Introduction

Sporadic duodenal adenomas are uncommon in comparison to other gastro-intestinal adenomas and often an incidental finding in upper gastrointestinal endoscopy. Recent studies indicate an increasing incidence of these lesions.¹

Aims & Methods

A retrospective review of upper endoscopies performed over the past 10 years was conducted to identify cases of duodenal adenomas. Patients with polyposis syndromes and ampullary adenomas were excluded, resulting in a sample of 41 patients with sporadic duodenal adenomas. In addition, a control group of 41 randomly selected individuals from the same 10-year span, matched by age and gender, was used for comparison. Potential risk factors for duodenal adenomas were collected.

Results

The prevalence of duodenal adenomas was 0.22%. The mean age of affected individuals was 69 years, out of which 24 were males. Most of the adenomas were endoscopically removed (68.3%), three patients had recurrent adenomas and one progressed into adenocarcinoma. A significant association was observed between smoking and the presence of duodenal adenomas (p = 0.037). Family history of gastrointestinal neoplasia was related to the occurrence of duodenal adenomas (p = 0.043). In addition, in comparison to the control group, the duodenal adenoma group had a significantly higher number of affected family members with gastrointestinal neoplasia (p = 0.001). Furthermore, the duodenal adenoma group had a significantly higher number of colorectal adenomas compared to the control group (p < 0.001). No statistically significant associations or differences to the control group were found amongst other variables.

Conclusion

Although sporadic duodenal adenomas are rare, their potential for recurrence and progression to adenocarcinoma warrants careful surveillance. Smoking and family history of gastrointestinal neoplasia appear to be potential risk factors for sporadic duodenal adenomas. Additionally, the higher prevalence of colorectal adenomas in these patients highlights the importance of colorectal cancer screening in this population.

References

(1) Culver, E., & McIntyre, A. (2011). Sporadic duodenal polyps: classification, investigation, and management. Endoscopy, 43(02), 144–155. https://doi.org/10.1055/s-0030-1255925

Introduction

Hepatic decompensation in patients with cirrhosis represents a critical point in the clinical course of the disease, associated with a significant increase in morbidity and mortality. ¹ Common clinical manifestations of decompensation include ascites, hepatic encephalopathy, and variceal bleeding.^2​ Cystatin C, a low molecular weight cysteine protease inhibitor produced by all nucleated cells, has emerged as a reliable endogenous marker of glomerular filtration rate (GFR). Unlike serum creatinine, cystatin C is not significantly influenced by age, sex, muscle mass, or dietary protein intake, making it a more precise indicator of renal function—particularly in populations with altered muscle mass, such as those with chronic liver disease.³ Beyond its role in renal assessment, cystatin C has demonstrated prognostic value in various clinical settings, including cardiovascular disease, sepsis, and general critical illness^​4,5; however, patients with liver cirrhosis have been underrepresented in these cohorts.

Aims & Methods

Prospective longitudinal study including 62 patients with confirmed Child-Pugh class A or B cirrhosis. Serum cystatin C levels were measured at baseline by ELISA (mg/L), using <0.95 mg/L as the normal cutoff. Patients were followed for 6 months to detect decompensation events. Clinical and biochemical variables (age, sex, creatinine, albumin) were analyzed using quartile stratification, linear trend tests, Pearson’s chi-squared test, and diagnostic performance metrics (odds ratio, sensitivity, specificity, likelihood ratios).

Results

Table 1. Clinical and Biochemical Characteristics According to Hepatic Decompensation During Follow-Up.

