Introduction

Antiplatelets and anticoagulants significantly increase the risk of upper gastrointestinal bleeding by impairing normal clotting mechanisms. Patients on dual or combined therapy often present with more severe bleeds and poorer endoscopic control. This leads to higher rates of rebleeding, complications, and mortality compared to those not on these therapies.

Aims & Methods

To evaluate the risk and outcomes of non-variceal upper gastrointestinal bleeding (UGIB) in patients on single antiplatelet therapy, dual antiplatelet therapy, and combined antiplatelet-anticoagulant therapy, and to assess associated morbidity, mortality, and rebleeding rates.
A prospective study was conducted involving 150 patients (90 males, 60 females) aged 40–60 years, presenting with upper GI bleeding between 1st January 2023 till 1st January 2025. Patients had co-morbid conditions including hypertension, diabetes mellitus, coronary artery disease, or prior cerebrovascular events, and were on their respective medications for at least 3 months. Patients using NSAIDs, having liver disease, or known bleeding disorders were excluded. Clinical presentations included melena, hematemesis, or both. All patients underwent upper GI endoscopy, with Forrest classification used to characterize ulcers. Laboratory investigations included CBC, LFTs, renal function, PT, and APTT. Bleeding profiles and endoscopic outcomes were analyzed across three medication groups: single antiplatelet (n=60), dual antiplatelet (n=50), and combined antiplatelet-anticoagulant therapy (n=40).

Results

UGIB was reported in 6 (10%) of the single antiplatelet group, 16 (32%) of the dual antiplatelet group, and 14 (35%) of the combined therapy group. Endoscopic findings predominantly revealed Forrest class IIA ulcers. Patients on dual or combined therapy had poorer endoscopic hemostasis. Four patients experienced rebleeding refractory to standard endoscopic measures, requiring angioembolization. One mortality was recorded in the dual antiplatelet group due to massive bleeding and shock.

Conclusion

Dual antiplatelet and combined antiplatelet-anticoagulant therapies significantly increase the risk and severity of non-variceal UGIB, with higher rates of poor endoscopic hemostasis, rebleeding, and mortality. These findings underscore the importance of risk stratification and prophylactic strategies in patients requiring long-term antithrombotic therapy.

References

1. Hao, W., Liu, A., Zhu, H. et al. Risk factors and management of gastrointestinal bleeding in patients with or without antiplatelet and anticoagulation therapy: a multicenter real-world prospective study. BMC Gastroenterol 24, 155 (2024). https://doi.org/10.1186/s12876-024-03238-3
2. Risk of Gastrointestinal Bleeding Increases With Combinations of Antithrombotic Agents and Patient Age Abraham, Neena S. et al. Clinical Gastroenterology and Hepatology, Volume 18, Issue 2, 337 - 346.e19

Introduction

International guidelines recommend performing emergency gastroscopy within 12 hours for variceal (V) bleeding and within 24 hours for non-variceal (NV) bleeding in cases of upper gastrointestinal bleeding (UGIB).

Aims & Methods

This study aimed to analyze the time elapsed between emergency department admission and time of endoscopy, referred to as "door-to-endoscopy time" (DET), and to identify factors influencing DET across different UGIB subgroups. We conducted a retrospective cohort analysis of patients who underwent emergency gastroscopy for UGIB between January 1, 2022, and December 31, 2023, at the Department of Emergency Medicine at Semmelweis University. Data were collected on clinical parameters and 30-day mortality. NV patients were categorized into high-risk (HNV) and low- risk (LNV) groups based on endoscopic findings (Forrest classification). Welch’s t-test was used for comparing mean DET among the subgroups, whereas for hemoglobin linear regression was applied. The significance level was set at 0.05 for all analyses.

