Introduction

Colorectal cancer (CRC) risk is increased in patients with long-standing colitis related to Inflammatory Bowel Disease (IBD). A higher frequency of mucinous and signet-ring colonic adenocarcinoma has been suggested in IBD, but risk factors for these histotypes of CRC are undefined.

Aims & Methods

Primary aim was to compare the frequency of mucinous and signet-ring adenocarcinoma in patients with vs without IBD. Secondary aims were to search for IBD-related risk factors for signet ring and mucinous adenocarcinoma and to compare the localization of these histotypes of CRC in patients with vs without IBD. From January 2002 to January 2023, all IBD patients with concomitant colorectal adenocarcinoma (Cases) were retrospectively enrolled. Each Case was matched with 2 patients with CRC and no IBD (Controls) for age at CRC diagnosis (±5 years). Inclusion criteria for Cases and Controls: 1) age ≥18; 2) well-defined diagnosis of CRC. Additional inclusion criteria for Cases: well-defined diagnosis of IBD, classified according to standard criteria. Exclusion criteria: Missing histological and surgical report. Data were expressed as median [range]. Student-t Test and χ2 test were used for comparisons. Univariate logistic regression model was applied for assessing risk factors for mucinous and signet-ring CRC (OR [95%CI]).

Results

The study population included 120 patients with colorectal adenocarcinoma: 40 IBD patients and 80 non-IBD Controls. CRC in the 40 IBD patients occurred in 24 (60%) patients with Ulcerative Colitis (UC) and in 16 (40%) with Crohn’s Disease (CD). In patients with CRC, no differences were observed between IBD and non-IBD Controls in terms of gender (F) (13 [32.5%] vs 35 [43.7%]; p=0.32) and median age at diagnosis of CRC (54 [29-80] vs 58 [31-83] years; p=0.19). CRC in IBD was histologically defined as mucinous/ signet-ring in 17 (42.5%) and standard adenocarcinoma in 23 (57.5%) patients. Mucinous/signet ring CRC more frequently occurred in patients with IBD vs non-IBD Controls (17 [42.5%] vs 18 [22.5%], p=0.03). In IBD patients, rectal localization of CRC was significantly more frequent in mucinous/signet-ring vs standard CRC (4 [17.4%] vs 8 [47.1%]; p=0.04). In stricturing CD, there was a significantly higher frequency of standard vs mucinous/signet-ring CRC (7 [77.8%] vs 1 [14.4%]; p=0.04). Other IBD characteristics did not differ in relation to the 2 CRC histotypes, including gender (F): 8 [34.8%] vs 5 [29.4%]; p=0.98 and IBD duration at CRC diagnosis (14 [1-45] vs 17 [1-36]; p=0.74). In IBD, CRC stage at diagnosis was comparable between patients with standard vs mucinous/signet-ring CRC (stage I: 6 [26.1%] vs 1 [5.9%]; p=0.21; II: 9 [39.1%] vs 4 [23.5%]; p=0.48; III: 5 [21.7%] vs 7 [41.2%]; p=0.71; IV: 3 [13.1%] vs 5 [29.4%]; p=0.37)). At univariate analysis, no IBD-related risk factors for mucinous/signet-ring CRC were detected.

Conclusion

In the tested cohort, mucinous and signet-ring adenocarcinoma was more frequently observed in IBD than in non-IBD controls, although no IBD-related risk factors were identified. A higher frequency of rectal involvement is suggested for mucinous/signet-ring vs standard adenocarcinoma in IBD.

Introduction

Effective colorectal cancer prevention relies on the quality of screening colonoscopy examinations. Cecal withdrawal time is significantly associated with adenoma detection rate (ADR), which is an established quality indicator for screening colonoscopy. Therefore, we introduced a real-time cecal withdrawal timer (CWT) that alerts the physician of the elapsed time since cecal intubation.

Aims & Methods

An observational, retrospective, single-center study to evaluate CWT in screening colonoscopy tests. The CWT is activated by a vocal command when the physician achieves cecal intubation. Following activation, the elapsed time is audio-announced every minute until the end of the procedure. The ADR of colonoscopies with and without the CWT was evaluated following CWT implementation from January 2023 to February 2024. Moreover, the ADR of the entire department in this period was compared with the year before.

Results

Of 1,557 colonoscopies between January 2023 and February 2024, 908 (58.3%) were performed with the CWT with a median withdrawal time of 8.75 (IQR: 6.9-12.0) minutes. During this period, the CWT usage was greater than 50% in 11 out of 14 months. Considering only months with CWT usage over 50%, the ADR of colonoscopies with CWT was 28.3% compared to 19.2% in those without (p<0.001). Among physicians who performed at least 20 tests with and 20 tests without the CWT, 6 out of 8 demonstrated improved ADR with the cecal timer. Notably, the 2 physicians who did not improve ADR had baseline ADR exceeding 30%. The overall ADR of the department between January 2023 and February 2024 was 25.5%, compared to 26.2% in 2022 (p=0.704).

Conclusion

Initial findings of the CWT program suggest its potential in enhancing screening colonoscopy quality indicators, although long-term prospective follow-up is warranted.

