Introduction

Gastric injury induces metaplasia is based on parietal cells loss and reprogramming chief cells into proliferative, mucin-rich spasmolytic polypeptide-expressing metaplasia (SPEM) cells. Previously, we demonstrated that parietal cell-selective Slc26a9 deficiency in mice promotes the development of SPEM and progress to gastric intraepithelial neoplasia in mice (Liu et al., Cellular oncology; 2022; Deng et al., DDW2023). However, the exact role of Slc26a9 in injury-induced metaplasia is need further investigated.

Aims & Methods

We used immunostaining to characterize the expression pattern of Slc26a9 during murine gastric development, homeostasis, and injury in homeostasis, after conditionial genetic deletion of Slc26a9. Furthermore, to reveal the functional role of Slc26a9, Injury-induced metaplasia was established in Slc26a9^fl/fl mice and Slc26a9^fl/fl/Atp4b-Cre mice with high-dose tamoxifen.

Results

Mice with parietal cell selective Slc26a9 deficiency first developed spontaneous parietal cell damage, which subsequently led to SPEM. Parietal cell injury was associated with the release of typical pyroptosis factors, including NRLP3, Caspase-1, ASC, GasderminD, IL-1β and IL-18. At the same time, SLC26A9 colocalized with caspase1, NLRP3, GSDMD, and NLRP3 and GSDMD, and produced a large number of reactive oxygen species (ROS), markers of mitochondrial damage, thereby expanding membrane perforation of GSDMD-N fragments and amplifying inflammasome-mediated parietic cell pyrodeath. At the same time, electron microscopy showed that after the knockout of the Slc26a9 gene, the mitochondria of the murine wall cells were obviously swollen, the cell membrane structure was blurred and damaged, the matrix was more dissolved, the ridge was broken and disappeared, and there were many bubble protrusions. This suggests that parietal cell specific SLC26A9 gene deletion may lead to parietal cell scorch death through mitochondrial damage mediated by GSDMD. However, with a large number of parietal cell damage and loss, gastric hypergastrinemia stimulates Tuft cell proliferation and migration to the gastric mucosa for colonization, and secretes a series of alarm hormones such as IL-25, IL-33, HMGB1. Moreover, ILC2 cell secretory factors such as IL-17RA and IL-17RB, GATA3, CD90, CD25 were up-regulated. M2 macrophage polarization-related markers such as Arg1, Fizz1, Ym1, Klf4 and secreted chemokines such as CCL24 and CCL22 were significantly up-regulated. The immunofluorescence staining of F4/80+ and CD163+ was significantly increased. This suggests that the spontaneous injury of parietal cells caused by the deletion of SLC26A9 gene in gastric parietal cells may lead to gastric dysfunction (hypoacid and hypergastrinemia) and mucosal epithelial injury, which may promote the occurrence of SPEM through IL-25 mediating the activation of ILC2 cells to regulate the cellular immune mechanism of macrophage M2 polarization.

Conclusion

Slc26a9 target deletion in parietal cells leads to spontaneous damage and scorch death of parietal cells, which is the core target and cell origin of initiating SPEM. After parietal cell specific Slc26a9 gene deletion leads to spontaneous injury of parietal cells, gastric dysfunction and mucosal injury result in the release of alarm hormone IL-25, which promotes the development of SPEM by activating IL-25-ILC2-macrophage M2 polarization axis. Slc26a9 plays an important protective role in stabilizing gastric epithelial cell differentiation and gastric mucosal immune homeostasis.

