Introduction

Massive gastrointestinal bleeding is a clinical condition that is poorly studied due to its abrupt presentation, involvement of various clinical services, and the high and rapid mortality of patients. We present the preliminary results of a multicenter registry that includes 21 hospitals from Spain and Hispanic America, analyzing factors related to mortality and need for intervention.

Aims & Methods

Since January 2023, 403 patients over 18 years old who presented to the emergency departments of participating hospitals with massive gastrointestinal bleeding, defined as bleeding accompanied by signs of shock and requiring transfusion of at least 2 units of blood within the first 24 hours of admission, were included. Demographic variables, comorbidities, treatments including NSAIDs, antiplatelets, and anticoagulants, clinical presentation variables, medical, endoscopic, and surgical variables, and a 6-month follow-up were collected.
The aim of this study was to analyze factors related to mortality and the need for intervention in patients with massive gastrointestinal bleeding.

Results

A total of 403 patients with a mean age of 64.5 ± 15.7 years were included (male 68.7%). Main comorbidities were cirrhosis (31%), diabetes (28%) and a previous UGIB (25%). 8.4% of patients had already been admitted to the hospital, and 29% were on antithrombotic (16.6% antiplatelets and 16.4% anticoagulants). On admission we observed SPB: 91±22 mmHg, heart rate 101 ± 21; and an altered mental status in 31%. Mean hemoglobin levels 7.6±2.5 g/dl, urea: 98±67, albumin 2.16±1.3, INR: 3.9±7. The most common causes were esophageal varices (29%), gastric ulcer (25%) and duodenal ulcer (25%). Endoscopic intervention was needed in 60%, with mortality rate of15.4%. Mean admission was 8.6±10 days, and patients needed 4±3 red blood cells units. When analyzing in-hospital mortality, we observed that the age of patients who died was higher than that of survivors (68.2±15 vs. 63.6±16; p=0.033), with the former requiring more packed red blood cells (5±5.5 vs. 3.5±2; p=0.043). Patients who died had a lower frequency of gastric ulcer (14% vs. 27%; p=0.034), a higher frequency of altered mental status (42.6% vs. 29%; p=0.036), and a lower rate of endoscopic therapy applied (43.3% vs. 63.6%; p<0.0001). In logistic regression, gastric ulcer etiology and endoscopic therapy were protective factors against mortality (Table 2).
Regarding the need for intervention, more patients with liver cirrhosis required it (73% vs. 60%, p=0.018), patients with hematemesis (73% vs. 52%; p<0.0001), patients without melena (60% vs. 76%; p=0.002), with syncope (76.3% vs. 61%; p=0.06), etiologies other than gastric ulcer (78% vs. 56%; p=0.028), and the presence of esophageal varices (83% vs. 57%; p<0.0001). In binary logistic regression, liver cirrhosis, hematemesis, and syncope were risk factors for the need for intervention.

Conclusion

Age, altered mental status, and lower frequency of endoscopic therapy are risk factors for mortality due to massive gastrointestinal bleeding. Gastric ulcer as an etiology and receiving endoscopic therapy acted as protective factors against mortality. Indeed, in both situations, it might be related to an opportunity window to receive appropriate treatment, especially when compared with more cataclysmic types of bleeding, such as variceal or posterior duodenal bulb wall, which sometimes can be challenging and utterly abrupt. Regarding the need for intervention, liver cirrhosis, hematemesis, and syncope were independent risk factors for the need for endoscopy, surgery, or interventional radiology.

Clinical Case Summary

A 52-year-old male, liver-transplanted in 2014 for alcohol- and HCV-related cirrhosis (HCV eradicated in 2017 with DAAs), was evaluated in May 2024 due to low-grade evening fevers. His immunosuppression regimen included tacrolimus 1 mg b.i.d., with stable trough levels around 11.5 ng/mL. However, during a routine check-up, tacrolimus levels spiked to 27 ng/mL. The result was confirmed on repeat testing despite Tacrolimus discontinuation.

