Tumor size discrepancy between endoscopic and pathological evaluations in colorectal endoscopic submucosal dissection

BACKGROUND Tumor size impacts the technical difficulty and histological curability of colorectal endoscopic submucosal dissection(ESD);however,the preoperative evaluation of tumor size is often different from histological assessment.Analyzing influential factors on failure to obtain an accurate tumor size evaluation could help prepare optimal conditions for safer and more reliable ESD.METHODS This was a retrospective study conducted at a single institution.A total of 377 lesions removed by colorectal ESD at our hospital between April 2018 and March 2022 were collected.We first assessed the difference in size with an absolute per-centage of the scaling discrepancy.Subsequently,we compared the clinicopatho-logical characteristics of the correct scaling group(>-33%and<33%)with that of the incorrect scaling group(<-33%or>33%),which was further subdivided into the underscaling group(-33%or less of the discrepancy)and overscaling group(33%or more of the discrepancy),respectively.As secondary outcome measures,parameters on size estimation were compared between the underscaling and correct scaling groups,as well as between the overscaling and correct scaling groups.Finally,multivariate analysis was performed in terms of the following relevant parameters on size estimation:Pathological size,location,and possible influential factors(P<0.1)in the univariate analysis.RESULTS The mean of absolute percentage in the scaling discordance was 21%,and 91 lesions were considered to be incorrectly estimated in size.The incorrect scaling was significantly remarkable in larger lesions(40 mm vs 28 mm;P<0.001)and less experience(P<0.001),and these two factors were influential on the underscaling(75 lesions;P<0.001).Conversely,compared with the correct scaling group,16 lesions in the overscaling group were significantly small(20 mm vs 28 mm;P<0.001),and the small lesion size was influential on the overscaling(P=0.002).CONCLUSION Lesions indicated for colorectal ESD tended to be underestimated in large tumors,but overestimated in small ones.This discrepancy appears worth understanding for optimal procedural preparation.

Protein-losing enteropathy caused by a jejunal ulcer after an internal hernia in Petersen's space: A case report

BACKGROUND The incidence of internal hernias has recently increased in concordance with the popularization of laparoscopic surgery.Of particular concern are internal hernias occurring in Petersen's space,a space that is surgically created after treatment for gastric cancer and obesity.These hernias cause devastating sequelae,such as massive intestinal necrosis,fatal Roux limb necrosis,and superior mesenteric vein thrombus.In addition,protein-losing enteropathy(PLE)is a rare syndrome involving gastrointestinal protein loss,although its relationship with internal Petersen’s hernias remains unknown.CASE SUMMARY A 75-year-old man with a history of laparotomy for early gastric cancer developed Petersen's hernia 1 year and 5 mo after surgery.He was successfully treated by reducing the incarcerated small intestine and closure of Petersen’s defect without resection of the small intestine.Approximately 3 mo after his surgery for Petersen’s hernia,he developed bilateral leg edema and hypoalbuminemia.He was diagnosed with PLE with an alpha-1 antitrypsin clearance of 733 mL/24 h.Double-balloon enteroscopy revealed extensive jejunal ulceration as the etiology,and it facilitated minimum bowel resection.Pathological analysis showed extensive jejunal ulceration and collagen hyperplasia with nonspecific inflammation of all layers without lymphangiectasia,lymphoma,or vascular abnormalities.His postoperative course was unremarkable,and his bilateral leg edema and hypoalbuminemia improved after 1 mo.There was no relapse over the 5-year follow-up period.CONCLUSION PLE and extensive jejunal ulceration may occur after Petersen's hernia.Doubleballoon enteroscopy helps identify and resect these lesions.

Clinical significance of programmed cell death-ligand expression in small bowel adenocarcinoma is determined by the tumor microenvironment