Disclosure

No conflict of interest

Clinical Case Summary

A 70-year-old patient with diabetes mellitus and cholecystectomy performed six months earlier was admitted to the emergency department for generalized abdominal pain, hyporexia and weight loss.
An abdominal CT scan showed a solid-cystic pancreatic lesion suggestive of mucinous neoplasia, together with peritoneal nodules in the right paracolic gout. In view of the suspicion of malignancy, an echoendoscopy with fine needle aspiration puncture (EUS-FNA) was performed, identifying an irregular lesion with heterogeneous and hypovascular ultrastructure in the pancreatic neck-body and a discrete dilatation of the main pancreatic duct. Finally, the histological study didn´t show neoplastic cells.
Suddenly the patient experienced a clinical worsening with severe pain and high fever. Laboratory tests showed a progressive increase in C-reactive protein and leukocytosis with left shift. In a control CT scan, a reduction in the size of the pancreatic lesion is observed, together with an increase in the peritoneal lesions which present a polyglobulated contour, hypercapillary margins and rarefaction of the surrounding fat. These finding suggesting the presence of peritoneal abscesses secondary to dropped gallstones. After broad-spectrum antibiotic therapy, the intra-abdominal abscesses improved radiologically, but the collection persisted in the right posterior pararenal space which was drained under ultrasound control with subsequent disappearance of fever and normalization of analytical parameters.
Dropped gallstones occur in approximately 7% of cholecystectomies. The secondary granulomatous reaction in paucisymptomatic patients can simulate peritoneal tumor processes in imaging tests, being one of the adverse effects described in relation to this pathology. In our case, the concomitant presence of peritoneal lesions together the pancreatic lesion oriented the initial case as a malignant process; however, the patient's evolution were key to the final diagnosis.

Introduction

Despite advances with chemotherapy regimens, Pancreatic adenocarcinoma (PDAC) is becoming the 2^nd cause of cancer-related death. Personalized medicine will be the game changer, but molecular characterization of pancreatic neoplasms is yet extremely cumbersome and has been performed on surgical samples or few EUS-tissue acquisition (TA) cases, mostly for DNA analysis. Our aim was to evaluate DNA and RNA extracted for research purposes from pancreatic neoplasms employing Endoscopic Ultrasound (EUS) Fine needle aspiration (FNA) and biopsy (FNB) and adequacy to molecular analyses.

Aims & Methods

From Oct 2022, patients with solid pancreatic neoplasms suggestive of either PDAC or neuroendocrine neoplasm (NEN) undergoing diagnostic EUS-TA were considered for enrollment. Employed needles were either FNA, or Franseen, Fork-tip or Three-prong, either 22G or 25G based on operator’s preference, with Rapid on Site Evaluation and, in case of adequacy within the first 2 passes, 1 additional pass with the same needle was performed for molecular analyses. DNA and RNA were then extracted with a new technique and nucleic acids were quantified and evaluated for adequacy for molecular analysis. Mann-Whitney was employed for comparison of continuous variables, and Kruskal-Wallis test for comparison between multiple groups; Logistic regression was applied to determine factors associated with adequacy to molecular tests.

Results

351 patients underwent sampling for molecular analyses, 309 with a definitive diagnosis of PDAC and 42 with NEN. 92,9% of patients were sampled with 25G FNA needles. Median quantity of DNA extracted was significantly lower in PDAC 2048 ng (95%CI: 1470 -3651) compared to NEN 6752 ng (95%CI: 3502-9655)(p<0.0144). Mean quantity of RNA extracted was similar, 312 ng for PDAC, and 444 ng for NEN (p=0.07), with a higher median RIN of 6,4 (95%CI:6,2-6,5) for PDAC versus 4,7 (95%CI:3,9-5) for NEN (p<0.0001). In terms of needle type, concerning DNA extraction, 25G FNA needles retrieved a median of 3384 ng, 25G Franseen needles (4312 ng), 22G Franseen (73864 ng), 25G Fork-tip or Three-prong (3104 ng), with no significant difference. In terms of needle type, concerning RNA extraction, 25G FNA needles retrieved a median of 310 ng (RIN 6,3), 25G Franseen needles 460 ng (RIN 5,5), 22G Franseen 884 ng (RIN 5,9), 25G Fork-tip or Three-prong 301 ng (RIN 5,15), with no significant difference. 295 (95,5%) of PDAC samples and 34 (80,9%) of NEN samples were considered adequate for sequencing. The only factor associated to adequacy for molecular analysis was tumor type, with PDAC having an OR of 5,44 (95%CI 2,06-14,37)(p=0.0006), while the type of employed needle was not

