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Waste manager: The police in endoscopy?

Anastasia Tsalouka 1

1 University General Hospital Attikon, Athens, Greece

Event

UEG Week Copenhagen 2023

Topics

Endoscopy Nurses

Session

Green endoscopy

Published

2023

UEG Poster

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Introduction

Patients with ulcerative colitis (UC) are at an increased risk of cytomegalovirus (CMV) infection. CMV infection in acute severe ulcerative colitis (ASUC) may worsen disease severity and clinical outcomes. Current guidelines recommend colonic biopsies for the exclusion of CMV in all patients with ASUC. One study found that CMV positivity in ASUC was associated with greater need for rescue therapy, longer hospital length of stay (LOS) and higher readmission rates but found no difference in rate of colectomy.¹ We aimed to investigate the impact of positive CMV result on clinical outcomes in patients presenting with ASUC.

Aims & Methods

A retrospective review included all ASUC presentations to a quaternary hospital over a 10-year period based on modified Truelove and Witts’ criteria. ASUC presentations were grouped based on CMV positivity as determined by colonic biopsy. Data on pre-admission medications was collected. Data was collected on rates of rescue therapy, referral to colorectal surgery, colectomy, total parenteral nutrition (TPN). Outcomes assessed included intensive care unit (ICU) admission, 30- and 90-day readmission rates, 30- and 90-day mortality rates and mean LOS.

Results

A total of 172 ASUC presentations were identified. Of these, 133 had available colonic biopsy CMV results. 11 patients (8%) had positive CMV. Positive CMV result was significantly associated with increased need for TPN (36% vs 11%, p=0.02), ICU admission (27% vs 5%, p=0.004) and referral to colorectal surgery (82% vs 43%, p=0.01). Patients with CMV had longer LOS (27.1±14.0 vs 11.0±7.4, p=0.003). There were no significant differences in rates of rescue therapy, inpatient colectomy, readmission or mortality rates. 9 of the patients (82%) were treated with ganciclovir or valganciclovir. Patients on maintenance advanced UC therapies, including biologics and small molecule inhibitors, had significantly higher rate of CMV (22% vs 5%, p=0.01). Biologic therapy alone was associated with higher rate of CMV (24% vs 7%, p=0.02), whereas small molecule inhibitor alone was not (p=0.6). Pre-admission use of 5-aminosalicylates, high dose steroids, thiopurines or combination therapies were not associated with CMV positivity.

Table 1: Comparison data of clinical outcomes in ASUC between patients with and without CMV positivity on colonic biopsy

	CMV on biopsy		p-value
	Positive	Negative
Rescue therapy (n)	7 (64%)	44 (36%)	p=0.07
TPN (n)	4 (36%)	14 (11%)	p=0.02*
Referral to colorectal surgery (n)	9 (82%)	52 (43%)	p=0.01*
Inpatient colectomy (n)	3 (27%)	14 (11%)	p=0.13
ICU admission (n)	3 (27%)	6 (5%)	p=0.004*
Readmission at 90 days (n)	4 (40%)	23 (19%)	p=0.11
Mortality at 90 days (n)	1 (9%)	2 (2%)	p=0.11
Length of stay (days)	27.1 ± 14.0	11.0 ± 7.4	p=0.003*

Conclusion

Patients with CMV positive colonic biopsies tend to require more inpatient interventions, including increased need for TPN, ICU admission, referral to colorectal surgery and longer hospital length of stay. Despite more complex admission course of ASUC patients with concurrent CMV infection, these patients were not observed to have worse outcomes than those without CMV diagnosis. Maintenance biologic and small molecule inhibitor use was associated with higher rates of CMV, reflecting the immunosuppressant effects of advanced UC therapies. CMV detection needs to be considered as a potential exacerbating factor in disease severity.

References

1. Huang D, Rennie M, Krasovec A, Nagubandi S, Liu S, Ge E, Khehra B, Au M, Sivagnanam S, Kwan V, Rogge C, Mitrev N, Kariyawasam V. Impact of cytomegalovirus on outcomes in acute severe ulcerative colitis: a retrospective observational study. Ther Adv Chronic Dis. 2024 Mar 28;15:20406223241233203. doi: 10.1177/20406223241233203. PMID: 38560721; PMCID: PMC10981253.

