o’clock position were more likely to be missed due to misdiagnosis of malignancy (15/19 vs. 3/9, P=0.03). In contrast, lesions within LSBE were more likely to be overlooked due to misdiagnosis of detection (6/9 vs. 4/19, P=0.03).

Conclusion

Our findings suggest that lesions located at the 0 to 3 o'clock position were frequently missed due to misdiagnosis as esophagitis, highlighting the importance of careful differential diagnoses between esophagitis and BAC at such sites. In contrast, most lesions within LSBE were likely missed due the lack of adequate observation. Therefore, careful observation of LSBE using all available modalities is recommended.

Introduction

A confirmed diagnosis of low-grade dysplasia (LGD) on two endoscopies is currently considered a predictor for neoplastic progression in patients with Barrett’s esophagus (BE), and, therefore, ablation therapy is offered to these patients. However, recent studies show that aberrant expression of the p53 tumor suppressor protein might be a stronger risk factor for neoplastic progression than dysplasia status.

Aims & Methods

The aim of this study was to evaluate the value of p53 expression compared to confirmed LGD in predicting neoplastic progression in BE patients. Data was analyzed from a large prospective cohort study of 1031 BE patients (73% males, median age 61 years) with index diagnosis of non-dysplastic BE (NDBE), indefinite for dysplasia (IND), and LGD. Confirmed LGD was defined as a LGD diagnosis on 2 separate occasions, each LGD diagnosis was confirmed by two pathologists. P53 immunohistochemistry staining was performed on biopsies of 1545 endoscopies from 655 (64%) patients; both overexpression and loss of expression were considered aberrant. Neoplastic progression was defined as high-grade dysplasia (HGD) and/or esophageal adenocarcinoma (EAC). Cox regression analysis was used to determine neoplastic progression risk.

Results

During a median follow-up of 8.4 (IQR 5.3-12.9) years, 68/655 (10%) patients developed HGD/EAC. Neoplastic progression was found in 20/411 (5%) NDBE patients, 25/149 (17%) patients with a single diagnosis of LGD, and 24/95 (24%) patients with confirmed LGD. P53 expression was aberrant in 28/411 (7%) NDBE patients, 50/149 (34%) single LGD patients, and 51/95 (54%) confirmed LGD patients. Aberrant p53 expression was strongly associated with an increased risk of neoplastic progression after adjusting for age, gender, segment length, esophagitis, and grade of dysplasia (HR 13.5, 95% CI 7.1-25.8). In NDBE patients, the absolute neoplastic progression risk increased from 2% with normal p53 expression to 50% with aberrant p53 expression. In patients with a single diagnosis of LGD, the progression risk increased from 6% to 35% when p53 expression was aberrant. Similar risks where found in patients with confirmed LGD, with a neoplastic progression risk of 2% with normal p53 expression and 43% with aberrant p53 expression.

Conclusion

Aberrant p53 expression is a strong predictor for neoplastic progression in BE patients. The predictive value of aberrant p53 expression is independent of the grade of dysplasia. Aberrant P53 expression may be a better parameter than (confirmed) LGD to identify patients who need close surveillance or could benefit from ablation therapy.

Introduction

Endoscopic resection (ER) is curative for Barrett’s oesophagus-related early-stage oesophageal adenocarcinoma (EAC) without high-risk features, such as lymphovascular invasion (LVI), positive margins (R1), and deep submucosal invasion (T1bsm2-3). Piecemeal endoscopic mucosal resection (pEMR), often used for lesions larger than 15mm, prevents assessment of lateral margins and therefore complicates precise risk estimation for residual EAC at the first post-ER endoscopy. Thus, we investigated alternative clinical factors that could potentially be used to assess the risk for residual and recurrent EAC post-ER.

Aims & Methods

We performed a longitudinal cohort study of patients who underwent ER between 2006-2023. Inclusion criteria were: T1a or well/moderately differentiated T1bsm1 EAC; LVI-, and R0 resection. ER was categorised as pEMR (n=105) or en-bloc ER (n=22 en-bloc EMR, n=9 endoscopic submucosal dissection). The primary outcome was residual EAC at first post-ER endoscopy. Secondary outcomes were residual HGD at first post-ER endoscopy, recurrence of EAC and HGD at any post-ER endoscopy, and remission of EAC, HGD and intestinal metaplasia (IM) at latest endoscopy. Multivariate logistic regression, receiver operating characteristics, chi-squared, and Kaplan Meier analyses were performed to investigate possible associated risk factors.

