Introduction

Orodispersible budesonide (ODB) is an effective treatment for eosinophilic oesophagitis (EoE), with clinical trials reporting clinical remission rates of 75% at 48 weeks. Real-world data is lacking, particularly for longer term ODB maintenance treatment. We have conducted the first UK multicentre review of real-world outcomes on adults with EoE taking ODB from 5 tertiary hospitals.

Aims & Methods

Databases at 5 UK centres were screened to identify adults taking ODB. Audit approval was obtained by each centre. Electronic results and documentation were reviewed. Patients were telephoned and validated surveys completed to assess symptoms – Reflux Disease Questionnaire (RDQ), Hospital Odynophagia Dysphagia Questionnaire (HODQ) and Adult EoE Quality of Life Survey (EoE-QoLS). A numeric rating scale was used for pts to gauge their response to ODB.

Results

104pts aged 24-86y (med 41y), 27F:77M, taking ODB for 3-60months (med8.5m, mean14.2m) were included.
97pts completed questionnaires – 98% reported ODB had improved their symptoms. Scores on ODB were low, suggesting clinical remission: RDQ 0-52 (med0), HODQ 0-29 (med2), and EoE-QoLS 37-120 (med60).
71% received PPI first line prior to ODB, of which 81% reported inadequate improvement in dysphagia and 94% did not achieve histological remission (HR, <15eos/hpf) on PPI prior to ODB. 21pts continued PPI in addition to ODB - 1/21 was not in HR.
82pts underwent OGD on ODB – 77% were in HR. 74% pts had fibrotic findings (stricture, trachealisation) which had improved or resolved for 49% on ODB. 78% pts had inflammatory findings (oedema, exudate, furrows) which had improved or resolved for 67% on ODB.
14% experienced oro-oesophageal candidiasis on ODB. ODB was not discontinued.
Following ≥8week induction with 1mg BD ODB, 51pts had tried a reduced maintenance dose of 1mg OD ODB – 77% reported no deterioration in their symptoms on 1mg OD vs BD. 10pts had undergone OGD on 1mg OD – 7/10 were in HR.

Conclusion

Symptomatic and histopathological remission rates on ODB in this multicentre UK study are comparable to clinical trial outcomes yet resolution of endoscopic signs was lower. 1mg OD ODB kept a majority with symptomatic control but this was not always accompanied by histological/endoscopic remission. QoL scores were not proportionately as low as symptom scores on ODB, suggesting a persisting psychological burden despite treatment and warrants further study.

References

Lucendo et al, Gastroenterology (2019)
Miehlke et al, UEG Journal (2022)
Straumann et al, Gastroenterology (2020)
Dhar et al, Gut (2022)

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.

Introduction

Hepatocellular carcinoma (HCC) is an end stage liver disease with increasing morbidity and mortality worldwide. Development of the disease is dependent on various genetic, dietary and environmental factors. While alcohol-related liver disease (ALD/MetALD) remains a major contributor, metabolic dysfunction-associated steatotic liver disease (MASLD) is becoming increasingly relevant in clinical practice. There is increasing evidence for the role of bacteria, for instance, such as Bifidobacterium and Blautia, which were considered protective, while Streptococcus has been associated with disease progression. However, little is known about the alteration of microRNAs (miRNAs) in liver diseases and its interrelationship with microbial environment in view of etiological factors.

Aims & Methods

This study aimed to elucidate gastrointestinal miRNA alterations and explore their relationship with microbiome composition in patients with different stages of liver disease in terms of disease etiology. Multi-omics analyses were performed in a subset of well characterized patients (n=59) with liver disease and healthy controls. Systematic characterization included clinical, laboratory, demographic and imaging characterization and dietary preferences. Patients subclassification included fibrosis stage (no fibrosis, fibrosis, liver cirrhosis(LC)) and etiology (MetALD/ALD vs. MASLD). Fecal miRNAs were extracted using the Qiagen miRNeasy Kit and profiled via Agilent miRNA microarray. Microbiome analyses were performed amplifying the V1-V2 region of the 16S rRNA gene following Illumina sequencing.

