Introduction

Eosinophilic Oesophagitis (EOE) has a mean estimate of 63 new cases per 100,000 in the Western World and is in increasing prevalence¹. It must be considered as a differential diagnosis amongst patients presented with dysphagia and food bolus obstruction. British Society of Gastroenterology (BSG) guideline recommends that patients undergoing endoscopy should have oesophageal biopsies taken if they have endoscopic signs associated with EOE or symptoms of dysphagia or food bolus obstruction with normal looking oesophagus. At least six biopsies should be taken from at least 2 different anatomical sites within the oesophagus for diagnosis of EOE². (GDG recommendation).

Aims & Methods

A single-centre, retrospective analysis of patients presenting for an oesophagogastroduodenoscopy (OGD) with an indication of dysphagia or food bolus obstruction and coded as oesophagitis over the past 5 years was performed. The study was undertaken at a tertiary NHS Hospital Trust in West Midlands which provides hospital services for approximately 900,000 people³. Data was then collected for demographics, sedation, macroscopic findings, quality and location of biopsies as well as histology. This is measured against BSG recommendations.

Results

In total, 31 patients were included. 68% of patients were male and the mean age was 53 (range 14-90) 35% (n=11) had pharyngeal anaesthesia only, 16% (n=5) had midazolam and pharyngeal anaesthesia, 35% (n=11) had midazolam and fentanyl and 6% (n=2) had general anaesthesia (GA). Both patients who had GA were 14 and 15 years old. In terms of macroscopic findings, 61 % (n=19) had normal findings, 19% (n=6) had oesophagitis, 10 % (n=3) had EOE changes and 3% (n=1) had benign stricture with the same number for achalasia and tertiary contraction. 81% (n=25) had biopsies taken from at least 2 different anatomical sites and 32% (n=10) had more than 6 biopsies taken in total. There were 29 % (n=9) patients with a histological diagnosis of EOE, 29% was normal, 29% (n=9) had inflammation, 6% (n=2) had gastric metaplasia, 3% (n=1) had basal hyperplasia with 7-8 eosinophils per high-power field (HPF) and 3% (n=1) had basal hyperplasia with lymphocytic infiltration. In all patients with EOE, the histopathological report explicitly documented the presence of >15 eosinophils per HPF.

Conclusion

Our data suggest that our practice for diagnosis of EOE falls short of national recommendation, both in the number of anatomical sites and the number of biopsies taken. In terms of histopathology, we have adhered to the recommended diagnostic criteria of >15 eosinophils per HPF. Further work must be done to improve awareness and adherence to the guidelines for the diagnosis of this treatable condition.

References

1. Navarro P, Arias Ángel, Arias-González L, et al. Systematic review with meta-analysis: the growing incidence and prevalence of eosinophilic oesophagitis in children and adults in population-based studies. Aliment Pharmacol Ther 2019;49:1116–25.
2. Dhar A, Haboubi HN, Attwood SE, et al. British Society of Gastroenterology (BSG) and British Society of Paediatric Gastroenterology, Hepatology and Nutrition (BSPGHAN) joint consensus guidelines on the diagnosis and management of eosinophilic oesophagitis in children and adults. Gut 2022;71:1459-1487.
3. University Hospitals of North Midlands. About us. https://uhnm-appointments.co.uk/about-us/ [Accessed 23^rd November 2023]

Introduction

Bowel urgency (BU), the sudden or immediate need to have a bowel movement, is an impactful symptom of Crohn’s disease (CD) that varies in intensity¹. We report the efficacy of the IL-23 p19 inhibitor, mirikizumab (miri) in improving BU among patients with moderately-to-severely active CD from the phase 3 VIVID-1 trial (NCT03926130). VIVID-1 co-primary and gated endpoints, including comparison with ustekinumab, are already reported².