Results

Among 654 patients, we identified 126 V and 528 NV UGIB cases, with the latter comprising 99 HNV and 429 LNV cases. Rebleeding occurred in 5.4% of patients (V: 12.7%, HNV: 10.1%, LNV: 2.1%), and 30-day mortality was 19.7% in the cohort (V: 24.8%, HNV: 22.6%, LNV: 17.6%). The mean DET was 7.28 hours (SD=±6.04), with subgroup averages as follows: V: 5.87±3.77 hours, HNV: 6.33±4.04 hours, and LNV: 7.92±6.83 hours, with significant differences between LNV-HNV (p=0.003) and LNV-V (p<0.0001) groups; no significant difference was observed between HNV-V (p=0.37). In the entire cohort, shorter DET was significantly associated with tachycardia (6.61 vs. 7.73 hours, 95% confidence interval (CI) -1.99 to -0.25, p=0.01), hematemesis (5.82 vs. 8.09 hours, 95% CI -3.11 to -1.43, p<0.0001), syncope (6.25 vs. 7.57 hours; 95% CI -2.30 to -0.33, p=0.009), and lower hemoglobin levels (1 g/L decrease in hemoglobin reduced DET by an average of 1 minute, p=0.029). DET was not associated with 30-day mortality (p=0.501), vasopressor use (p=0.857), shock index (p=0.091), coffee-ground emesis (p=0.192), hematochezia (p=0.564), intubation (p=0.566), rebleeding rate (p=0.462), or melena (p=0.961). In the V group, DET was significantly shorter in case of hematemesis (5.20 vs. 7.25 hours, 95% CI -3.61 to -0.49, p=0.011) and tachycardia (5.19 vs. 6.64 hours, 95% CI -2.84 to -0.08, p=0.039); whereas in HNV patients with coffee-ground emesis, DET was significantly reduced (4.94 vs. 6.58 hours, 95% CI -3.08 to -0.20, p=0.026); in LNV patients, DET was shorter in patients with hematemesis (6.42 vs. 8.38 hours, 95% CI -3.20 to -0.71, p=0.002) and syncope (6.56 vs. 8.25 hours, 95% CI -3.10 to -0.29, p=0.019).

Conclusion

In our retrospective cohort study, DET significantly differed between LNV-V and LNV-HNV subgroups. Shorter DET correlated with tachycardia, hematemesis, syncope, and lower hemoglobin levels. DET showed no association with 30-day mortality or rebleeding rate.

Introduction

The current universal standard of care in primary biliary cholangitis (PBC) is ursodeoxycholic acid (UDCA), although its clinical benefit in PBC has never been reported in absolute measures.

Aims & Methods

This cohort aimed to assess the prevalence of incomplete response to UDCA and determine non-response predictors.
Patients with PBC as main diagnosis were included from the hospital's centralized electronic medical records system, over a 10-year period. Overlap syndromes (PBC-Auto-Immune Hepatitis) were also included. Main endpoints included incomplete response to UDCA treatment according to Paris I, Paris II criteria, and Globe score.

Results

A total of 50 patients were included in this study. The mean age at diagnosis was 52.74 years (24-73 years) and 92% females. Only one patient was asymptomatic at onset and 82% had positive anti‐mitochondrial antibodies. All patients were treated with ursodeoxycholic acid (UDCA). Corticosteroids and immunosuppressive therapies were associated in 26% of cases. Incomplete response to UDCA was observed in 28% and 34% of patients according to Paris I and II criteria, respectively. Non-response predictors were poor therapeutic adherence, Overlap syndrome and hepatocellular carcinoma in 14%, 6% and 4% respectively. Five patients were lost to follow-up and five cases died from cirrhosis ’complications. The median ΔGLOBE score was 0.42 (IQR: -1.58 to 3.92). The 5, 10 and 15 years liver transplantation-free survival (median) was: +10%, +7.38% and +5% respectively. Liver transplantation (LT) was considered in one patient with excellent outcomes at last follow-up.

Conclusion

A considerable proportion of patients showed incomplete response to UDCA treatment according to Paris II criteria. Early identification of patients at risk of incomplete response could improve patient management and overall disease prognosis.

References

- Treatment response to ursodeoxycholic acid in primary biliary cholangitis: A systematic review and meta-analysis. DOI: 10.1016/j.dld.2022.12.010
- Pretreatment prediction of response to ursodeoxycholic acid in primary biliary cholangitis: development and validation of the UDCA Response Score. doi: 10.1016/S2468-1253(18)30163-8. Epub 2018 Jul 13.

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.

Introduction

Oesophageal food bolus impaction [OFBI] is a common presentation to emergency room [ER] and often requires endoscopic intervention. We aimed to describe the incidence of OFBI in Canterbury, New Zealand and examine factors predicting the need for endoscopic intervention and complications in the population-based cohort.

Aims & Methods

All ER presentations of OFBI in Canterbury between October 2018 and August 2023 were included. Population data for the Canterbury population was obtained from Statistics NZ. Ethnicity was defined according to hospital records based on patients’ self-identification. Endoscopic intervention was defined as the presence of bolus during the endoscopy requiring any endoscopic manoeuvre for clearance. Complications were defined as unsuccessful attempts requiring a repeat procedure or procedure-related injuries.