IMPACT OF CMV DETECTION IN COLONIC BIOPSIES ON CLINICAL OUTCOMES IN ACUTE SEVERE ULCERATIVE COLITIS

Carmen Tung 1, Michael Yulong Wu 1, Christopher John Kiely 1, Steffanie Nario 1

1 Royal North Shore Hospital, St Leonards, Australia

Conference

UEG Week Berlin 2025

Topics

IBD

Submission format

Abstract

Session

Predicting outcomes in IBD (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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Organisation of an IBD centre

Federica Furfaro 1

1 Department of Biomedical and Clinical Sciences, L. Sacco University Hospital, Milan, Milano, Italy

Event

UEG Week Copenhagen 2023

Topics

IBD Nurses Standards & Guidelines

Session

IBD nurses: All around the gut

Published

2023

UEG Presentation

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PRO-TUMORIGENIC INFLAMMATORY RESPONSE INDUCED BY ONCOSTATIN M / ONCOSTATIN M RECEPTOR Β AXIS IN NASH-RELATED HCC

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Introduction

Oncostatin M (OSM) is a pleiotropic cytokine belonging to the interleukin (IL)-6 family that acts on a large variety of cells involving two distinct heterodimeric receptor complexes: leukemia inhibitory factor receptor beta (LIFRβ) and OSM receptor beta (OSMRβ) that is the receptor able to mediate the most relevant biological effects of OSM in mice. OSM has been proposed to contribute to the progression of chronic liver diseases, hepatocellular carcinoma (HCC) development and metastasis. High levels of OSM were found in cirrhotic patients with different etiology carrying HCC. In particular we observed that OSM serum levels are significantly higher in patients carrying non-alcoholic steatohepatitis (NASH)-related HCC, as compared to those whit viral etiologies, and their increase paralleles the disease progression from simple steatosis to HCC. Noteworthy, OSM serum levels are significantly higher in patients with intermediate/advanced HCC and correlate with poor survival.

Aims & Methods

This work discusses the role of OSM in relation to the development of HCC in a NASH background. We investigated the role of OSM taking advantage of: a) cohort of NASH patients with HCC; b) human THP1 macrophage cell lines exposed to human recombinant OSM (hrOSM); c) Wild type (wt) mice fed with a control diet (CSAA) or a lipogenic diet (CDAA) for 24 weeks in order to reproduce the non-alcoholic fatty acid disease (NAFLD)/NASH pathogenic phenotype (CSAA-CDAA protocol); d) Wild type (wt) and OSMRβ knock out (OSMRβ^-/-) mice treated with a protocol of NASH-related liver carcinogenesis (DEN/CDAA protocol).

Results

In patients with NASH-related HCC, OSM is expressed in cancer cells and its expression increases with patient tumor grade. In in vitro experiments, conducted on human THP1 macrophages exposed to hrOSM, we found that OSM is able to promote an M2 pro-tumorigenic phenotype, which is due to the activation of STAT3 and PI-3K/Akt signaling pathways. Accordingly, OSM expression, which was found increased in NASH-related liver tumours of wt mice during the progression of NAFLD/NASH towards HCC, correlates with F4/80 gene expression. This data suggests an interplay between OSM and macrophages recruitment/functions in the tumor microenvironment. In particular, wt mice treated with the DEN-CDAA protocol show a stronger promotion of the M2 phenotype compared with the M1 and in these mice OSM transcript levels correlate better with M2 macrophage polarization markers. As OSMRβ is fundamental for the activation of the OSM-related STAT3 and PI-3K/Akt signaling pathways, the OSMRβ^-/-murine model was employed to exploit the role of OSM in this regard. In this respect, the data obtained in the OSMRβ^-/-murine models shows that the livers of these animals develop smaller tumours. This event appears to be due to: i) a decreased amount of M2 Tumor Associated Macrophages (TAMs) in the nodules as revealed by the reduction of transcription levels of CD163, PDL1, ARG1, CCL2 and CCR2 compared with wt mice; ii) a impairment of the angiogenic process as shown by lower transcript levels of VE-cadherin, VEGFR2 and CD105 compared with wt mice; iii) a reduction of tumor growth demonstrated by decreased levels of proliferation markers (PCNA, Ki67).

Conclusion

Experimental data highlight a pro-carcinogenic contribution for OSM in NASH, by promoting pro-tumorigenic inflammation, suggesting a possible role for the OSM/OSMRβ axis as therapeutic target for NASH-related HCC.