Aims & Methods

Adult patients (N=1065) were randomised to placebo (PBO) or miri 900mg intravenously at weeks (W) 0, 4, and 8, then 300mg subcutaneously every 4 weeks (Q4W) from W12 to W52. At W12, PBO responders continued PBO to W52, non-responders received the blinded miri regimen per protocol. BU was assessed at W12 and W52 using the Urgency Numeric Rating Scale (UNRS)³. We evaluated the proportion of patients with baseline (BL) UNRS ≥3 and ≥6 who achieved BU Clinically Meaningful Improvement (CMI; >3 change in UNRS) and BU remission (UNRS ≤2). Treatment comparisons used Cochran-Mantel-Haenszel tests with non-responder imputation for missing values.

Results

Study population: 55.1% male. Mean (SD) age 36.2 (13.0) years. Disease duration 7.4 (7.9) years. At BL, median (Q1, Q3) UNRS 6.9 (5.2, 8.1), 94.5% patients achieved UNRS ≥3 and 66.0% patients achieved ≥6. In patients with BL UNRS ≥3, nominally significantly higher proportions of miri versus PBO patients achieved BU CMI and BU remission at both W12 and W52 (Table). A nominally significantly greater proportion of miri-treated patients achieved W52 BU CMI-composite and BU remission-composite (Table). Similar results were seen with BL UNRS ≥6.

		W12 PBO	W12 Miri	W12 p-value	W12 95% CI	W52 PBO	W52 Miri	W52 p-value	W52 95% CI
	UNRSa CFB (LSM ±SE)	-1.58 (0.168)	-2.44 (0.099)	0.00011	-1.24, -0.48	-1.23 (0.180)	-3.24 (0.106)	<0.0001	-2.42, -1.60
Patients with BL UNRS ≥3	BU CMI-TT	50/186 (26.9)	227/547 (41.5)	0.0004	6.7, 22.0	38/186 (20.4)	301/547 (55.0)	<0.0001	28.0, 42.1
	BU CMI-compositeb					38/186 (20.4)	251/547 (45.9)	<0.0001	18.5, 32.8
	BU Remissionc-TT	29/186 (15.6)	134/547 (24.5)	0.01	2.3, 15.0	21/186 (11.3)	209/547 (38.2)	<0.0001	21.0, 33.2
	BU Remission-composite					21/186 (11.3)	180/547 (32.9)	<0.0001	15.7, 27.8
Patients with BL UNRS ≥6	BU CMI-TT	38/137 (27.7)	180/376 (47.9)	0.0001	9.8, 28.2	31/137 (22.6)	229/376 (60.9)	<0.0001	30.1, 47.3
	BU CMI-composite					31/137 (22.6)	188/376 (50.0)	<0.0001	18.4, 36.0
	BU Remission-TT	11/137 (8.0)	70/376 (18.6)	0.007	3.8, 15.8	13/137 (9.5)	126/376 (33.5)	<0.0001	17.1, 31.1
	BU Remission-composite					13/137 (9.5)	111/376 (29.5)	0.0002	13.2, 27.0

PBO, N=199; Miri, N=579. Data are N (%) unless otherwise stated. ^aUNRS scale: 0 (no urgency)-10 (worst possible urgency)³. ^bComposite=Clinical response by PRO (2 of the patient-reported items of the CDAI, AP and SF) at W12 and W52 parameter (CMI or Remission). ^cBU remission=no to minimal BU (UNRS≤2). Treatment comparison: CFB used a mixed model for repeated measures model containing treatment, BL value, visit, stratification factors and interaction of BL value by visit and treatment by visit. Response rates usedCochran-Mantel-Haenszel tests with non-responder imputation. AP=abdominal pain; BL=baseline; CFB=change from BL; CI=confidence interval; CMI=clinically meaningful improvement; LSM=least squares mean; PBO=placebo; PRO=Patient Reported Outcome; SD=standard deviation; SE=standard error; SF=stool frequency; TT=treat-through; UNRS=Urgency Numeric Rating Scale; W=week.

Conclusion

BU is one of the most unrecognised symptoms in patients with CD. Patients enrolled in VIVID-1 had high BU scores at BL. Compared to PBO-treated pts, miri-treated pts achieved nominally significantly higher rates of BU CMI and remission at W12 and W52.

References

1. Dulai PS, et al. Aliment Pharmacol Ther 2020; 51(11): 1047-66.
2. Ferrante, M et al. (2024). Journal of Crohn's and Colitis, 18(Supplement_1), i7-i9.
3. Dubinsky MC, et al.. Qual Life Res 2023; 32(12): 3403-15.