Results

For miRNA analysis stringent criteria were applied to identify high quality miRNA targets. From approximately 4,000 candidates filtering resulted in selection of 202 high-quality miRNAs with reliably measurable concentrations. 28 of these miRNAs showed significantly positive alterations in concentration in patients with liver disease and 7 miRNAs significant negative alterations. Specifically, miR-642a-3p, miR-5006, miR-6781, and miR-6849 were elevated in feces in patients with LC. In contrast, miR-6869, miR-4467, and miR-5001 were present in lower concentration in LC patients. Notably, miR-4467 also showed strong negative associations with liver-specific laboratory markers, including gamma-glutamyl transferase (GGT) (r=-0.34; p=0.026) and M65, a marker of apoptosis (r=-0.42; p=0.005). Cross-sectional comparison of miRNA and microbiome data revealed miRNA alterations associated with specific microbial signatures. MiR-6795-5p, which was associated with liver stiffness (r = 0.39, p = 0.01), also correlated positively with the abundance of Streptococcus, a genus linked to disease progression (r=0.29; p=0.047). Conversely, miR-6869, miR-4467, and miR-5001 showed positive correlations with the potentially protective genera Blautia and Bifidobacterium (miR-6869: r_{Bifidobacterium}=0.35; p_{Bifidobacterium}=0.012; r_Blautia=0.37; p_Blautia=0.008; miR-4467: r_Blautia=0.41; p_Blautia=0.002; miR-5001: r_Blautia=0.38; p_Blautia=0.006).

Conclusion

Multi-omics analysis reveals distinct alterations in fecal miRNAs and gut microbiota across different stages of liver disease. Changes in microbial composition were associated with shifts in miRNA profiles, suggesting a functional link in maintaining intestinal homeostasis. These findings highlight the potential of integrated microbiome–miRNA signatures as novel diagnostic and therapeutic targets. Further studies are warranted to validate these associations and explore their clinical applications.

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

Tofacitinib, filgotinib, and upadacitinib, are Janus kinase inhibitors (iJAKs) approved for inflammatory bowel disease (IBD) treatment. Although no direct comparative studies exist, potential differences in efficacy and safety are attributed to in vitro-demonstrated affinity of each molecule for different JAK isoforms. JAK1 plays a crucial role in modulating cytokine-mediated immune responses, such as IL-6 and interferon, which are involved in inflammation and skin homeostasis. Its inhibition can promote conditions that may trigger acne.
Acne may be increased in iJAK-treated patients, meaning a clinical challenge for gastroenterologists.

Aims & Methods

A retrospective study was conducted at ten referral centers in Spain, including all IBD patients who had received iJAK therapy and had at least 3 months of follow-up. Demographic data, disease-related variables, and acne characteristics when appropriate, were collected. Univariate and multivariate logistic regressions were used to identify risk factors for acne; model discrimination was assessed by AUC.

Results

A total of 549 patients included: 258 (47%) were women; 354 (64%) had ulcerative colitis, 191 (35%) had Crohn’s disease and 1% had indeterminate colitis. Mean age was 41 years (IQR 30-52). 219 patients (40%) were treated with tofacitinib, 281 (51%) with upadacitinib, and 49 (9%) with filgotinib.
Ninety patients (16%) developed acne during iJAK treatment: 69% were mild, with only 4 severe cases (4%). Acne occurred early (median onset 42 days, IQR 7-122), predominantly on the face (56%), trunk (13%) or both (31%). Acne morphology included comedones (60%), papules (59%), pustules (39%), nodular-cystic (12%), scarring (9%); 48% showed more than one morphology.
Thirty-six patients received specific acne treatment: 89% topical (antiseptics, benzoyl peroxide, retinoids), 69% systemic (antibiotics, retinoids, antiandrogens), and 44% combined treatment. 83% of those patients responded to acne specific treatment, and only 8 patients (9% of those with acne; 1.5% overall) had to discontinue iJAK treatment, with acne resolving in all cases.
Acne developed in 26%, 6% and 6% of upadacitinib, tofacitinib and filgotinib treated patients respectively (p=0.001). Multivariate analysis showed that acne development was associated with upadacitinib (OR 10.28;IC95%=4,7–22,6; p<0,001) and history of acne (OR 3.52; IC95%=1,5–8,3; p=0,004), while older age (>35 years, OR 0.31; IC95% 0,11–0,83; p=0,02) and Crohn’s disease (OR 0.47; IC95% 0,25–0,90; p=0,02) showed to be protective. This model was reliable in predicting acne development (AUC 0.79). Additionally, univariate analysis showed high dose of iJAK was also associated with acne development, which could not be confirmed in multivariate analysis.