	Total (n = 187)
Age (years)	Mean 55 Median 54.9
Gender - Male (%) : Female (%)	113 (60.4) : 74 (39.6)
Ethnicity - European (%) : Non-European (%)	163 (87.2) : 24 (12.8)
Cause of oesophageal impaction (%)	EoE 42 (22.5) Stricture 43 (23)£ Other 15 (8)* Idiopathic/unknown 87 (46.5)¥
Food type (%)	Meat 141 (86.5) Non-meat 46 (24.5)
Spontaneous clearance of food bolus clinically, without endoscopy performed (inpatient or outpatient) (%)	42 (22.5)
Spontaneous clearance of food bolus diagnosed on endoscopy as an inpatient (%)	37 (19.8)
Inpatient endoscopic intervention required (%)	92 (49.2)
Total complications (%)	8 (4.3)

£ cause of impaction from Schatzi ring or benign esophageal stricture
* cause of impaction from severe reflux oesophagitis (Los Angeles Grade C or D), esophageal dysmotility, malignant stricture, or esophageal candidiasis
¥ no cause for impaction found; either no endoscopy performed as an inpatient or outpatient or no pathology found on endoscopy

Results

There were 187 ER presentations of OFBI between October 2018 and August 2023. Clinical characteristics of the population-based cohort are presented in Table 1.
The average annual incidence of ER presentations of OFBI in Canterbury region between 2019 – 2022 was 5.82 per 100,000 population (95% CI 3.96-7.68/100,000). The incidence of ER presentations of OFBI in Europeans and non-Europeans over the same period was 8 per 100,000 European population (95% CI 5.27-10.73/100,000) and 1.94 per 100,000 non-European population (95% CI 0.15-3.73/100,000).
A total of 92 cases (49%) required endoscopic intervention. Factors predicting the need for endoscopic intervention were meat bolus [p= 0.01], stricture [p<0.01], and early endoscopy performed <12hrs [p<0.01]. There were only 8 complications. Predictors with a trend associated with complications were after-hours presentation [p=0.06] and early endoscopy performed <6hrs [p=0.06].

Conclusion

Our population-based cohort showed a significantly higher incidence of ER presentations of OFBI in Europeans than in non-European ethnic groups. Factors predicting the need for endoscopic intervention were meat bolus, stricture and early endoscopy. After-hours presentation and early endoscopy <6hrs showed a trend towards a higher risk of complications. The results suggest that a delayed approach may be associated with a higher chance of spontaneous clearance and a lower risk of complications, although further study is needed.

Disclosure

Not applicable

Clinical Case Summary

Autoimmune gastritis (AIG) is an immune-mediated disease characterized by destruction of gastric parietal cells, which leads to the loss of internal factor Casl and decreased production of hydrochloric acid. When conducting endoscopic examination, it is possible to visualize a specific picture of the gastric body mucosa: diffuse atrophy, revealing changes occurring on the background of long-term hypergastrinemia.
Female patient, 45 years old, complaining of increased gas formation, burning sensation and heaviness in the epigastrium after eating, air burping. Chronic diseases: chronic iron deficiency anemia, B12 deficiency, autoimmune thyroiditis. Notes restriction of eating red meat, which causes heaviness in the abdomen. Heredity for cancer is not aggravated. Esophagogastroduodenoscopy revealed pallor of the mucous membrane of the stomach body, single islets of preserved mucous membrane of the stomach body, presence of multiple point whitish inclusions (WGA - white globe appearance) on all walls, forming the effect of “stardust”.
The diagnosis of autoimmune atrophic gastritis was confirmed by laboratory tests: Gastrin dated 01/20/2024 - 746 pg/mL, Chromogranin A CgA dated 01/2024 - 150.4 ng/mL, antibodies to gastric parietal cells -2560. Gastropanel from 20.01.2024 - gastrin-17 baseline > 30.6 pmol/l; pepsinogen I 21.89 µg/l; pepsinogen II 11.80 µg/l, pepsinogen I/II ratio - 1.9. 13C-urease breath test for HP dated 01.2024 - 1.3. Antibodies to Helicobacter, IgG < 13. Histologic conclusion: Moderate atrophy of the gastric body mucosa with the presence of cystic-expanded glands filled with opaque content.
The “stardust” phenomenon was first described in a case of long-term administration of potassium-competitive hydrochloric acid blockers. Given that elevated gastrin levels always accompany AIG, detection of this phenomenon is also possible in cases of AIG.The present case is the first description of the "stardust" phenomenon in a patient with autoimmune gastritis.

References

"Propensity score matching analysis: incidence and risk factors for "stardust" gastric mucosa, a novel gastric finding potentially induced by vonoprazan" Tetsuya Yoshizaki et al. DOI: 10.1111/apt.16151
https://pubmed.ncbi.nlm.nih.gov/33159407/

Disclosure

Yes