Conclusion

Molecular analysis on EUS-acquired tissue of pancreatic neoplasms will be the mainstay of personalized therapies but how to best perform tissue acquisition and sample handling for this specific purpose is yet to be defined. This is the largest study ever performed on DNA and RNA extraction from EUS-acquired samples, demonstrating superior adequacy for molecular analysis in PDAC compared to NEN. All needle types result similar in terms of performance despite the low number of needles other than 25G FNA needles.

Introduction

Inflammatory cells and cytokines play an instrumental role in the pathogenesis and disease course of ulcerative colitis (UC) and are thus accepted therapeutic targets. NX-13 is a first-in-class, orally active, once-daily, gut-selective NLRX1 agonist in development for UC. NLRX1 is a mitochondrial associated protein with a novel, bimodal, immunometabolic mechanism which upregulates mitochondrial metabolism, reduces oxidative stress, and decreases pro-inflammatory cell differentiation and cytokine release broadly in mouse models of IBD¹. NX-13 was well tolerated and showed gut selectivity with low systemic drug exposure in Phase 1 studies reported previously^2,3. We now present data from the phase 1b study describing changes in tissue cytokine levels and related to clinical response.

Aims & Methods

In this double-blind phase 1B trial (NCT04862741)³, 36 patients with active UC (Total Mayo Score 4-10; Mayo endoscopic subscore 2-3) were randomly assigned to NX-13 250mg Immediate Release (IR), 500mg IR, 500mg Delayed Release (DR) or Placebo QD for 4 weeks. Protein levels of IFNγ, IL-10, IL-12(p40), IL-17, IL-4, IL-6, IL-8, MCP1, and TNFα in colonic tissue from NX-13 treated patients collected at screening (baseline) and week 4 of treatment were determined by Human Cytokine/Chemokine Panel – Immunology Multiplex Assay (Millipore Sigma) normalized to total protein concentrations. Patients from all NX-13 dose groups with paired baseline and week 4 samples (n=18) were included in this analysis. Mann-Whitney U testing was used for comparisons between responders (Resp) and non-responders (NR).

Results

Baseline cytokines levels were not different between Resp (change from baseline of at least –3, or –30% in total Mayo Score) and NR. NX-13 treatment resulted in a decrease of multiple proinflammatory cytokines at week 4 compared to baseline in most patients, and especially in Resp. compared to NR at week 4 (Table 1). Primarily, the reduction (% change from baseline) of Th1 cytokines IL-12(p40) and IFNγ was greater in NX-13 treated patients with clinical response compared to NR, resulting in significantly lower values in Resp compared to NR at the end of the 4-week study. Similarly, IL-6 also tended to be lower among Resp. after 4 weeks of treatment with NX-13. Additionally, Th2 cytokine IL-4 values were significantly lower after 4 weeks of NX-13 in patients in clinical response compared to NR. Myeloid cell recruitment may also have been affected by cytokine changes induced by NX-13 as IL-8 and MCP levels were lower in clinical Resp. Reduced myeloid cell recruitment is consistent with higher levels of histologic remission in NX-13 treated patients³.

Conclusion

Broad changes in tissue cytokine expression were specifically observed in patients that responded to NX-13- after 4 weeks of treatment, compared to non-responders. These changes mirror those seen in preclinical mouse colitis models where a broad array of cytokines is reduced¹. The early onset of cytokine shifts associated with clinical response to NX-13 at week 4 is notable and will be assessed in the ongoing phase 2 NEXUS study in patients with moderate to severe UC (NCT05785715).

