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IMPACT OF DIAPHRAGMATIC RELAXING INCISION ON RECURRENCE RATE AFTER PARAESOPHAGEAL HERNIA REPAIR; 1 YEAR RESULTS OF A DOUBLE-BLIND, RANDOMIZED CLINICAL TRIAL

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IMPACT OF DIAPHRAGMATIC RELAXING INCISION ON RECURRENCE RATE AFTER PARAESOPHAGEAL HERNIA REPAIR; 1 YEAR RESULTS OF A DOUBLE-BLIND, RANDOMIZED CLINICAL TRIAL

Alexandros Tsoposidis 1, Srdjan Kostic 1, Lars Lundell 2, Ville Wallenius 1, Hans Axelsson 1, Anders Thorell 3, Bengt Håkanson 3, Marcus Reuterwall Hansson 3

Affiliations

1 University of Gothenburg, Gothenburg, Sweden

2 Karolinska Institutet, Stockholm, Sweden

3 Karolinska Institutet, Stockholm, Sweden|||Ersta Hospital, Stockholm, Sweden

Summary

AI Generated

A double-blind randomized trial of 76 patients found that adding a left-sided diaphragmatic relaxing incision to standard laparoscopic paraesophageal hernia repair did not reduce anatomical recurrence rates at 12 months (54% vs 66%, p=0.313).

CT-confirmed recurrence at 12 months occurred in 54% of patients receiving the relaxing incision with mesh versus 66% in the control group receiving standard crural repair with fundoplication, a difference that was not statistically significant (p=0.313).
Both groups showed significant improvements in dysphagia, reflux, indigestion, and abdominal pain postoperatively, with no differences between groups in symptom relief or quality of life.
90-day mortality was 2.6% (2 deaths, 1 per group), with other complications including 1 mediastinal abscess and 5 patients requiring postoperative endoscopic dilatation.
Three patients in the intervention group developed asymptomatic herniation at the diaphragmatic incision site.
The authors concluded that the relaxing incision technique should not be recommended for routine use and alternative strategies to reduce paraesophageal hernia recurrence need to be explored.

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Abstract

Introduction

The optimal surgical approach to reduce recurrence rates after laparoscopic repair of paraesophageal hernia (PEH) is yet to be defined. The crural repair is challenged by both axial and transverse-lateral tension, which may compromise durability. The aim of this double-blind randomized clinical trial was to investigate whether a left-sided diaphragmatic relaxing incision in addition to standard crural repair and fundoplication reduces anatomical recurrence rates at one year postoperatively.

Aims & Methods

This study was conducted at two high-volume Swedish centers—Ersta Hospital (Stockholm) and Sahlgrenska University Hospital (Gothenburg)—between August 2019 and August 2023. Adult patients undergoing surgery for PEH were randomized 1:1 to either standard crural repair with total (360°) fundoplication (control) or the same procedure with the addition of a left-sided diaphragmatic relaxing incision covered by synthetic mesh (intervention). Patients with prior hiatal surgery, ASA class IV or above, type I hernia, major esophageal motility disorders, or any contraindication to fundoplication were excluded. Blinding for patients and assessors was maintained throughout follow-up. Pre- and postoperative assessments included computed tomography (CT), symptom questionnaires (Dakkak dysphagia score, Gastrointestinal Symptom Rating Scale [GSRS]), and quality of life (QoL, RAND-36). The primary outcome was radiologically confirmed PEH recurrence at 12 months.

Results

Of 103 patients screened, 76 were randomized (38 per group). Baseline characteristics were well balanced. CT was completed in 72 patients (95%) at 12 months. The recurrence rate was 66% in the control group and 54% in the intervention group (p=0.313). Three patients in the intervention group had asymptomatic CT verified herniation at the site of the diaphragmatic incision. There were no differences in recurrence size distribution (<4 cm vs >4 cm) between groups. Postoperative symptom assessment revealed significant improvements in dysphagia, reflux, indigestion, and abdominal pain in both groups, without intergroup differences. Physical QoL (PCS) improved significantlywhereas mental QoL (MCS) remained unchanged. Two deaths occurred within 90 days postoperatively (1 per group), yielding a 90-day mortality of 2.6%. Other complications included mediastinal abscess (n=1, intervention group) and need for postoperative endoscopic dilatation (n=5 in total). Operation time tended to be longer in the intervention group (150 vs 133 min; p=ns).