BACKGROUND Comprehensive genomic analysis has shown that small bowel adenocarcinoma(SBA)has different genomic profiles from gastric and colorectal cancers.Hence,it is essential to establish chemotherapeutic regimens based on SBA characteristics.The expression of programmed cell death-ligand 1(PD-L1)and programmed cell death-ligand 2(PD-L2)in SBA is not fully understood.Anti-PD-L1/PD-1 therapy uses tumor-infiltrating lymphocytes(TILs);therefore,the status of TILs in the tumor microenvironment(TME)may influence their efficacy.The ratio of FoxP3+to CD8+T cells has been reported to be useful in predicting the prognosis of digestive system cancers.AIM To investigate the clinicopathological significance of PD-L1/2 expression according to the status of TILs in SBA tissues.METHODS We performed immunohistochemical analysis for PD-L1,PD-L2,CD8,FoxP3,and DNA mismatch repair(MMR)proteins using formalin-fixed,paraffin-embedded tissues from 50 patients diagnosed with primary SBA.The immunoreactivities of PD-L1 and PD-L2 were determined separately in tumor cells and tumor-infiltrating immune cells throughout the tumor center and invasive margins,and finally evaluated using the combined positive score(CPS).We assessed CD8+and FoxP3+T cells in the intratumoral and tumor-surrounding stroma.Subsequently,we calculated and summed the ratio of FoxP3 to CD8+T cell counts.Immune-related cell densities were graded as low or high.Immunohistochemical results were compared with clinicopathological factors and patient prognosis.The distribution of cancer-specific survival(CSS)was estimated using the Kaplan–Meier method,and the log-rank test was used to test for significant differences in CSS.A Cox proportional hazard model was also used to assess the effect of tumor variables on CSS.RESULTS PD-L1 expression was positive in 34%in tumor cells(T-PD-L1)and 54%in tumor-infiltrating immune cells(I-PDL1)of the cases examined.T-PD-L2 was positive in 34%and I-PD-L2 was positive in 42%of the cases.PD-L1 CPS≥10 and PD-L2 CPS≥10 were observed in 50%and 56%of the cases,respectively.Deficient MMR(dMMR)was 14%of the cases.T-PD-L1,I-PD-L1 and PD-L1 CPS≥10 were all significantly associated with dMMR(P=0.037,P=0.009,and P=0.005,respectively).T-PD-L1,I-PD-L1,and PD-L1 CPS≥10 were all associated with deeper depth of invasion(P=0.001,P=0.024,and P=0.002,respectively).I-PD-L2 expression and PD-L2 CPS≥10 were significantly higher in the differentiated histological type(P=0.015 and P=0.030,respectively).The I-PD-L1 and IPD-L2 levels were significantly associated with better CSS(P=0.037 and P=0.015,respectively).CD8-high was significantly associated with less lymph node metastasis(P=0.047),less distant metastasis(P=0.024),less peritoneal dissemination(P=0.034),and earlier TNM stage(P=0.047).The CD8-high group had better prognosis than the CD8-low group(P=0.018).FoxP3 expression was not associated with any clinicopathological factors or prognosis.We found that patients with PD-L2 CPS≥10 tended to have worse prognosis in the FoxP3/CD8-low group(P=0.088).CONCLUSION The clinicopathological significance of PD-L1/2 expression may differ depending on the TME status.Immune checkpoint inhibitors may improve the prognosis of SBA patients with low FoxP3/CD8 ratio and PD-L2 expression.

Risk factors for small intestinal adenocarcinomas that are common in the proximal small intestine

The frequency of primary small intestinal adenocarcinoma is increasing but is still low.Its frequency is approximately 3%of that of colorectal adenocarcinoma.Considering that the small intestine occupies 90%of the surface area of the gastrointestinal tract,small intestinal adenocarcinoma is very rare.The main site of small intestinal adenocarcinoma is the proximal small intestine.Based on this characteristic,dietary animal proteins/lipids and bile concentrations are implicated and reported to be involved in carcinogenesis.Since most nutrients are absorbed in the proximal small intestine,the effect of absorbable intestinal content is a suitable explanation for why small intestinal adenocarcinoma is more common in the proximal small intestine.The proportion of aerobic bacteria is high in the proximal small intestine,but the absolute number of bacteria is low.In addition,the length and density of villi are greater in the proximal small intestine.However,the involvement of villi is considered to be low because the number of small intestinal adenocarcinomas is much smaller than that of colorectal adenocarcinomas.On the other hand,the reason for the low incidence of small intestinal adenocarcinoma in the distal small intestine may be that immune organs reside there.Genetic and disease factors increase the likelihood of small intestinal adenocarcinoma.In carcinogenesis experiments in which the positions of the small and large intestines were exchanged,tumors still occurred in the large intestinal mucosa more often.In other words,the influence of the intestinal contents is small,and there is a large difference in epithelial properties between the small intestine and the large intestine.In conclusion,small intestinal adenocarcinoma is rare compared to large intestinal adenocarcinoma due to the nature of the epithelium.It is reasonable to assume that diet is a trigger for small intestinal adenocarcinoma.