Variable	Total (n = 62)	With decompensation (n =27)	Without decompensation (n = 35)
Age (mean ± SD, years)	58.05 ± 11.4	59.1 ± 10.9	57.2 ± 11.9
Male sex, n (%)	32 (51.6%)	14 (43%)	18(56%)
Serum cystatin C (mg/L, mean ± SD)	1.07 ± 0.42	1.25 ± 0.40	0.90 ± 0.40
Elevated cystatin C (>0.95 mg/L), n (%)	35 (56.4)	22 (81.5)	20 (57.1)
Serum albumin (g/dL, mean ± SD)	3.1 ± 0.5	2.8 ± 0.5	3.4 ± 0.4
Creatinine/cystatin C ratio (mean ± SD)	8.7 ± 5.8	7.6 ± 5.1	9.7 ± 6.1
Main etiology: Alcoholic liver disease, n (%)	26 (41.9)	12 (44.4)	14 (40.0)

Of 62 patients (32 men, 51.6%; mean age 58.05 ± 11.4 years), major etiologies were alcohol use (41.9%), metabolic liver disease (38.7%), and autoimmune disease (19.3%). Patients with infectious or undefined etiologies were excluded.
During follow-up, 27 patients (43.5%) developed at least one decompensation event (ascites, encephalopathy, or variceal bleeding). Among them, 81.5% had elevated cystatin C (mean 1.25 ± 0.40 mg/L) versus non-decompensated (mean 0.9 ± 0.40 mg/L, p<0.001). Chi-square analysis showed a significant association (χ² = 4.132; p = 0.042), supported by likelihood ratio (χ² = 4.293; p = 0.038) and linear-by-linear association (χ² = 4.065; p = 0.044). The estimated OR was 3.3.
Decompensated patients had a lower creatinine/cystatin ratio (mean 7.6 ± 5.1 vs 9.7 ± 6.1), though not statistically significant (p=0.162). Albumin levels were lower (2.8 ± 0.5 g/dL vs 3.4 ± 0.4 g/dL, p<0.001).
Quartile analysis showed a higher risk of decompensation in the highest cystatin C quartile (>1.25 mg/L; p<0.001, linear trend), even after excluding patients with eGFR <60 mL/min/1.73 m². This trend was confirmed by linear-by-linear association (χ² = 39.88; df = 1; p < 0.001).

Conclusion

Cystatin C is significantly associated with the development of decompensation events in patients with chronic liver disease, providing an OR of 3.3 and a consistent dose-response trend across quartiles. Although the final sample size was relatively small due to exclusions for loss to follow-up or incomplete biochemical studies, the results were statistically significant and clinically relevant. These findings, based on a prospective design and strict follow-up, suggest that cystatin C could be a prognostic marker, and its inclusion in clinical practice warrants prospective validation.

References

1. Zhai M, Long J, Liu S, Liu C, Li L, Yang L, Li Y, Shu B. The burden of liver cirrhosis and underlying etiologies: results from the global burden of disease study 2017. Aging (Albany NY). 2021 Jan 12;13(1):279–300. doi: 10.18632/aging.104127.
2. D'Amico G, Bernardi M, Angeli P. Towards a new definition of decompensated cirrhosis. J Hepatol. 2022 Jan;76(1):202–207. doi: 10.1016/j.jhep.2021.06.018.​
3. Chen DC, Potok OA, Rifkin D, Estrella MM. Ventajas, limitaciones y consideraciones clínicas en el uso de la cistatina C para estimar la TFG. Riñón360. 2022;3(10):1807-14.
4. Wang Y, Li W, Yang J, Zhang M, Tian C, Ma M, Zhang Q. Association between cystatin C and the risk of ischemic stroke: a systematic review and meta-analysis. J Mol Neurosci. 2019;69(3):444–449. doi:10.1007/s12031-019-01373-1.
5. Luo J, Wang LP, Hu HF, Zhang L, Li YL, Ai LM, et al. Cystatin C and cardiovascular or all-cause mortality risk in the general population: a meta-analysis. Clin Chim Acta. 2015 Oct 23;450:39–45. doi: 10.1016/j.cca.2015.07.016.

Disclosure

I declare that I have no conflicts of interest related to this work.

Introduction

Several risk stratification scores have been developed for predicting endoscopic treatment or patient survival in non-variceal upper gastrointestinal bleeding (NVUGIB).

