Introduction

Musculoskeletal disorders (MSDs) are the leading cause of occupational disease and represent a major public health concern. Endoscopy plays a central role in hepatogastroenterology, and its practice is associated with a high prevalence of MSDs, ranging from 40% to 90% among endoscopists. The increasing complexity of endoscopic procedures may further exacerbate musculoskeletal strain on practitioners. However, few studies have been conducted on this topic, and most rely on observational and self-reported data, limiting their level of evidence. Quantitative studies assessing the impact of digestive endoscopy, particularly endoscopic retrograde cholangiopancreatography (ERCP), on MSD risk under real working conditions remain scarce.

Aims & Methods

To obtain objective and reliable data, we used the KIMEA tool, which analyzes an operator’s movements by generating a digital twin based on data collected through a depth camera and wrist-mounted sensors. This system allows for an objective assessment of musculoskeletal strain by estimating MSD risk using the Rapid Upper Limb Assessment (RULA) method. Our study was conducted on two experienced endoscopists performing a total of 10 ERCP procedures.

Results

Motion analysis revealed an average global RULA score of 4.2, indicating a moderate risk of MSDs. Musculoskeletal strain was predominantly observed in the forearms, particularly in the wrists, which remained in constrained postures for more than 50% of the procedure time. The musculoskeletal load was asymmetrical, with greater strain on the left side. These findings were consistent across all 10 procedures.

Conclusion

Discussion: This study confirms the significant musculoskeletal strain on the upper limbs during ERCP procedures. Our findings align with existing literature. The KIMEA tool appears to be a suitable method for analyzing movements in digestive endoscopy and represents a methodological advancement for the objective evaluation of musculoskeletal strain in this field.
Conclusion: Motion analysis using the KIMEA tool provides objective evidence that ERCP practice poses a risk for MSD development. Further studies with larger sample sizes are needed to strengthen the level of evidence, assess the impact of factors such as age, experience, gender, and procedure type, and promote the integration of ergonomic measures into endoscopic practice to reduce MSD risk.

Clinical Case Summary

A 69-year-old male presented with dysphagia, food regurgitation, weight loss, and halitosis with a 12-month evolution. An upper endoscopy revealed, at 32 cm from the dental arch, a large food bolus impacted in an area consistent with a large esophageal diverticulum (Figure 1), along with isolated esophageal contractions suggestive of tertiary contractions. A barium swallow study confirmed a distal esophageal diverticulum measuring 6x5 cm (Figure 2). Subsequently, a chest CT scan showed the diverticulum with a large amount of food content inside (Figure 3). High-resolution esophageal manometry (HRM) demonstrated a hypercontractile pattern of the esophageal body in more than 20% of swallows, consistent with a diagnosis of hypercontractile esophagus or Jackhammer esophagus (Figures 4 and 5). Due to the symptoms and the size of the diverticulum, thoracoscopic diverticulectomy was performed, with favorable outcomes.
Esophageal diverticulum are uncommon, with a reported prevalence of 0.06% to 4%. In the case of hypercontractile esophagus, a pulsion mechanism is involved, with mucosal and submucosal protrusion secondary to increased intraesophageal pressure. HRM is useful for diagnosing underlying and triggering motility disorders, as well as guiding therapeutic decisions. Management should be individualized and may range from peroral endoscopic myotomy (POEM) to laparoscopic or open surgery.

References

Figure 1. Endoscopic view of the esophageal diverticulum. A: esophageal lumen. B: diverticular lumen with food bolus inside.

Figure 2. Barium swallow study showing an epiphrenic esophageal diverticulum with a 1 cm diverticular neck.

Figure 3. Chest computed tomography showing a large esophageal diverticulum with food content and an air-fluid level. A: sagittal view. B: axial view.

Figure 4. High-resolution manometry: hypercontractile contraction pattern (Distal Contractile Integral -DCI- >8000 mmHg·s·cm). Horizontal notch in the wave contour (arrow) corresponding to the diverticular neck.

Figure 5. Image of the resected diverticulum compared with a standard surgical scissor (18 cm long).

Introduction

Chronic liver disease—including alcoholic liver disease (ALD), metabolic dysfunction-associated steatotic liver disease (MASLD), and liver fibrosis/cirrhosis (LFC)—has emerged as a major global health challenge, accounting for over 2 million deaths annually^1-2. Often progressing silently, chronic liver disease is frequently diagnosed at advanced stages, underscoring the urgent need for early identification of at-risk populations through reliable markers³. While recognized risk factors such as insulin resistance, alcohol overuse, and aging contribute to disease development, recent attention has focused on biological ageing acceleration (BioAgeAccel) as a comprehensive, integrative metric reflecting physiological decline, yet the utility in large populations remains underexplored^4-6. In parallel, genetic susceptibility and phenotypic data hold promise for identifying individuals predisposed to chronic liver disease⁷.