No changes in liver function were observed, and tacrolimus was temporarily discontinued. The patient was hospitalized and developed mild upper limb tremors. Erythrocytapheresis was performed due to suspected tacrolimus toxicity, reducing levels only modestly (from 22 to 21.2 ng/mL). Given the discrepancy between assay results and clinical context, the lab performed a dilutional linearity test, revealing non-linearity suggestive of assay interference.

Autoantibody screening (RF, ANA, ASMA, LKM, ANCA, etc.) was negative. However, treatment of the sample with heterophile antibody blocking reagent (HBR) significantly reduced tacrolimus concentrations, confirming heterophile antibody interference. The patient underwent plasmapheresis to eliminate interfering antibodies, which normalized tacrolimus readings. Unfortunately, he developed candidemia (Candida parapsilosis) and died from cardiovascular complications.

This case illustrates how heterophile antibodies may falsely elevate tacrolimus levels in immunoassays, potentially leading to inappropriate clinical decisions. Clinicians must consider assay interference when pharmacokinetics and clinical findings are discordant, and collaborate closely with laboratory services to ensure accurate therapeutic drug monitoring.

Introduction

Emerging experimental and clinical data suggest that the gut microbiome can significantly influence the antitumor efficacy of key chemotherapy agents, including 5-fluorouracil, oxaliplatin, and docetaxel. These agents form the backbone of the neoadjuvant chemotherapy (NAC) regimen, FLOT, which is widely used for the treatment of locally advanced gastric cancer (GC). However, despite growing evidence from preclinical models, clinical studies investigating the direct association between gut microbiome composition and the response to NAC in GC patients remain scarce.

Aims & Methods

This study aims to address this gap in knowledge by exploring the relationship between the gut microbiome and therapeutic outcomes in this clinical context. In this longitudinal observational study, we explored the association between pre-treatment fecal microbiome composition analyzed via 16S rRNA gene sequencing and histological tumor regression, as assessed by the Becker score, in GC patients undergoing NAC with the FLOT regimen, followed by gastrectomy.

Results

Among the 38 enrolled patients, 19 (50%) achieved a Becker score of 1–2 and were classified as ‘Responders,’ while the other 19 (50%) were classified as ‘Non-responders’. Responders exhibited a higher abundance of Parabacteroides distasonis, Alistipes sp. AL-1, and Bacteroides plebeius. A combined biomarker of these species demonstrated robust predictive accuracy for a favorable response to NAC, with sensitivity of 89%, specificity of 63%, and an AUC of 0.8 (95% CI: 0.66–0.94). In contrast, non-responders showed a predominance of bacterial genera, including Ruminococcaceae UCG-014, Ruminococcus 1, Ruminococcaceae UCG-005, and the [Eubacterium] eligens group. The combined biomarker of these genera demonstrated excellent predictive performance for poor NAC response, with sensitivity of 89%, specificity of 95%, and an AUC of 0.93 (95% CI: 0.85–1.0).

Conclusion

The results of our study support the hypothesis that the pre-treatment gut microbiome composition can serve as a reliable biomarker for predicting both positive and negative responses to NAC in GC patients. By identifying specific microbial signatures associated with chemotherapy outcomes, this research provides critical insights into how microbiome-based strategies might enhance personalized treatment regimens for GC. Future studies are needed to validate these findings and explore potential therapeutic interventions targeting the microbiome to improve clinical outcomes in GC patients.