Disclosure

VP consulting/advisory board fees from AbbVie, Alimentiv Inc., Arena pharmaceuticals, Asahi Kasei Pharma, Asieris, Astra Zeneca, Avoro Capital, Bristol Myers Squibb, Celltrion, Lilly, Endpoint Health, Enthera, Ferring, Flagship Pioneering, Fresenius Kabi, Galapagos, Gilde Healthcare, GlaxoSmithKline, Genentech, Gilead, Innomar, JAMP, Janssen, Merck, Metacrine, Mylan, Pandion, Pendopharm, Pfizer, Protagonist, Prometheus Biosciences, Reistone Biopharma, Roche, Roivant, Sandoz, SCOPE, Second Genome, Sorriso, Takeda, TD Securities, Teva, Topivert, Ventyx, and Vividion; speaker’s fees from, Abbvie, Ferring, Bristol Myers Squibb, Galapagos, Janssen Pfizer Shire, Takeda, and Fresenius Kabi.
BES consulting fees from Abbvie, Alimentiv, Amgen, Arena Pharmaceuticals, Artugen Therapeutics, Astra Zeneca, Boehringer IngelheSim, Boston Pharmaceuticals, Calibr, Celgene, Celltrion, ClostraBio, Equillium, Enthera, Evommune, Fresenius Kabi, Galapagos, Genentech (Roche), Gilead Sciences, GlaxoSmithKline, Gossamer Bio, Index Pharmaceuticals, Innovation Pharmaceuticals, Inotrem, Kaleido, Kallyope, Merck, Morphic Therapeutics, MRM Health, Progenity, Prometheus Biosciences, Prometheus Laboratories, Protagonist Therapeutics, Q32 Bio, Sun Pharma, Surrozen, Target RWE,Teva, TLL Pharmaceutical, and Ventyx Biosciences; consulting/speaking fees from Abivax; consulting/speaking fees/other support from Lilly, Bristol Myers Squibb, Janssen, Pfizer, and Takeda; research grants and consulting fees from Theravance Biopharma; stock options from Ventyx Biopharma.
MC speaker, consultant, or has received research/education funding from MSD, AbbVie, Hospira, Pfizer, Takeda, Janssen, Ferring, Shire Pharmaceuticals, Dr Falk Pharma, Tillotts Pharma, Biogen, Gilead, and Lilly.
MChen provided educational activities for AbbVie, China Medical System, IPSEN, Janssen, and Takeda; advisory board for Boehringer Ingelheim and Janssen; support for clinical research from Janssen and Takeda.
GD’H adviser and/or speaker for Abbvie, Alimentiv, Amgen, Bristol Meiers Squibb, Boehringer Ingelheim, Celltrion, Ferring, Lilly, Engene, Galapagos, Glaxo Smith Kline, Immunic, Index Pharmaceuticals, Johnson and Johnson, Merck, Polpharm, Prometheus biosciences, Prometheus Laboratories, Procise diagnostics, Protagonist, Sandoz, Takeda, Tillotts, and Ventyx.
MD consultant for AbbVie, Arena, Astra Zeneca, Boehringer Ingelheim, Celgene, Lilly, Gilead, Janssen, Merck, Pfizer, Prometheus Laboratories, Takeda, and UCB; research grants from Janssen, AbbVie, and Prometheus Laboratories.