	Crural repair alone	Crural repair with relaxing diaphragmatic incision	P value
Completed CT chest at 1 year	35/38	37/38
Radiological recurrence	23 (66%)	20 (54%)	.313
Recurrence<4cm	12 (34%)	11 (30%)	.522
Recurrence>4cm	11 (31%)	9 (24%)	.457

Table 1: Radiological recurrences 1 year after surgical repair of PEH

Conclusion

In this randomized, double-blind trial, the addition of a left-sided diaphragmatic relaxing incision to standard laparoscopic PEH repair did not improve anatomical recurrence rates, symptom relief or QoL at 12 months after surgery and should not be recommended for routine use. Alternative strategies to improve recurrence rates after PEH need to be explored in the future.

Event

UEG Week Berlin 2025

Topics

Neurogastroenterology & Motility Oesophagus

Submission format

Abstract

Session

Burning issues in GERD

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Who is at risk: Is it all about anticoagulants?

Franco Radaelli 1

Affiliations

1 Valduce Hospital, Como, Italy

Summary

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Abstract

Event

UEG Week Berlin 2025

Topics

Endoscopy Radiology & Imaging

Session

Crash course: Lower GI bleeding

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Radiologic intervention

Miltiadis Krokidis 1

Affiliations

1 National and Kapodistrian University of Athens, Athens, Greece

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Abstract

Event

UEG Week Berlin 2025

Topics

Endoscopy Radiology & Imaging

Session

Crash course: Lower GI bleeding

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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JIng Li

Metabolic dysfunction-associated fatty liver disease (MASLD)

Philip Newsome

Chronic constipation (Complete Session)

UEG Presentation

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

Exploiting the immune response in GI cancer: Next chapter

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Exploiting the immune response in GI cancer: Next chapter

Tamara Matysiak-Budnik 1

Affiliations

1 CHU de Nantes IMAD, Nantes, France

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Abstract

Event

UEG Week Berlin 2025

Topics

Digestive Oncology Hepatobiliary Immunology Mechanisms & Personalised Medicine Small Intestine & Nutrition

Session

The art of making clinical research precise: What will be new in therapy in 2030?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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UEG Presentation

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

MYELOID MAS REGULATES PKM2-MEDIATED SPI1 LACTYLATION TO PROGRAM THE METABOLIC-INFLAMMATORY SENESCENCE AXIS OF MONONUCLEAR PHAGOCYTE SYSTEM DURING THE METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE (MASLD)

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MYELOID MAS REGULATES PKM2-MEDIATED SPI1 LACTYLATION TO PROGRAM THE METABOLIC-INFLAMMATORY SENESCENCE AXIS OF MONONUCLEAR PHAGOCYTE SYSTEM DURING THE METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE (MASLD)

Luying Zhao 1, Shujing Xu 1, Shikai Qiao 1, Changqing Yang 1, JIng Li 1

Affiliations

1 Tongji Hospital, Tongji University School of Medicine, Shanghai, China

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Abstract

Introduction

Metabolic dysfunction-associated steatotic liver disease (MASLD) is closely related to the metabolic syndrome of chronic liver disease and its pathogenesis involves a variety of cell types of metabolic disorders and inflammatory response, however, treatment is limited. Mas is a G protein-coupled receptor highly expressed by myeloid cells. It may play a key role in regulating myeloid-associated inflammation and metabolic homeostasis in the process of MASLD. However, its specific mechanism of action in MASLD remains unclear.

Aims & Methods

This study aims to explore the regulatory mechanism of MAS in myeloid cells in the occurrence and development of MASLD. In this study, liver tissues of patients with MASLD and animal models of MASLD induced by high-fat diet (HFD) were analyzed. In this study, myeloid-specific Mas1 knockout (Lysm^creMas1^f/f) mice were constructed. Single-cell RNA sequencing and multi-omics analysis were used to explore the role and mechanism of myeloid Mas in HFD-induced MASLD mice.