Aims & Methods

Our aim was to compare the performance of some previously described scores Forrest, (Canada-United Kingdom-Adelaide (CANUKA) score, Glasgow-Blatchford score (GBS), HARBINGER score, neutrophil-to-lymphocyte ratio (NLR), red cell distribution width (RDW), Rockall pre-endoscopy and complete scores) in predicting the following outcomes in patients with NVUGIB: need for endoscopic intervention, in-hospital rebleeding rate, need for red blood cell (RBC) transfusion, need for surgical or interventional radiological procedure, 30-day mortality.
Patients undergoing emergency endoscopy for upper GI bleeding at the Department of Emergency Medicine at Semmelweis University between January 1, 2022 and December 31, 2023 were included in a retrospective cohort analysis. Endoscopic treatment was applied to lesions with high-risk stigmata (HRS) defined by ESGE, based on the Forrest classification. Statistical methods included ROC analysis, through which we obtained the AUROC values.

Results

There were 528 patients with NVUGIB, including 99 patients (61 males, 38 females, mean age 72) with high-risk stigmata (HRS) and 429 patients (246 males, 183 females, mean age 70) with low-risk stigmata (LRS). In-hospital rebleeding rate was 3.6% (n=19/528), All-caused 30-day mortality was 17.8% (n=94/528). Due to missing data in 51 patients, scoring systems were analyzed in 477 patients. Area under receiver operator characteristic curves (AUROC) were generated for predicting need for endoscopic intervention: Forrest: 0.91, CANUKA: 0.57, GBS: 0.58, NLR: 0.55, RDW: 0.46, Rockall (pre-endoscopy): 0.53, Rockall (complete): 0.69, HARBINGER: 0.57; in-hospital rebleeding rate: Forrest: 0.65, CANUKA: 0.67, GBS: 0.55, NLR: 0.50, RDW: 0.51, Rockall (pre-endoscopy): 0.54, Rockall (complete): 0.70, HARBINGER: 0.67; need for RBC transfusion: Forrest: 0.64, CANUKA: 0.79, GBS: 0.80, NLR: 0.51, RDW: 0.68, Rockall (pre-endoscopy): 0.62, Rockall (complete): 0.66, HARBINGER: 0.64; need for surgical or interventional radiological procedure: Forrest: 0.77, CANUKA: 0.62, GBS: 0.56, NLR: 0.64, RDW: 0.46, Rockall (pre-endoscopy): 0.57, Rockall (complete): 0.72; 30-day mortality: Forrest: 0.53, CANUKA: 0.70, GBS: 0.65, NLR: 0.67, RDW: 0.60, Rockall (pre-endoscopy): 0.70, Rockall (complete): 0.70, HARBINGER: 0.62.

Conclusion

Currently used risk stratification scores have a suboptimal performance (AUROC ≤ 0.8) as per ESGE guideline in predicting the need for endoscopic therapy, in-hospital rebleeding, need for surgical or interventional radiological procedure and 30-day mortality. GBS and CANUKA scores proved to be effective in estimating the need for RBC transfusion, whereas CANUKA and Rockall scores seem to be acceptable in estimating 30-day mortality. Further prospective studies on larger patient cohorts exploiting artificial intelligence are needed to analyze and optimize risk stratification scores for NVUGIB.

Introduction

Colectomy is the primary treatment for dysplastic lesions in inflammatory bowel disease (IBD). Since the development of advanced endoscopic techniques, the management of dysplasia is evolving. Endoscopic submucosal resection (ESD) could be used in selected cases at referral centres as an alternative to colectomy. However, the feasibility and safety in IBD remains limited.

Aims & Methods

To evaluate en-bloc resection rate and the need of colectomy due to ESD failure in IBD.
Secondary aims: to assess the complications of ESD, the local recurrence of dysplastic lesions, the presence of synchronous and metachronous lesions and the risk of IBD relapse following the procedure.
Multicentre, retrospective study of IBD patients who underwent ESD for suspected colonic dysplastic lesions at least one month before the inclusion date. Patients with total colectomy before ESD, invisible dysplasia at the time of ESD, or pregnancy were excluded. En-bloc resection rate and colectomy due to ESD failure at the short term were evaluated by logistic regression analysis. The risk of IBD relapse was evaluated by Cox regression analysis.