MF research grants from AbbVie, Biogen, EG, Janssen, Pfizer, Takeda, and Viatris; consultancy fees from AbbVie, AgomAb Therapeutics, Boehringer Ingelheim, Celgene, Celltrion, Lilly, Janssen-Cilag, MRM Health, MSD, Pfizer, Takeda, and ThermoFisher; speakers’ fees from AbbVie, Biogen, Boehringer Ingelheim, Falk, Ferring, Janssen-Cilag, MSD, Pfizer, Takeda, Truvion Healthcare, and Viatris.
LP-B personal fees from Galapagos, AbbVie, Janssen, Genentech, Ferring, Tillots, Celltrion, Takeda, Pfizer, Index Pharmaceuticals, Sandoz, Celgene, Biogen, Samsung Bioepis, Inotrem, Allergan, MSD, Roche, Arena, Gilead, Amgen, BMS, Vifor, Norgine, Mylan, Lilly, Fresenius Kabi, OSE Immunotherapeutics, Enthera, Theravance, Pandion Therapeutics, Gossamer Bio, Viatris, and Thermo Fisher Scientific; grants from AbbVie, MSD, Takeda, and Fresenius Kabi; holds stock options in Clinical Trials Mobile Application.
SS consultant/speaker fees from AbbVie, Allergosan, Amgen, Arena, BMS, Celltrion, Falk Pharma, Ferring, Galapagos, Gilead, Genentech (Roche), GSK, IMAB, Janssen, Lilly, MSD, Pfizer, Shire, Takeda, and Ventyx.
ST consultancy from Biogen, Bristol-Myers Squibb, Celgene, ChemoCentryx, Cosmo, Enterome, Ferring, Giuliani, GlaxoSmithKline, Genentech, Immunocore, Immunometabolism, Janssen, Lilly, MSD, Merck, Neovacks, Novonordisk, Novartis, NPS Pharmaceuticals, Pfizer, Proximagen, Receptos, Roche, Shire, Sigmoid Pharma, Takeda, Topivert, UCB, VHsquared, Vifor, Zeria, Sensyne, Satisfai, Bioclinica, Equillium, Mestag, Sorriso, Protagonist; research support from AbbVie, the International Organization for the Study of Inflammatory Bowel Diseases, Lilly, UCB, Vifor, Norman Collisson Foundation, Pfizer, UK–India Education and Research Initiative, ECCO Health Care, the Helmsley Trust; honoraria from AbbVie, Amgen, Biogen, Ferring, Takeda, Lilly; travel expenses covered or reimbursed from AbbVie, Lilly, Johnson & Johnson, Pfizer, Takeda, Ferring, Amgen, and Biogen.
HC, ZL, RM, MP, AV and KT are employees and stockholders of Lilly.
SG speaking commitments with AbbVie, Takeda, Janssen, Pfizer, Gilead, Galapagos, Ferring, Lilly and Company, and Celltrion; drug monitoring committees with Janssen; advisory committees with Janssen, AbbVie, Takeda, Gilead, Galapagos, Lilly, Pfizer, Celltrion, and Ferring; steering committees with Janssen, Bristol Myers Squibb, and AbbVie.