Conclusion

Acne occurred in a relevant proportion of iJAK-treated patients, was generally mild and manageable with dermatological care, and rarely required treatment discontinuation. Risk factors for iJAK-associated acne included use of upadacitinib (probably reflecting a greater affinity for JAK1) and history of acne, while older age and Crohn’s disease were protective.
Gastroenterologists should be aware of both likelihood and management of this specific adverse event when considering iJAK therapy.

Disclosure

Y G-L, MC, GB, ER, IB, DC, M B-dA, LM, I M-J, DG, IV have provided scientific advisory / participated in educational activities / received unrestricted research grants / received payments for lecturing from Johnson & Johnson, ​Takeda, Pfizer, Amgen, AbbVie, Lilly, AlfaSigma, Ferring, Gilead.

Introduction

The coexistence of HBV and hepatic steatosis is frequent, but its impact on the progression of liver disease remains poorly characterized and much debated.

Aims & Methods

We aim by this study to determine the prevalence, associated factors, consequences of this association and response to treatment.
A retrospective analysis was conducted over 20 years from 2005 to 2025 on a single-center cohort of 124 patients with chronic HBV, of whom 16.1% (n=20) had steatosis (confirmed by imaging). Demographic, virological, metabolic and histological (fibrosis stage) characteristics were compared between the groups with and without steatosis. And statistical tests (Chi², Mann-Whitney, logistic regression) were used.
For the comparison, we defined:
- Group A: combining steatosis and HBV
- Group B: HBV without steatosis.

Results

The prevalence of steatosis in patients with HBV in our series was 16.1%, with a mean age of 52.1 years higher than that of patients with HBV without steatosis, (45.8 years), with a p-value of 0.02. Furthermore, in our work there was a clear female predominance, with a sex ratio of 3 F/H in group A vs 0.9F/H in group B with a p-value of 0.04.
In the history of our patients, we found that 30% of patients had high blood pressure in group A compared with 18% in group B, 10% had diabetes in group A compared with 8% in the other group, and there was no significant difference in smoking habits (15% compared with 12%). Statistical regression did not find any significant correlation in those signs. On the other hand, in the case of dyslipidemia, there was a slight predominance of group A (15% vs. 10%) with a p-value of 0.045.
The analysis of hepatic test didn’t show any big difference between results of GGT, PAL and ASAT but for ALAT there was a higher in patients with steatosis with a median of 62 vs 52,1 and a p-value of 0,02.
Our study also found no difference in serological results: 95% of patients with steatosis were Hbs Ag positive, with the presence of Hbc Ab in all patients at the time of diagnosis. These results were not very different from those of patients without steatosis (Hbs Ag positive in 96.8% and Hbc Ab positive in all patients). Only 10% of patients had a positive Hbe Ag in group A vs 7.2% in group B. The median viral load before treatment was 1870 UI/ml vs 2450 UI/ml with no real difference noted between the 2 groups, confirmed by statistical regression which found a p=0.82 value.
Our study found no real impact on liver disease, showing no worsening of fibrosis (30% F≥2 with steatosis vs 25% without, p=0.62*).
After analysis using the association Chi² test, our study found similar virological responses under treatment (83% in group A vs 78% in group B, p=0.75*).

Conclusion

In this cohort, steatosis in HBV patients (16.1%) was associated with age and female sex. Hepatic test showed a higher ALAT fold among patient with steatosis. However, higher viral load or more severe fibrosis was not demonstrated. Steatosis in HBV does not appear to have a negative influence on the course of the disease. These results suggest that the management of HBV with steatosis should primarily target virological control, without requiring any specific therapeutic adaptation.

Disclosure

no conflict of interest