Results

The study found that the expression of MAS protein on myeloid cells in the livers of MASLD patients and MASLD animal models was significantly increased. Mononuclear phagocyte system（MPs）undergo metabolic disorders in the MASLD model, with elevated glycolysis levels, increased lactic acid production, and at the same time, the expression of cellular senescence markers (such as p16 and p21) is upregulated, and the secretion of inflammatory factors is increased. Single-cell multi-omics analysis revealed that myeloid MAS1 knockout activated the FN1⁺CCR2⁺monocytes first. Pseudo-temporal analysis showed that the FN1⁺CCR2⁺ monocytes had spatiotemporal metabolic responses with the macrophages, significantly involving the activation of glycolysis and inflammatory senescence by myeloid MAS. Non-target metabolomics of MASLD patients also revealed elevated glycolytic metabolism and increased lactic acid secretion. Mass spectrometry revealed that Mas specifically bound to the key glycolytic protein pyruvate kinase M2 (PKM2) and activated the lactylation of transcription factor Spi1-K208 site mediated by PKM2. The lactylation of Spi1-K208 promoted the transcription of senescence-associated secretory phenotype (SASP) -related proteins. Myeloid Mas1 knockout inhibited the nuclear translocation of PKM2 and blocked the lactylation of Spi1, inhibiting the transcriptional initiation of SASP. Screening of over 100,000 small molecule compounds through a virtual drug library revealed that Theaflavin 3,3'-digallate (TFDG) might reduce the protein expression of Mas and PKM2, and block the binding of the MAS-PKM2 complex. We synthesized macrophage membrane to encapsulat PLGA nanoparticles loaded with TFDG (MM@NP-TFDG) and found that MM@NP-TFDG effectively reduced the expression level of Mas-PKM2 complex protein expression in the MASLD mouse model, inhibited the glycolytic - inflammatory senescence axis of FN1⁺CCR2⁺ monocytes and macrophages, and alleviated liver inflammation and tissue damage. While the lipid deposition in the liver is reduced and the fatty acid oxidation is enhanced.

Conclusion

This study reveals that myeloid MAS1 protein participates in the occurrence and development of MASLD by regulating PKM2-mediated Spi1 lactylation and reprogramming the metabolic-inflammatory senescence axis of MPs during the process of MASLD. This discovery provides new potential targets for the treatment of MASLD patients and is expected to offer new clinical treatment strategies for MASLD patients.

Disclosure

The authors declare no conflict of interest.

Event

UEG Week Berlin 2025

Topics

Gut Microbiota Hepatobiliary Mechanisms & Personalised Medicine

Submission format

Abstract

Session

MASLD: Inflammatory mechanisms

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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UEG Presentation

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

Metabolic dysfunction-associated fatty liver disease (MASLD)

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Not sure what you can access? Learn more about account types.

Metabolic dysfunction-associated fatty liver disease (MASLD)

Philip Newsome 1

Affiliations

1 University of Birmingham, Birmingham, United Kingdom

Summary

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Summary is not available for this content yet.

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Abstract

Event

UEG Week Berlin 2025

Topics

Hepatobiliary Nurses Small Intestine & Nutrition Pancreas

Session

Mistakes in …: Hepatobiliary and pancreas

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Franco Radaelli

Radiologic intervention

Miltiadis Krokidis

Exploiting the immune response in GI cancer: Next chapter

Tamara Matysiak-Budnik

MYELOID MAS REGULATES PKM2-MEDIATED SPI1 LACTYLATION TO PROGRAM THE METABOLIC-INFLAMMATORY SENESCENCE AXIS OF MONONUCLEAR PHAGOCYTE SYSTEM DURING THE METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE (MASLD)

JIng Li

Metabolic dysfunction-associated fatty liver disease (MASLD)

Philip Newsome

Chronic constipation (Complete Session)

UEG Presentation

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Not sure what you can access? Learn more about account types.

Chronic constipation (Complete Session)

Summary

AI Generated

Summary is not available for this content yet.

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Thanks for your feedback.

Abstract

Event

UEG Week Berlin 2025

Topics

Primary Care

Session

Chronic constipation

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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