Introduction

C-reactive protein (CRP) and fecal calprotectin (FeCal) are non-invasive inflammatory biomarkers used to assess disease activity in UC. The Phase 3 QUASAR induction study evaluated the efficacy and safety of guselkumab (GUS), an IL-23 p19 subunit antagonist, in patients (pts) with moderately to severely active UC. Here, we analyze the effect of GUS treatment on CRP and FeCal through Week (Wk) 12 in pts with elevated CRP and/or FeCal.

Aims & Methods

Pts with a modified Mayo score of 5-9 and a Mayo endoscopy subscore ≥2 at baseline (BL) were randomized 3:2 to receive either GUS 200mg IV or placebo (PBO) IV at Wks0, 4, and 8. CRP and FeCal were assessed at BL, Wk4, Wk8 (for CRP only), and Wk12.

Results

A total of 701 pts were evaluated and approximately 50% of randomized pts had a history of inadequate response/intolerance to advanced therapies (ADT) for UC; 47.4% of these pts had inadequate response/intolerance to ≥2 ADT classes. Median BL concentrations of CRP and FeCal were similar between the GUS-treated and PBO-treated pts (4.34 vs 3.83mg/L and 1651 vs 1606mg/kg, respectively). Among pts with elevated CRP and/or FeCal at BL, greater reductions in CRP and FeCal were observed at the earliest timepoint assessed (Wk4) with GUS and continued through Wk12 compared with PBO (Table).
At BL, 248 GUS-treated pts and 160 PBO-treated pts had elevated CRP (>3mg/L); the proportions were similar between treatment groups (58.9% vs 57.1%, respectively). Among these pts, median change from BL in CRP concentration (mg/L) at Wk12 for the GUS and PBO cohorts were -3.99 and -0.51mg/L, respectively (nominal p<0.001); the proportions of pts achieving 50% and 75% reduction in CRP levels (or ≤3mg/L) at Wk12 were higher for GUS-treated pts than those receiving PBO (59.7% vs 28.1% and 47.2% vs 19.4%, respectively; both nominal p<0.001). Similarly, a higher proportion of GUS-treated pts achieved CRP≤3mg/L at Wk12 than PBO-treated pts (40.3% vs 16.3%, nominal p<0.001).
At BL, 333 GUS-treated pts and 225 PBO-treated pts had elevated FeCal (>250mg/kg); the proportions were similar between treatment groups (79.1% vs 80.4%, respectively). Median change from BL in FeCal concentration (mg/kg) for pts with elevated FeCal at BL at Wk12 were -800 and -86mg/kg for the GUS and PBO cohorts, respectively (nominal p<0.001); the proportions of pts achieving 50% and 75% reduction in FeCal levels (or ≤250 mg/kg) at Wk12 were higher for GUS-treated pts than those receiving PBO (51.1% vs 33.8% and 41.4% vs 23.6%, respectively; both nominal p<0.001). A larger percentage of pts treated with GUS achieved FeCal≤250mg/kg at Wk12 than pts treated with PBO (29.4% vs 17.3%, nominal p<0.001).

Table. Change from baseline in CRP and FeCal through Week 12 among patients with elevated CRP (>3mg/L) or FeCal (>250mg/kg) at baseline
	Placebo IV	Guselkumab 200 mg IV
CRP (mg/L) Baseline, N Median [IQR]	160 8.02 [5.40; 16.85]	248 9.26 [5.31; 18.05]
Wk 4, N Median change from baseline [IQR]	158 -2.06 [-5.70; 1.58]	245 -3.35 [-8.60; -0.23]***
Wk 8, N Median change from baseline [IQR]	156 -1.75 [-5.68; 1.46]	239 -3.80 [-10.77; -0.19]***
Wk 12, N Median change from baseline [IQR]	153 -0.51 [-4.64; 2.72]	239 -3.99 [-11.46; -0.85]***
FeCal (mg/kg) Baseline, N Median [IQR]	225 1743 [1120; 3395]	333 1787 [920; 4009]
Wk 4, N Median change from baseline [IQR]	213 -227 [-1041; 658]	308 -603 [-1866; 230]***
Wk 12, N Median change from baseline [IQR]	201 -86 [-1254; 504]	293 -800 [-2532; 0]***
***Nominal P≤0.001. Patients who had a prohibited change in UC medication, an ostomy or colectomy, or discontinued study agent due to lack of efficacy or an AE of worsening of UC or other reasons except for COVID-19 related reasons (excluding COVID-19 infection) or regional crisis in Russia and Ukraine prior to the designated timepoint had their baseline value carried forward from the time of the event onward. The p-values of treatment comparison were based on the mixed-effect model repeated measures with CRP and FeCal values being log-transformed.

Conclusion

In this phase 3 induction study, pts with moderately to severely active UC and elevated inflammatory markers treated with GUS 200mg IV induction showed greater improvement from BL in both CRP and FeCal levels compared with PBO. Differences were observed as early as the first assessments at Wk4 and continued through Wk12.

Disclosure

Tadakazu Hisamatsu received consulting fees from Janssen Research & Development, LLC.
Laurent Peyrin-Biroulet reports personal fees from Janssen.
Axel Dignass reports fees for participation in clinical trials, review activities such as data monitoring boards, statistical analysis and end point committees from Janssen; consultancy fees from Janssen; and payment from lectures including service on speakers bureaus from Janssen.
Kuan-Hsiang G. Huang, Matthew Germinaro, Nicole Houck,Ye Miao, and Hongyan Zhang are employees of Johnson & Johnson and own company stock/stock options.
Marjorie Argollo reports consulting fees from Janssen.
Ken Takeuchi has served as a speaker for Janssen.
Rafal Filip reports lecture fees and research/education support from Janssen.
Jessica R. Allegretti is a consultant and speaker for Janssen.
Brian G. Feagan received consulting fees from Janssen; a member of the speakers bureau for Janssen; support for attending meetings and/or travel from Janssen; and participation on a Data Safety Monitoring Board or Advisory Board from Janssen.
Bruce E. Sandsreports grants, consulting and speaking fees and other support from Janssen.