Results

Sixty patients from 22 centres were included: 47 with ulcerative colitis, 11 with Crohn’s disease and 2 with IBD-unclassified. The mean age at ESD was 64 years (SD 13). The majority of the lesions (n=33, 55%) were located in rectum. Fifty lesions (83%) were located in areas previously inflamed. En-bloc and R0 were achieved in 58 (97%) and 50 patients (83%), respectively. Colectomy due to ESD failure was required in 5 patients (8.3%), all of them occurred within 6 months after ESD. No risk factors were associated with colectomy in multivariable analysis, including inflammatory activity, IBD treatments or characteristics of the lesions. Complications occurred in 17 patients (28%): 3 did not required any treatment, 6 required pharmacologic therapy, 6 needed endoscopic or radiologic intervention, and 2 underwent surgery (Table 1). No deaths were reported.
At least one surveillance colonoscopy after ESD was performed in 42 patients (70%). Local recurrence was observed in 2 patients (4.7%) while other dysplastic lesions were detected in 11 (26%) during the follow-up (median 1.5 years, IQR 0.5-3.4). All these lesions were removed endoscopically. Synchronous and metachronous lesions were identified in 4 (20%) and 9 patients (19%), respectively. IBD relapse occurred in 8 patients during the follow-up, with an incidence rate of 7% person-year (CI 95%:3-13). The occurrence of relapses was gradually throughout the follow-up period.

Table 1. Complications of endoscopic submucosal dissection

	Frequency, n (%)	Time of onset: during the ESD, n (%)	Serious complication, n (%)	Resolution with endoscopy, n (%)	Resolution with no sequelae, n (%)
Perforation	9 (15)	8 (13)	2 (3.3)	6 (10)	8 (13)
Bleeding	3 (5)	1 (1.6)	0 (0)	3 (5)	3 (5)
Post polypectomy syndrome	4 (6.7)	0 (0)	0 (0)	0 (0)	4 (6.7)
Other complication	1 (1.6)	0 (0)	0 (0)	0 (0)	1 (1.6)

Other complication: fever with no evidence of infection.
n: number, ESD: endoscopic submucosal infection.

Conclusion

ESD avoids colectomy in 90% of IBD patients with dysplastic lesions. One-third of the patients experienced complications, all of them resolved with no sequelae. Given the risk of new dysplastic lesions, ongoing monitoring with surveillance colonoscopies is recommended.

Disclosure

María José García has received financial support for travelling and educational activities from Janssen, Pfizer, AbbVie, Takeda, Kern Pharma, Faes Farma and Ferring.
Edoardo Vincenzo Savarino has served as speaker for Abbvie, Abivax, Agave, AGPharma, Alfasigma, Apoteca, Biosline, CaDiGroup, Celltrion, Dr Falk, EG Stada Group, Fenix Pharma, Galapagos, Johnson&Johnson,consultant for Abbvie, Agave, Alfasigma, Biogen, Bristol-Myers Squibb, Celltrion, Dr. Falk, Eli Lilly, Fenix Pharma, Ferring, Giuliani, Grunenthal, Johnson&Johnson, JB Pharmaceuticals, Merck & Co, Nestlè, Pfizer, Reckitt Benckiser, Sanofi/Regeneron, SILA, Sofar, Takeda, Unifarco; he received research support from Bonollo, Difass, Pfizer, Reckitt Benckiser, Sanofi/Regeneron, SILA, Sofar, Unifarco, Zeta Farmaceutici.
Irene González-Partida has received support for conference attendance and speaker fees from AbbVie, Dr. Falk Pharma, Ferring Pharmaceuticals, Janssen, MSD, Kern, Pfizer, Shire, Takeda, Teva and Tillotts Pharma AG.
Alicia López has served as speaker for Chiesi, Takeda, ABBVIE, Lilly. I have received support for conference attendance from Pfizer, Lilly, Kern Pharma, Falk, Ferring, and Janssen
Jordina Llao has received educacional suport from Abbvie, Tillots, Ferring and Lilly.