Clinical Case Summary

The patient was a 39-year-old man admitted to the emergency department for sudden onset of diffuse abdominal pain. The patient had a pathological history of chronic smoking. The clinical history dates back 10 hours to the onset of abdominal pain, initially localized to the epigastrium and rapidly generalized to the entire abdomen, unrelieved by usual treatment and without other associated signs. The patient was conscious, normocardiac, normotensive, slightly tachypneic and apyretic. A diffuse abdominal tenderness was noted, with no other particular pathological signs. Biological work-up revealed hyperleukocytosis at 20430/mm3 , C-reactive protein (CRP) at 5.80 mg/L , no hydroelectrolytic disorders, and the rest of the biological work-up returned normal. Abdominal CT revealed pneumo bubbles with infiltration of mesenteric fat, predominantly at the supra-mesocolic level, in favor of a hollow organ perforation. The patient underwent surgery, which revealed a pre-pyloric gastric perforation measuring approximately 1 cm with a clean edge and the presence of 2 hepatic nodules measuring 0.25 and 0.5 cm in segment II. The rest of the exploration was without anomalies, and the gastric perforation was sutured, with biopsy of the edges of the gastric perforation and biopsy of the hepatic nodules. Histopathological examination revealed the presence of subacute and chronic nonspecific inflammatory remodeling in the gastric margin biopsy, whereas the liver biopsy showed epithelial and gigantocellular granulomatous inflammation with caseous necrosis consistent with tuberculosis.The diagnosis of hepatic tuberculosis was made.The patient was put on standard anti-tuberculosis treatment for 6 months.

Clinical Case Summary

A 36-year-old man with a history of chronic diarrhea was admitted with isolated oedemato-ascitic syndrome and general deterioration.On examination,he had conjunctival subicterus bilateral lower limb edema, thoracoabdominal collateral venous circulation and ascites.As part of the etiological work-up of the oedemato-ascitic syndrome,Cardiac and renal causes were ruled out.Chest X-ray showed a hilar opacity with tracheal retraction.GeneXpert test on sputum confirmed pulmonary tuberculosis.Paracentesis showed non-infected transudate ascites with a serum-ascites albumin gradient at 11 g/L.Blood tests showed microcytic hypochromic anemia,normal platelet count,and elevated liver tests with AST at 18 times the upper limit of normal (ULN), ALT at 11× ULN, alkaline phosphatase at 3.3× ULN,normal GGT,prothrombin time at 25%,and a direct hyperbilirubinemia of 24 mg/L.Viral serologies were negative.Serum protein electrophoresis showed a beta-gamma bridging pattern with hypergammaglobulinemia.Antinuclear antibodies were positive, while the remaining autoimmune panel and Wilson's disease screening were negative.Abdominal CT angiography showed hepatomegaly with hypertrophy of the caudate lobe,a “flip-flop” pattern,stenosis of the intrahepatic inferior vena cava, and non visualization of the hepatic veins confirming Budd-Chiari syndrome(BDS).The etiological work-up of the chronic diarrhea revealed negative HIV serology,normal TSH,and elevated IgA anti-transglutaminase antibodies.Ileocolonoscopy showed partial villous atrophy in the ileum,supporting the diagnosis of coeliac disease (CD).Given the radiological features suggestive of BDS,a thrombophilia work-up was performed and was negative.An autoimmune etiology related to CD was retained as the most likely cause of BDS.A gluten-free diet resolved the diarrhea.Anticoagulation was started, but persistent portal hypertension and difficulty maintaining therapeutic anticoagulation led to referral for a portosystemic shunt.

References

An actual image of the thoracoabdominal collateral venous circulation of the patient, and his abdominal CT angiography.