Introduction

Transmural response (TR) and healing (TH) assessed by intestinal ultrasound (IUS) are gaining increasing relevance as treatment targets in Crohn’s disease (CD) [1]. Even though less established in ulcerative colitis [UC], in which the inflammation mainly affects mucosa and submucosa, there is clear evidence that applying IUS in UC is beneficial to monitor short-term response to therapy [2]. However, the long-term IUS outcome, its association to clinical and lab parameters as well as the predictive value of early TR remain elusive.

Aims & Methods

The TRUST BEYOND study is an ongoing, prospective, non-interventional, multi-centre study in patients with active CD or UC who receive a biologic- or Januskinase-inhibitor (JAKi)-therapy at baseline. The study aims to assess the predictive value of TR or TH, evaluated at week 12 for the disease outcome after 52 weeks (TR: reduction of bowel wall thickness (BWT) of at least 25% and/or normalization; TH: normalization of BWT and Colour Doppler signal). For this interim analysis, we report IUS and clinical results as well as fecal calprotectin levels of 77 UC patients on the same therapy after 12 (W12) and 52 weeks (W52) and assessed the predictive value of TR at W12 for clinical remission at W52.

Results

Seventy-seven UC patients (63.6% were male, median age was 38.6 years (30.6 – 55.7) median disease duration of 5.85 years (2.49–12.77)) with clinically active disease (SCCAI 8.5 ± 2.2) with increased BWT at baseline had a documented visit after 52 weeks until February 2023. For the vast majority, the most affected bowel wall segment was the sigmoid colon with a mean BWT of 5.22 ± 1.28 mm at baseline.
At W12 after induction of therapy, the proportion of UC patients with TR and TH was 67.5% (n = 52) and 31.2% (n = 24). At W52, the rates of UC patients increased to 77.9% (n = 60) for TR and 41.6% (n = 32) for TH. Over the study course, patients with TR at W12 and W52 had a numerically lower SCCAI score and reduced fecal calprotectin levels than patients without TR.
Of note, 72.2% (n = 39) of patients with TR at W12 were in clinical remission at W52 compared to 27.8% (n = 15) of patients without early transmural response (p = 0.178).

Conclusion

In this interim analysis of the TRUST BEYOND study, UC patients demonstrated substantial rates of transmural improvements on IUS after 12 and 52 weeks. Patients with early transmural response were more likely to be in remission after one year. This suggests that in UC, IUS has to some degree a predictive value as observed for CD.

References

1. Kucharzik T, Wittig BM, Helwig U, et al. Use of Intestinal Ultrasound to Monitor Crohn's Disease Activity. Clin Gastroenterol Hepatol. 2017; 15:4, 535-42 e2.
2. Maaser C, Petersen F, Helwig U On behalf of the German IBD Study Group and the TRUST&UC study group, et alIntestinal ultrasound for monitoring therapeutic response in patients with ulcerative colitis: results from the TRUST&UC studyGut 2020;69:1629-1636.

Disclosure

T. Kucharzik, U. Helwig, F. Seibold, L. Biedermann, C. Högenauer and C. Maaser have received lecture and consulting fees from AbbVie.
I. Fischer has received consulting fees from AbbVie. L. Hammer and S. Rath are AbbVie employees and may own AbbVie stock or options.
AbbVie sponsored the study; contributed to the design; participated in the collection, analysis, and interpretation of data; in writing, reviewing, and approval of the final version. No honoraria or payments were made for authorship.

Introduction

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD), is a widespread chronic liver condition closely associated with obesity, insulin resistance, and dyslipidemia. Recent evidence points to gut microbiota dysbiosis as a key player in MASLD pathogenesis, affecting intestinal barrier function and systemic inflammation.