Aims & Methods

We conducted research to explore the association between BioAgeAccel, the risk of chronic liver diseases, incorporating genetic susceptibility.

This study included participants from the UK Biobank (UKB) and the All of Us (AoU) two cohort databases. BioAgeAccel was defined as the deviation between an individual’s phenotypic age (PhenoAge) or Klemera-Doubal age (KDMAge) and chronological age. Cox proportional hazards models analyzed the associations between BioAgeAccel and the risk of MASLD, ALD, and LFC, with hazard ratios (HRs) and 95% confidence intervals (CIs), and combined polygenic risk scores (PRS) to quantify genetic predisposition to chronic liver diseases.

Results

In the UKB cohort, accelerated PhenoAge was associated with significantly higher risks of ALD (HR 2.29; 95% CI 2.03-2.58), MAFLD (1.10; 1.04-1.16), and LFC (2.22; 2.01-2.46). Similarly, in the AoU cohort, accelerated PhenoAge was associated with higher risks of ALD (1.97; 1.00-3.88), MAFLD (1.35; 1.15-1.58), and LFC (2.19; 1.48-3.22). Comparable trends were observed for KDMAgeAccel in the UKB. Greater BioAgeAccel was associated with progressively higher risks of ALD and LFC, with these trends consistently. In the UKB, accelerated biological ageing was associated with chronic liver diseases independently of genetic risk and remained significant across PRS levels. Furthermore, compared to individuals with biologically younger ages and low genetic risk, participants with high genetic risk and accelerated PhenoAgeAccel exhibited the highest risk of developing chronic liver diseases, and LDSC revealed a positive genetic correlation between ageing and ALD, with SMR identifying three shared genes.

Table 1: Association between biological ageing acceleration (PhenoAgeAccel) and incident of chronic liver diseases in two datasets

Conclusion

Accelerated biological ageing was associated with increased risk of chronic liver diseases, independently of genetic risk. Identifying individuals with higher BioAgeAccel is crucial for predicting the risk of chronic liver diseases, and indicators related to the calculation of BioAgeAccel can serve as potential targets for interventions.

References

1. GBD 2019 Diseases and Injuries Collaborators. Global burden of 369 diseases and injuries in 204 countries and territories, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet. 2020;396(10258):1204-1222. doi:10.1016/S0140-6736(20)30925-9
2. Devarbhavi H, Asrani SK, Arab JP, Nartey YA, Pose E, Kamath PS. Global burden of liver disease: 2023 update. J Hepatol. 2023;79(2):516-537. doi:10.1016/j.jhep.2023.03.017
3. Wang Y, Huang Y, Chase RC, et al. Global Burden of Digestive Diseases: A Systematic Analysis of the Global Burden of Diseases Study, 1990 to 2019. Gastroenterology. 2023;165(3):773-783.e15. doi:10.1053/j.gastro.2023.05.050
4. Lee YB, Ha Y, Chon YE, et al. Association between hepatic steatosis and the development of hepatocellular carcinoma in patients with chronic hepatitis B. Clin Mol Hepatol. 2019;25(1):52-64. doi:10.3350/cmh.2018.0040
5. Klemera P, Doubal S. A new approach to the concept and computation of biological age. Mech Ageing Dev. 2006;127(3):240-248. doi:10.1016/j.mad.2005.10.004
6. Cohen AA, Milot E, Yong J, et al. A novel statistical approach shows evidence for multi-system physiological dysregulation during aging. Mech Ageing Dev. 2013;134(3-4):110-117. doi:10.1016/j.mad.2013.01.004
7. Martin K, Hatab A, Athwal VS, Jokl E, Piper Hanley K. Genetic Contribution to Non-alcoholic Fatty Liver Disease and Prognostic Implications. Curr Diab Rep. 2021;21(3):8. doi:10.1007/s11892-021-01377-5

Disclosure

The authors have declared no conflict of interest.

Clinical Case Summary

A middle-aged man underwent screening colonoscopy during which a diminutive (3–4 mm) polyp was removed by cold snare polypectomy. The procedure was uneventful. Within hours, he developed painless scrotal swelling. Examination revealed subcutaneous emphysema confined to the scrotum (scrotal crepitus) with a soft, non-tender abdomen. He remained afebrile with stable vital signs. Abdominal computed tomography (CT) demonstrated retroperitoneal free air tracking into the scrotum (pneumoscrotum) with no intraperitoneal free air or fluid. Despite the absence of peritoneal signs, the atypical location of free air prompted surgical consultation. An exploratory laparotomy was performed. Intraoperatively, no colonic perforation or contamination was identified, including at the polypectomy site. The air leak was presumed to stem from a sealed microperforation or mucosal defect that allowed retroperitoneal air dissection. The patient had an uneventful recovery and was discharged on postoperative day five. Pneumoscrotum is a rare but recognized complication of colonoscopy, usually resulting from retroperitoneal air dissection without overt perforation (1–3). Most reported cases have been managed conservatively; however, when air dissects into atypical anatomical compartments or if clinical uncertainty exists, surgical exploration may be warranted to exclude a full-thickness injury (2,3). This case highlights the need for individualized management based on clinical and radiological findings, and underscores a rare complication of a routine colonoscopic polypectomy.