Results

The cumulative incidence of recurrence of HGD was higher post-pEMR compared to en-bloc ER (HR = 2.43, 95% CI: 1.1-5.36; p=0.021), with residual EAC at first post-ER endoscopy accounting for 35% of such post-pEMR recurrence. The percentage of pEMR specimens with EAC was an independent risk factor for residual EAC at first post-pEMR endoscopy (p=0.013, Table 1). A 53.5% cut-off of involved pEMR specimens was identified as the optimal threshold for residual EAC prediction (specificity=0.68, sensitivity=0.67, AUC=0.66). Indeed, rate of residual (p=0.013) and recurrent (p=0.00041) EAC were higher when EAC involvement was >50%.However, rates of remission of EAC (p=0.13), HGD (p=0.20) and IM (p=0.81) were unaffected by high EAC burden.

Conclusion

High burden of cancer in pEMR specimens correlates with increased risk of residual and recurrent EAC at post-pEMR endoscopy. Post-pEMR site check is recommended prior to endoscopic ablation, particularly in patients where more than 50% of pEMR specimens show EAC, where repeat ER should be performed in cases of flat subtle lesions. This will ensure eradication of any focus of residual disease and high success rates for treatment of early EAC using endotherapy.

Introduction

With the recent rise in the occurrence of esophageal adenocarcinoma (EAC) in Western nations, there is an escalating worry regarding Barrett’s esophagus (BE). In contrast, Asian countries exhibit a lower prevalence of BE compared to their Western counterparts. Given the annual increase in chronic gastroesophageal reflux disease (GERD) cases, there is an expectation of a concurrent rise in the prevalence of BE. Consequently, we are embarking on a multicenter prospective study to assess the current prevalence of BE and pinpoint its risk factors in Taiwan.

Aims & Methods

Aim: to evaluate current prevalence and risk factors of Barrett's esophagus in Taiwan.
Methods: We carried out a prospective multicenter study involving consecutive outpatients who underwent upper gastrointestinal endoscopy for various upper gastrointestinal symptoms. Biopsies were taken from endoscopically suspected esophageal metaplasia (ESEM), clearly visible at least 1 cm above the gastroesophageal junction during endoscopy. The biopsy procedure involved obtaining standardized random samples, with four pieces taken every 2 cm from the four quarters of the esophagus exhibiting the ESEM lesion. BE was defined based on the histological confirmation of specialized intestinal metaplasia in the metaplastic esophageal epithelium.

Results

A total of 8925 subjects were enrolled in this study. The prevalence of BE was 2.6%. A total of 228 subjects with BE were detected among 751 ESEM subjects. Short segment BE (78.1 % , n = 178) was more prevalent than long segment BE (22.9 % , n = 50). The prevalence of GERD symptoms, erosive esophagitis (EE), and hiatal hernia (HH) was 52.5%, 27.3% and 7.85%, respectively. Multivariate analysis disclosed that old age [odds ratio (OR) = 1.59; 95% CI, 1.20-2.11; P <0.01], male gender (OR = 2.27; 95%CI, 1.65-3.11; P < 0.01),alcohol consumption (OR = 1.70, 95%CI, 1.19-2.44; P< 0.01), GERD symptoms (OR = 1.45, 95%CI, 1.10-1.92; P< 0.01), EE (OR = 1.94, 95%CI, 1.47-2.56; P< 0.01) and presence of hiatal hernia (OR = 2.49; 95%CI, 1.78-3.47; P < 0.001) were significant risk factors predicting BE.
Risk factors for Barrett esophagus: multivariable analysis.

Conclusion

The prevalence of BE was identified as 2.6%. Notably, advanced age (>50), male gender, alcohol consumption, symptoms of gastroesophageal reflux disease (GERD), erosive esophagitis, and the presence of hiatal hernia emerged as independently significant risk factors for Barrett's esophagus.

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