References

¹Leber, et al. J Immunol 203(12); ²Leber, et al. UEGW J 9(Supp); ³Verstockt, et al. JCC epub 11NOV2023

Disclosure

BS has received grant support from Pfizer (to institution); served as a consultant (served as a representative of Charité) for AbbVie, Arena, BMS, Boehringer, Celgene, Endpoint Health, Falk, Galapagos, Janssen, Landos, Lilly, Pfizer, PredictImmune, and Takeda; and has received speaker’s fees (served as a representative of Charité) from AbbVie, CED Service GmbH, Falk, Ferring, Galapagos, Janssen, Lilly, Pfizer, and Takeda; support for attending meetings/travel from Falk; and served as president of ECCO. | SV has received grants from AbbVie, J&J, Pfizer, Takeda, and Galapagos; consulting and/or speaking fees from AbbVie, Abivax, AbolerIS Pharma, AgomAb, Alimentiv, Arena Pharmaceuticals, AstraZeneca, Avaxia, BMS, Boehringer Ingelheim, Celgene, CVasThera, Cytoki Pharma, Dr Falk Pharma, Ferring, Galapagos, Genentech-Roche, Gilead, GSK, Hospira, Imidomics, Janssen, J&J, Lilly, Materia Prima, MiroBio, Morphic, MrMHealth, Mundipharma, MSD, Pfizer, Prodigest, Progenity, Prometheus, Robarts Clinical Trials, Second Genome, Shire, Surrozen, Takeda, Theravance, Tillots Pharma AG, and Zealand Pharma. | AY reports consulting fees from Takeda, Prometheus Labs, Arena Pharmaceuticals, and Bristol Myers Squibb; and speaker bureau fees from Bristol Myers Squibb. | SS has received personal fees from AbbVie, Amgen, Arena Pharmaceuticals, Bristol Myers Squibb, Boehringer Ingelheim, Celltrion, Dr Falk Pharma, Ferring, Fresenius, Galapagos, Genentech, GSK, Gilead, I-MAB Biopharma, Janssen, Lilly, Merck, Novartis-Sandoz, Pfizer, Protagonist, Takeda, and Theravance. | SD reports consultancy fees from AbbVie, Alimentiv, Allergan, Amgen, AstraZeneca, Athos Therapeutics, Biogen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Celltrion, Dr Falk Pharma, Eli Lilly, Enthera, Ferring Pharmaceuticals Inc., Gilead, Hospira, Inotrem, Janssen, Johnson & Johnson, MSD, Mundipharma, Mylan, Pfizer, Roche, Sandoz, Sublimity Therapeutics, Takeda, TiGenix, UCB Inc., and Vifor; he reports lecture fees from Abbvie, Amgen, Ferring Pharmaceuticals Inc., Gilead, Janssen, Mylan, Pfizer, and Takeda. | RM is an employee of Landos. | FC is an employee of Landos. | BV has received grants from Abbvie, Biora Therapeutics, Landos, Pfizer, Sossei Heptares, and Takeda; Speaker’s fees from Abbvie, Biogen, Bristol Myers Squibb, Celltrion, Chiesi, Falk, Ferring, Galapagos, Janssen, MSD, Pfizer, R-Biopharm, Takeda, Truvion and Viatris. Consultancy fees from Abbvie, Alimentiv, Applied Strategic, Atheneum, Biora Therapeutics, Bristol Myers Squibb, Galapagos, Guidepoint, Landos, Mylan, Inotrem, Ipsos, Janssen, Progenity, Sandoz, Sosei Heptares, Takeda, Tillots Pharma and Viatris. | MCD reports consulting fees from AbbVie, Arena, Bristol Myers Squibb, Celgene, Eli Lilly, Genentech, Gilead, Janssen, Pfizer, Prometheus Labs, and Takeda; and is founder and a shareholder of Trellus Health.