Disclosure

Nothing to declare

Introduction

Complete endoscopic resection and accurate histological evaluation for T1 colorectal cancer (CRC) is critical to determine subsequent treatment. Endoscopic full-thickness resection (EFTR) and endoscopic submucosal dissection (ESD) are potential curative methods for treatment of T1 CRC.

Aims & Methods

Primary aims were R0 resection rate, histopathological risk-assessment, and curative resections. Secondary aims were short-term outcomes of patients with T1 CRC after endoscopic and surgical resection.
​Consecutive EFTR and ESD procedures for T1 CRC at one tertiary endoscopic centre, prospectively recorded in National CRC Registry between 2015 and 2023, were retrospectively analysed. High risk factors included positive resection margin, low-grade differentiation (G3, G4), deep submucosal invasion (DSI) and lymphovascular invasion (LVI).

Results

We analysed 178 procedures: 114 (64 %) ESD and 64 (36 %) EFTR. From all resected lesions, 24 (13 %) were T1 carcinomas, 10 (6 %) subepithelial lesions (GIST/NET), 9 (5 %) T2 carcinomas, 2 (1%) T3 carcinomas, 58 (33 %) intramucosal carcinomas and 75 (42 %) low-grade adenomas. From 24 T1 CRC (54 % men, average diameter of lesion 25 mm) were 15 (63 %) lesions resected by EFTR, 7 (29 %) lesions resected by ESD, and 2 (8 %) lesions resected by hybrid technique ESD/EFTR. Overall R0 resection was achieved in 18 (75 %) lesions. Seven (29 %) T1 CRC had superficial submucosal invasion (≤ 1000µm), 17 (71 %) T1 CRC had deep submucosal invasion, including 1 lesion with lymphovascular invasion. Curative resection rate for resected T1 CRC was 29 % and 71 % after excluding deep submucosal invasion as a risk factor. Additional oncologic surgery was performed in 9 (38 %) patients, with residual cancer in 1 patient. Endoscopic follow-up was available in 22 (92 %) patients with a median of 3 years and no residual cancer were observed.

Conclusion

EFTR and ESD techniques are effective methods for treatment T1 CRC. Appropriate surveillance without additional surgery may be considered as another option in selected cases after endoscopic resection of T1 CRC.
Supported by programme projects of the Ministry of Health of the Czech Republic with Reg. No. NU22-08-00424, Reg. No. NV18-08-00246, DZVRO - MO1012 and Cooperatio.

Introduction

Primary sclerosing cholangitis (PSC) is an idiopathic cholestatic disease. Recent genome-wide studies (GWAS) have identified about 30 disease susceptible genes to PSC. We investigated the expression profiles of these genes in the liver biopsy samples of the patients with PSC, and revealed that the expression of TNFRSF14, which is a one of the risk genes for PSC, was upregulated in the biliary epithelial cell (BEC) of PSC compared to that in normal liver tissue and primary biliary cholangitis (PBC) liver tissue. TNFRSF14 is a member of the tumor necrosis factor receptor superfamily associated with inflammation and fibrosis. We also clarified that the expression of LIGHT, an active ligand for TNFRSF14, was elevated in the BEC of PSC^１). These molecules are mainly expressed on lymphocytes, and in other inflammatory diseases, many reports have mentioned to the associations between these molecules in the sera and the disease progression.

Aims & Methods

Aims: In this study, we aimed to evaluate the concentrations of these molecules in the sera and bile of PSC.
Methods: The concentrations of soluble TNFRSF14 and LIGHT in the sera and bile were measured by enzyme-linked immunosorbent assay. The samples were collected from the following cases:
• Serum: 73 patients with PSC, 35 patients with PBC and 53 healthy controls.
• Bile: 15 patients with PSC, 12 patients with malignant biliary obstruction (MBO), 19 patients with biliary lithiasis (BL).
The bile samples were obtained during endoscopic retrograde cholangiopancreatography. The median values of the serum (s) and bile (b) concentrations of each group were evaluated by Mann-Whittney U test.

Results

sTNFRSF14 in the PSC group was significantly higher than those in the healthy controls (6.301 v.s. 4,247 pg/mL, P < 0.001) and the PBC group (4,987 pg/mL, P < 0.001).
sLIGHT in the PSC group was 87 pg/mL, which was higher than those in the healthy controls (61 pg/mL, P = 0.012), and was comparable to those in the PBC group (106 pg/mL, P = 0.142).
bTNFRSF14 in the PSC group was 2,005 pg/mL, showing no significant difference compared to those in the MBO (1,794 pg/mL, P = 0.516) and the BL group (1,987 pg/mL, P = 0.504).
bLIGHT in the PSC group was 523 pg/mL, remarkably higher than those in the MBO (82 pg/mL, P < 0.001) and the BL group (268 pg/mL, P = 0.024).

Conclusion

sTNFRSF14 in the PSC group was higher than those in the healthy control and the PBC group, and this result was equivalent to the previous report about the upregulated expression in the liver biopsy samples. While soluble LIGHT was secreted non-specifically in the sera of cholestatic liver disease, the elevated bile concentration of LIGHT can be involved in in the unique biology of PSC. ​Further research is needed to elucidate the involvement of these two molecules in the pathogenesis of PSC.

References

1) Digestive Liver Disease 2024 Feb;56(2):305-311.