Aims & Methods

The aim was to investigate gut microbiota composition in patients with MASLD and assess its association with disease progression and gut barrier dysfunction. A total of 152 MASLD patients and 150 matched controls without liver pathology were examined. Diagnosis was confirmed by ultrasound and steatometry, alongside assessment of cardiometabolic risk factors. Gut microbiota composition was analyzed using real-time PCR, focusing on Bacteroidetes, Firmicutes, and Actinobacteria. Hydrogen breath testing was used to diagnose small intestinal bacterial overgrowth (SIBO), and the presence of Akkermansia muciniphila was evaluated as a marker of gut barrier integrity.

Results

MASLD patients demonstrated a significant increase in Firmicutes (50.3%) and Actinobacteria (15.3%) proportions compared to controls, with a higher Firmicutes/Bacteroidetes (F/B) ratio. SIBO was detected in 52% of MASLD patients versus 40.5% in controls (p<0.05). The presence of Akkermansia muciniphila was notably lower in MASLD patients (33%) compared to controls (63%), suggesting impaired gut barrier function. Strong positive correlations were observed between Actinobacteria abundance and the F/B index (r=0.75, p<0.05), while Akkermansia muciniphila presence negatively correlated with MASLD development (r=–0.69, p<0.05).

Conclusion

Gut microbiota dysbiosis, characterized by elevated Firmicutes and Actinobacteria and reduced Akkermansia muciniphila, is closely associated with MASLD pathogenesis. The findings highlight the potential of microbiota-targeted interventions for improving gut barrier function and modifying disease progression in MASLD patients.

Clinical Case Summary

Introduction: Tuberculosis (TB) is a transmissible disease associated to a high morbidity and mortality. Within the extrapulmonary forms, peritoneal TB corresponds to 11% of reported cases in the literature (1). Despite its high prevalence, its diagnosis remains a challenge due to its pauci-bacillary nature, and its nonspecific clinical findings.
Clinical case: 29 years old male patient, who consulted for abdominal pain and ascites. Abdominal and pelvis Contrast enhanced tomography revealed infiltrative material in the omental fat, ascites, irregular peritoneal thickening, and retroperitoneal mesenteric adenopathies (Fig.1). Paracentesis fluid: seroascitic albumin gradient (SAAG) estimated 1.8. The adenosine deaminase (ADA) of the ascitic fluid 181.1U/L. In diagnostic laparoscopy, it was observed miliary infiltration in the peritoneum. The pathology report described a caseating necrotizing granulomatous inflammatory process (Fig.2); confirming the diagnosis of PTB. Isoniazid, rifampicin, pyrazinamide, and ethambutol was initiated for 2 months, followed by isoniazid and rifampicin for 4 months with total improvement of the patient.
Discussion: The diagnostic approach of the patient with ascites is based on the study of ascitic fluid and the determination of SAAG; a value of >1.1 points towards ascites due to portal hypertension (PHT) and <1.1 towards ascites due to non-PHT. (2) In our patient, the biochemical analysis of the ascitic fluid determined (SAAG>1.1) with a high probability of PHT, leading the physician to initially suspect this cause and dismiss other neoplastic, infectious, and granulomatous diseases. However, the medical history did not correlate with PHT. In contrast, ADA study was positive. The sensitivity and specificity of this measure in PTB is 98 and 95% respectively, with a positive predictive value of 100% and a negative predictive value of 98%. (3)
Conclusión: The measurement of ADA in ascitic fluid , constitutes an essential, rapid diagnostic tool, with high sensitivity and negative predictive value for diagnostic PTB.

References

1. Gómez-Piña JJ. Tuberculosis peritoneal. Med Int Méx. 2018 mayo-junio;34(3):490-496
2. Rodríguez Brainy, Monge Eduardo, Montes Pedro, Salazar Sonia, Guzmán Edson. Eficacia de gradiente de albúmina sangre-ascitis y los análisis de proteínas en líquido ascítico en el diagnóstico de ascitis hipertensiva portal. Rev. gastroenterol. Perú 2014
3. Vasen Walter, Mauriño Eduardo, Ferro Diego, Brotto Claudia, Fernández Marty, Cabanne Ana. Acta Gastroenterol Latinoam 2016;46: 205-212.

Disclosure

No conflict of interest.