Introduction

In patients with chronic pancreatitis (CP), pancreatic exocrine insufficiency (PEI) and poor nutritional intake may cause nutritional deficiencies. Guidelines advise monitoring key nutrients and supplementing is case of deficiency to prevent malnutrition-related complications. However, adherence remains low, possibly due to limited evidence on the clinical relevance of single nutrient deficiencies and the benefit of targeted supplementation. The aim of this study is to evaluate the prevalence of nutritional deficiencies in patients with CP and to identify predictors of those at highest risk. Secondary, we seek to explore association between nutritional deficiencies and malnutrition-related complications, and to provide insight into the natural course of nutritional deficiencies.

Aims & Methods

We analyzed data from the COMBO-trial, a nationwide stepped-wedged cluster randomized trial to evaluate the effect of an evidence-based algorithm for the management of CP. Measurements of fat-soluble vitamins, minerals, and albumin conducted in the outpatient clinic during the 35-month study period were included. PEI was defined as fecal elastase-1 concentration <200 µg/g or the use of pancreatic enzyme replacement therapy (PERT). The Pancreatic Exocrine Insufficiency Questionnaire (PEI-Q), designed to evaluate the severity of PEI symptoms, was administered at four distinct time points throughout the study. Supplement use was collected from health records and patient questionnaires. Multivariate logistic regression analysis was performed for the presence of multiple deficiencies. Potential predictors included patient and disease characteristics at baseline and the mean score of the PEI-Q during follow-up.

Results

In total 409 patients were included in this study. At baseline 327 (80.0%) had PEI and PERT was used by 297 (72.6%). Nutritional deficiencies were present in 195 patients (47.7%) of which 81 (19.8%) had multiple deficiencies. The prevalence of deficiencies included vitamin A in 13/172 (7.6%) patients, vitamin D 111/289 (38.4%), vitamin E 15/168 (8.9%), vitamin K 52/88 (59.1%), iron 44/137 (32.1%) calcium 4/198 (2.0%), magnesium 24/132 (18.2%) zinc 13/67 (19.4%), selenium 4/42 (9.5%), and albumin in 41/288 (14.2%) patients. No abnormal coagulation was observed in the 20 patients with vitamin K deficiency and available INR measurements. Osteopenia was diagnosed in 110/236 (46.6%) and osteoporosis in 56/236 (23.7%). Deficiencies in vitamin K and vitamin D, micronutrients critical to bone metabolism, were not associated with osteopenia or osteoporosis. Of 44 patients with an iron deficiency, 22 (50%) were anemic. Deficiency resolved without single nutrient supplementation in 71.4% (vitamin A), 75.0% (vitamin D), 50.0% (vitamin E) , 33.3% (vitamin K), 63.6% (iron), 100% (magnesium), 80.0% (zinc) of cases. Independent predictors for multiple deficiencies were more severe PEI symptoms (OR 1.86, 1.09 – 3.17) and daily alcohol consumption (OR 2.80, 1.27 – 6.18).

Conclusion

Nutritional deficiencies are present in approximately half of the patients with CP. Most nutritional deficiencies resolve without single nutrient supplementation. Predictors for multiple nutritional deficiencies were severity of PEI symptoms and daily alcohol consumption. Therefore, nutritional deficiencies should be considered a marker of malnutrition, with treatment focused on addressing the underlying cause rather than isolated correction through single nutrient supplementation.

Introduction

Acute pancreatitis (AP) is associated with an intense catabolic, local-regional and systemic inflammatory state, which can lead to changes in body composition, with prognostic implications.