Clinical Case Summary

Acute Esophageal necrosis (AEN) is a rare clinical entity, with fewer than 150 reported cases in literature and endoscopic prevalence ranging from 0.01 to 0.28%(1). First described by Goldenberg and later characterized by Gurvits in 2007, this condition predominantly affects the distal esophagus due to its relatively poor blood supply, resulting in its characteristic black appearance. AEN typically occurs in male patients with predisposing risk factors such as chronic liver disease, chronic kidney disease, alcoholism, malnutrition and cardiovascular comorbidities(2). It is also associated with sepsis and carries a high mortality rate. Upper gastrointestinal endoscopy remains the gold standard (3). Given the rarity of AEN, the standardized management guidelines are not well defined and the primary therapeutic focus remains on optimizing medical condition.
We present the case of an 81-year old female, marking the first documented instance of AEN in Ireland, who presented with septic shock, profound hypoglycemia with hypothermia and workup revealed Acute Esophageal Necrosis. The development of AEN in our patient was multifactorial, with esophageal ischemia secondary to septic shock induced hypotension playing a key role. The condition may have been exacerbated by reduced cardiac output and vasoconstriction of splanchnic blood vessels secondary to hypothermia. Furthermore, gastric reflux likely contributed to additional mucosal injury. The patient was managed successfully with conservative yet aggressive approach with inotropic support, antibiotics and total parenteral nutrition.
We conclude that AEN should be considered in any patient with predisposing risk factors, particularly in presence of critical illness. This case highlights the urgent need for development of standardized guidelines to ensure timely diagnosis and optimal management for this rare but serious condition.
The poster will include pictures of Upper GI endoscopy of the patient

References

1. Goldenberg SP, Wain SL, Marignani P. Acute necrotizing esophagitis. Gastroenterology. 1990 Feb;98(2):493-6. doi: 10.1016/0016-5085(90)90844-q. PMID: 2295407.

2. https://pubmed.ncbi.nlm.nih.gov/17322991/

3. Sina (2023). Acute Esophageal Necrosis: A Rare and Serious Cause of Digestive Bleeding - Clinical Case Reports Journal (ISSN 2767-0007). [online] Clinical Case Reports Journal. Available at: https://clinicalcasereportsjournal.com/article/1000264/acute-esophageal-necrosis-a-rare-and-serious-cause-of-digestive-bleeding [Accessed 28 Feb. 2025].

Clinical Case Summary

A 62-year-old woman with hypothyroidism and multiple sclerosis presented to our care to underwent outpatient esophagogastroduodenoscopy (EGD) after one episode of hematemesis, which had occurred 20 days earlier following the use of Naproxen (440 mg/day) for low back pain. Proton pump inhibitor (PPI) therapy had been initiated afterward. EGD revealed a 20 mm ulcer in the gastric body with an adherent clot. Upon gastric distension, oozing bleeding from the ulcer was observed and treated with adrenaline injection and endoscopic clips. Diffuse oozing from the gastric mucosa and multiple suction-related hematomas were also noted. The patient was hospitalized and started on high-dose intravenous PPI therapy and fasting. H. pylori serology was negative. Physical exam showed hepatomegaly and lower limb edema. Lab tests revealed elevated cholestatic enzymes, proteinuria, leukocytosis, hypoalbuminemia, mild anemia, and a monoclonal spike on serum protein electrophoresis. Abdominal ultrasound confirmed hepatomegaly. Autoimmune, viral, and metabolic liver diseases were excluded. Liver magnetic resonance raised suspicion of a storage disorder. Liver biopsy confirmed AL-type amyloid deposits. A follow-up EGD was performed, in absence of further GI bleeding, to obtain gastric biopsies. It showed a 1 cm ulcer with an adherent clot in the fundus. Again, insufflation triggered diffuse oozing from the ulcer and gastric mucosa with suction-related hematomas. Histology confirmed amyloid deposits. Suspecting multiple myeloma, immunofixation identified Bence-Jones proteinuria and hypergammaglobulinemia. Spinal MRI showed vertebral collapse at D12–L1; cardiac MRI excluded cardiac involvement. MM with secondary AL amyloidosis was diagnosed. Treatment with targeted therapy led to symptom resolution.This case highlights the importance of considering rare systemic diseases in atypical GI bleeding, especially when triggered by minimal stimuli such as gastric distension.

References

1. Histological images of liver and stomach with amyloid deposits.
2. Endoscopic images of gastrointestinal bleeding manifestations in patients with gastric amyloidosis