References

1) Singh S, Thakur M. Pneumoscrotum after colonoscopy. Can J Gastroenterol. 2008;22(4):411–413.
— This case report describes an instance of pneumoscrotum following colonoscopic polypectomy, managed conservatively. It highlights air dissection from retroperitoneum into the scrotum and notes the rarity of the condition.

2) Graepler F, Lauer UM, Horger MS, et al. Pneumoscrotum after colonoscopic polypectomy. Endoscopy.2007;39(Suppl 1):E90.
— A rare case of post-polypectomy pneumoscrotum requiring laparotomy. No perforation was found intraoperatively, underscoring that extensive air can dissect without overt bowel rupture.

3) Fu KI, Sano Y, Kato S, et al. Pneumoscrotum: a rare manifestation of perforation associated with therapeutic colonoscopy. World J Gastroenterol. 2005;11(32):5061–5063.
— This article presents pneumoscrotum as a clinical manifestation of colonic microperforation and describes the potential retroperitoneal air pathway into the scrotum.

Introduction

A large proportion of Inflammatory Bowel Disease (IBD) patients also develop liver diseases, predominantly primary sclerosing cholangitis (PSC), and more than 80% of PSC patients also have IBD. Coexistence of both diseases in patients, increase of five times the risk of developing a colorectal cancer, and causes liver transplantation failure. Both of IBD and PSC have no curative treatment yet, and the impact of IBD on liver homeostasis and reciprocally the impact of PSC on intestinal barrier (IB) remain largely unknown.

Aims & Methods

The aims of the study were to investigate the impact of (1) mouse models of IBD on liver homeostasis and (2) the impact of mouse models of PSC on IB integrity. Two models of colitis have been used. A model was conducted by adding 3% DSS in drinking water for five days, followed by two days of regular water. The second model of colitis was performed using a pre-sensitizing step involving subcutaneous injection of 2% oxazolone and five day later, a rectal injection of 1.5% oxazolone. As PSC mouse models, we used intra-peritoneal injection of 1µL/g mice weight of CCl₄ twice a week for 8 weeks and another model with a 0.1% diethyl 1,4-dihydro-2,4,6-trimethyl-3,5-pyridinedicarboxylate within diet for 3 weeks. Colitis and cholangitis severities were monitored by food consumption, macroscopic observations as well as calculation of Disease Activity Index which sum up scores of weight loss, bleeding and stool consistency. Fecal samples were tested for calprotectin and lipocalin by ELISA to estimate gut inflammation. Intestinal permeability (IP) was investigated in vivo by estimation of FITC-Dextran quantity in mice’s sera after oral administration and at mice sacrifice in ileum and colon tissues by measuring the flux of fluorescein sodium salt in Ussing chamber. To study liver homeostasis, we performed pathological analysis (H&E and Sirius red staining), and real-time PCR with a focus on fibrosis markers, bile acids metabolism and metabolic pathways.

Results

IBD models induced strong alteration of colonic homeostasis including increased fecal markers of inflammation (Calprotectin and Lipocalin-2) and tissues mRNA expression of inflammatory cytokines (Ifng…). These models of colitis were also accompanied by elevated IP and impaired liver genes expression level of fibrosis (Col3a1) and fatty acids metabolism (Fasn…), as well as cholesterol and bile acids transporters (Abcb11…). This was found to be correlated with impaired enterohepatic circulation of bile acids in the gut. Furthermore, an increase expression of mRNA markers of inflammation (Cxcl1…) was only observed in the liver of the DSS colitis model. However, no alteration of liver homeostasis, including infiltrated immune cells or fibrosis was revealed by histological analysis. PSC mouse models induced strong alterations of liver homeostasis and were associated with altered gut homeostasis shown by a strong increased IP.

Conclusion

Our data demonstrate that IBD colitis models impair liver homeostasis, while PSC models disrupt intestinal integrity. The data obtained from both IBD and PSC models demonstrated a significant increase in intestinal permeability, thereby underscoring it’s potential as an association between those diseases. Further investigations are ongoing in ours models as a next step will be to study a combination of both protocols to explore disease progression and severity.