Aims & Methods

Aims: To evaluate the body composition by anthropometry, bioelectrical impedance analysis (BIA) and computed tomography (CT) and its influence in AP severity, endocrine insufficiency (EnPI-AP), pancreatic exocrine (EPI-AP) and post-pancreatic enzyme replacement therapy (PERT).
Methods: Prospective longitudinal study of consecutive adult patients diagnosed with first AP episode. EPI-AP patients were randomized to receive PERT (4000IU/meal+20000IU/snack) vs. placebo (clinicaltrials.gov:NCT05480241). Body composition was assessed using anthropometry, BIA (InBody 570) and CT (cross-sectional areas L1/L3). Obesity was diagnosed for body mass index (BMI)≥30Kg/m², waist-to-hip ratio (WHR)>0.9(men)/0.85(women) and percentage total fat mass (TFM)>20%(men)/28%(women). Visceral obesity was defined by abdominal circumference (AC)>94(men)/80(women)cm, visceral fat area (VFA)≥100cm² and visceral/subcutaneous fat ratio (VSFR)≥0.4. Sarcopenia was diagnosed by skeletal muscle mass (SMM)<20(men)/15(women)Kg, SMM index (SMMi)<7.0/5.5Kg/m² and skeletal muscle area index (SMAi)<41(men)/38.5(women)cm². The three methods were correlated using spearman test and Bland-Altman plots.

Results

A total of 105 patients (65.7%(n=69) males; mean age:63.8±17.1yo) were enrolled and followed-up. AP was moderately-severe/severe in 32.4%/16.2%. EPI-AP and EnPI-AP occurred in 47.6%(n=50) and 17.1%(n=18). EPI-AP was persistent (≥6months after AP diagnosis) in 58%. After 6-month post-randomization, 44%(n=11/25) under PERT and 40%(n=10/25) under placebo resolved EPI-AP (p=0.598).
Obesity was diagnosed in 19.0%(n=20) by BMI, 97.1%(n=102)/72.4%(n=76) by WHR in antropometry/BIA, and 57.1%(n=60) by TFM. Visceral obesity was diagnosed in 78.1%(n=82) by AC, in 41.9%(n=44)/ 97.2%(n=103) by VFM in BIA/CT and in 90.5%(n=95) by VSFR. Sarcopenia was diagnosed in 1.0%(n=1) by MMS.
Considering outcomes, moderately-severe/severe AP was strongly associated with WHR by BIA (OR=10.2; p=0.034) and VFA by BIA (OR=1.08; p=0.029) and CT (OR=1.003; p=0.038). EPI-AP was statically associated with WHR by BIA (OR=11.6; p=0.048) and SMMi by BIA (OR=77.4; p=0.048) and TFM (OR=2.3; p=0.048). Severe EPI-AP was strongly associated with VSFR (OR=20;95%CI; p=0.048) and SMMi by BIA (OR=23.2; p=0.003) and CT (OR=2.3; p=0.041). SMMi by BIA (OR=14.1; p=0.030) and CT (OR=1.6; p=0.031) predicted EnPI-AP.
For obesity, TFM by BIA had a strong correlation with BMI (r=0.61; p<0.001) and a weak correlation with WHR by anthropometry (r=0.37; p<0.001). Regarding visceral obesity, VFA by BIA was weakly correlated with WHR by anthropometry (r=0.29; p=0.004) and VFA by CT (r=0.20; p=0.045). For sarcopenia, SMM by BIA was strongly correlated with SMM by CT (r=0.78; p<0.001).
In EPI-AP patients, a significant decrease of WHR (t(52)=2.262; p=0.028) and TFM (t(53)=1.695; p=0.046) by BIA was observed after 6months of PERT.

Conclusion

Body composition is significantly changed in AP, with >2/3 of patients with obesity, especially the visceral component. Obesity, including visceral obesity, correlates with AP severity. Obesity, including visceral obesity and sarcopenia are correlated with the EPI-AP and its severity, while sarcopenia is correlated with EnPI-AP. PERT has led to a significant reduction in obesity markers. Body composition assessment by BIA (TFM, VFA and SMM) and CT (VFA and SMM) were of clinical value and comparable.

References

1. Kim J, Kim S-s, Hwang HK, Kang CM, Kim KS, Kim SH. Body composition assessment using bioelectrical impedance analysis and computed tomography in patients who underwent pancreatoduodenectomy in Korea: a before and after study. Ann Nutr Metab 2023;15(3):72-80.
2. Wang S, Wang M, Jiang L, Zhao X. Low skeletal muscle quality extracted from CT is associated with poor outcomes in severe acute pancreatitis patients. Eur J Radiol 2024;170:111215.
3. Zhou Y, Hao N, Duan Z, Kong M, Xu M, Zhang D, et al. Assessment of acute pancreatitis severity and prognosis with CT-measured body composition. Int J Gen Med 2021;14:3971-3980.
4. Chaigneau T, Morello R, Vannier E, Musikas M, Piquet M-A, Vupont B. Impact of sarcopenic obesity on predicting the severity of acute pancreatitis. Did Liver Dis 2023;55(7):926-932.

Introduction

The incidence of elderly-onset ulcerative colitis (EO-UC) and Crohn’s disease (EO-CD) is increasing globally. However, whether the initial disease presentation of EO-UC and EO-CD differs from that in adult-onset (AO) is currently poorly investigated.

Aims & Methods

The aims of this study were to explore the initial presentation, severity, and disease course of newly diagnosed EO-UC and EO-CD (age ≥60 years) in comparison to AO-UC and AO-CD (18–59 years). The study was conducted as an ongoing prospective population-based inception cohort, IBD Prognosis Study, with enrollment between May 2021 and April 15^th, 2023, within a catchment population of 1.050.000 citizens (~20% of the Danish population). We defined severe disease course as requiring surgery or initiation of biological therapies within six months of diagnosis.

Results

The cohort comprised 501 patients, including 398 (79.4%) with AO disease (AO-UC: 223 (56.0%), AO-CD: 145 (36.4%), AO-IBDU: 30 (7.5%)), and 99 (19.8%) with EO disease (EO-UC: 64 (64.6%), EO-CD: 35 (35.4%), EO-IBDU: 5 (5.1%)). A comparison of the clinical presentation, severity, and initial disease course is presented in Table 1. As shown, EO-UC and EO-CD did not differ significantly from AO-UC and AO-CD in terms of demographic factors, disease phenotype, severity, and initial therapy. However, a significantly higher proportion of patients with EO-UC had left-sided UC, and tended to be treated less frequently with biological therapies and immunomodulators.
In a Cox multivariable regression model with Bonferroni correction adjusting for disease type and gender, patients with EO-UC (adjusted hazard ratio (aHR)=1.9 (95% confidence interval (CI) 0.5-7.3)) and EO-CD (aHR =4.1 (95% CI 0.3-12.3)) were not at different risk of requiring surgery or initiation of biological therapies within six months of diagnosis than patients with adult-onset IBD.
Table 1: Pairwise comparison of newly diagnosed elderly-onset and adult-onset inflammatory bowel diseases

Conclusion

In this population-based study, we found no difference between EO-IBD and AO-IBD in terms of initial disease presentation, severity, and course. However, patients with EO-IBD tended to be treated with less biological therapies and immunomodulators.

Disclosure

Mohamed Attauabi: None
Gorm Roager Madsen: None
Flemming Bendtsen: Tillotts, Ferring
Klaus Theede: Ferring, Janssen, Takeda, Pfizer, and Tillotts
Jakob Benedict Seidelin: has received research grants from Takeda, Janssen and is national coordinator of studies from AbbVie, Arena Pharmaceuticals, Ely Lilly, and Boehringer Ingelheim. None of these pertain to the research submitted here.
Johan Burisch: reports grants and personal fees from AbbVie, grants and personal fees from Janssen-Cilag, personal fees from Celgene, grants and personal fees from MSD, personal fees from Pfizer, grants and personal fees from Takeda, grants and personal fees from Tillots Pharma, personal fees from Samsung Bioepis, grants and personal fees from Bristol Myers Squibb, grants from Novo Nordisk, personal fees from Pharmacosmos, personal fees from Ferring, personal fees from Galapagos, outside the submitted work.