References

Rabiee, Anahita, and Marina G Silveira. “Primary sclerosing cholangitis.” Translational gastroenterology and hepatology vol. 6 29. 5 Apr. 2021, doi:10.21037/tgh-20-266
Kim, You Sun et al. “Primary sclerosing cholangitis (PSC) and inflammatory bowel disease (IBD): a condition exemplifying the crosstalk of the gut-liver axis.” Experimental & molecular medicine vol. 55,7 (2023): 1380-1387. doi:10.1038/s12276-023-01042-9

Clinical Case Summary

Introduction: Aortoesophageal fistula (AEF) is a rare but fatal cause of upper gastrointestinal bleeding. The disease progression is often rapidly if not promptly recognized.
The most common etiologies include thoracic aortic aneurysm (TAA) and prior aortic surgery. Early diagnosis remain challenge due to nonspecific symptoms. This case series highlights endoscopic features of AEF and the critical role of endoscopists in early detection.
Case present: We report three elderly patients (aged 76–82) who presented to the emergency department with massive hematemesis. One had a history of type B aortic dissection post thoracic endovascular aortic repair (TEVAR) ; the others had no known thoracic disease. None reported mid-thoracic pain. Laboratory data showed hemoglobin 5.1 to 6.2 g/dL without coagulopathy. Esophagogastroscopy (EGD) was performed within 1 hour in two patients, and at 9 hours in the third. EGD showed consistent findings in three cases: a subepithelial bulging mass with central blood clot adherent to the left quadrant (6–9 o’clock) of the mid-esophagus. CT confirmed AEF secondary to ruptured TAA in two patients. Unfortunately, one patient collapsed suddenly in the ED; the others underwent emergent surgery but died within 1 and 21 days postoperatively.(esophagectomy +/- TEVAR).
Discussion: Chiari’s triad (mid-thoracic pain, sentinel bleeding, fatal hematemesis) is classically associated with AEF but was absent in half patients. In our report, EGD can be a most timely and specific modality to early diagnosis of AEF, especially in patients without clear prior aortic disease. The typical endoscopic feature : bulging submucosal mass with central blood adherent clot may serve as a diagnostic clue. And the “hot-zone” of the AEF in EGD was located at left quadrant (six to nine o’clock) of mid esophagus .
Conclusion: Early recognition of typical characteristic and “hot zone” of AEF on EGD may improve timely diagnosis of AEF and guide life-saving interventions.

References

1. Bergqvist D. Arterioenteric fistula. Review of a vascular emergency. Acta Chir Scand 1987;153:81–6.
2. Hollander JE, Quick G. Aortoesophageal fistula: a comprehensive review of the liter- ature. Am J Med 1991;91:279–87.
3. Mortensen A, Hansen NF, Schiodt OM. Fatal aortoesophageal fistula caused by but- ton battery ingestion in a 1-year-old child. Am J Emerg Med 2010;28(984):e5-6.
4. Takeno S, Ishii H, Nanashima A, Nakamura K. Aortoesophageal fistula: review of trends in the last decade. Surg Today. 2020 Dec;50(12):1551-1559.

Introduction

This study aims to assess the impact of antithrombotic therapy on endoscopic findings in patients hospitalized for upper gastrointestinal bleeding.

Aims & Methods

We carried out a prospective, single-center cross-sectional study including 332 patients between June 2020 and February 2025. Patients were classified as antithrombotic (AT) users if they were receiving antiplatelet agents (such as low-dose aspirin or thienopyridines) and/or anticoagulants (including vitamin K antagonists, direct oral anticoagulants, or heparin).

Results

The mean age of the study population was 59 ± 16.7 years, with a marked male predominance (77.1%). Among them, 63 patients (19%) were receiving antithrombotic (AT) therapy—41 on antiplatelet agents and 39 on anticoagulants. Patients in the AT group were significantly older (68 vs. 57 years; p < 0.001) and had a higher burden of comorbidities (75.8% vs. 16.7%; p < 0.001). However, there were no significant differences between the AT and non-AT groups regarding the presence of active bleeding at endoscopy (12.7% vs. 16.8%; p = 0.425) or the need for endoscopic hemostasis (7.9% vs. 16%; p = 0.1).
In multivariate analysis, after adjustment for age, sex, comorbidities, active bleeding, and AT use, only the presence of active bleeding was independently associated with the need for endoscopic hemostasis. Specifically, active bleeding at endoscopy increased the odds of requiring hemostasis by 26-fold (OR: 26, 95% CI: 12.9–62.15; p < 0.001), whereas AT therapy was not an independent predictor (OR: 0.386, 95% CI: 0.105–1.42; p = 0.154).

Conclusion

In older patients receiving antithrombotic therapy and admitted for upper gastrointestinal bleeding, the risk of active bleeding during endoscopy and the need for endoscopic hemostasis do not appear to be increased.