Introduction

A novel device intended to evaluate motility in patients at risk for dysmotility and enteral feeding intolerance was developed. This VIPUN Gastric Monitoring System (GMS) consists of a feeding tube with a balloon attached to its distal end and a control unit. Once the balloon is positioned in the stomach the control unit can inflate the balloon, record intra-balloon pressure and analyze gastric motility.

Aims & Methods

Our aim was to validate the GMS as a gastric motility monitoring system by comparing its performance to the gold standard, high-resolution manometry. The primary hypothesis was that the contraction durations recorded by the GMS and manometry are strongly correlated (ρ > 0.70). Secondary objectives: To correlate the contraction frequency observed by expert gastroenterologists and by GMS analysis software on GMS and manometry, and to observe gastric accommodation upon nutrient intake.
In this monocentric, single-arm, interventional study, a GMS prototype (VIPUN Medical, Belgium) was tested in healthy adults. A solid state manometry catheter (UniTip, Unisensor AG, Switzerland) was used as comparator. The balloon catheter was inserted through the nose. The manometry catheter was inserted through the other nare and positioned with the tip in the duodenum, as verified using fluoroscopy. Afterwards, the GMS catheter balloon was inflated with 120 mL air. The participant was placed in semi-recumbent position for the 2.5 h pressure measurement. After 2 h, a liquid meal (400 kcal, 1.5 kcal/mL) was infused via the GMS catheter.
For manometry, only the channels that were consistently in the stomach were analyzed. Duration of contractility (primary outcome) was calculated as the time baseline-corrected pressure waves exceeded a subject- and technology-specific pressure threshold (1). The identification of individual gastric contractions (secondary outcome) was done by two independent readers, a third reader served as adjudicator. Additionally, GMS software was used for the detection of individual gastric contractions. Results are shown as mean (standard deviation).

Results

13 healthy volunteers (6 women, 27.5 (8.1) years) were included. GMS catheter placement was feasible and safe. Intragastric balloon inflation was well-tolerated. No serious or unanticipated adverse events occurred.
For the primary outcome, the Spearman correlation between the contraction duration recorded by GMS and manometry was 0.96 (p < 0.01). The sum of contractile activity per subject was similar: 2588.7 (1872.2) and 2722.3 (1768.7) seconds on manometry and GMS, respectively (p = 0.44, paired t-test, see Table 1).
For the number of contractions identified visually by readers, the correlation between GMS and manometry was 0.71 (p < 0.01) . Using GMS software for detection of individual contractions on GMS, the correlation with reader-identified contractions on manometry was 0.87 (p < 0.01).
Nutrient infusion resulted in a significant decrease in tonic (-1.7 (0.96) mmHg) and phasic (-3.4 (3.1) contractions/10 min) contractility.

Conclusion

The observed strong correlations with the gold standard, manometry, validate the performance of the VIPUN GMS as a gastric monitoring system.

References

1. Janssen P, Goelen N, Tack J. A comparison of various intragastric balloons for the assessment of gastric motility. Neurogastroenterol Motil. 2018;30(12):e13453.

Introduction

Ozanimod (OZA), a sphingosine 1-phosphate (S1P) receptor modulator that selectively targets S1P₁ and S1P₅, is approved in the European Union, United States, and other countries for the treatment of moderately to severely active ulcerative colitis (UC). Mucosal healing (MH), a key treatment goal for patients (pts) with UC, is associated with improved long-term pt outcomes.

Aims & Methods

The goal of this analysis was to determine the rate of early MH after treatment with OZA at Week (W) 10 using stringent MH criteria (mucosal endoscopy subscore [MES] = 0 plus histologic remission [Geboes score <2.0]) and to assess the relationship between achievement of stringent MH at W10 and clinical outcomes at W52. Outcomes were compared to pts achieving MH using a standard definition (MES ≤1 plus histologic remission). This analysis included pts from True North (NCT02435992) who achieved clinical response on once-daily oral OZA 0.92 mg at W10 and continued OZA during the 42-wk maintenance period. In this post hoc analysis, we examined MH, clinical remission, and corticosteroid (CS)–free remission at W52 in pts with stringent MH vs without stringent MH at W10 and with stringent MH vs with standard MH.

Results

Of the 230 pts who achieved clinical response on OZA at W10 and continued OZA during the maintenance period, 44 (19.1%) achieved MH using a standard definition and 13 (5.7%) achieved stringent MH at W10. Demographic and clinical characteristics were generally balanced between OZA-treated pts with stringent MH (n=13) and without stringent MH (n=217) at W10. Notably, there were fewer male pts with stringent MH vs without stringent MH, all pts with stringent MH had moderate disease (based on endoscopy), and more pts with stringent MH vs without stringent MH had left-sided UC disease. CS use at screening and prior tumor necrosis factor inhibitor (TNFi) use were lower in those with stringent MH vs without stringent MH. Similar differences in disease severity, extent of disease, and CS and TNFi use were seen in pts with stringent MH vs standard MH. At W52, more pts treated with OZA with stringent MH at W10 vs without stringent MH at W10 had clinical remission (53.8% vs 35.9%), CS-free remission (53.8% vs 30.4%), MH (61.5% vs 27.6%), endoscopic improvement (61.5% vs 44.7), and histologic remission (61.5% vs 31.8%). Except for endoscopic improvement, a slightly higher percentage of pts with stringent MH vs standard MH at W10 achieved clinical outcomes at W52 (Table).

Conclusion

While difficult to achieve, a small proportion of pts treated with OZA experienced stringent MH by W10. Compared with pts who achieved standard MH at W10, those with stringent MH at W10 demonstrated numerically better clinical outcomes at W52 on OZA treatment. Achieving stringent MH at W10 correlated with better clinical, endoscopic, and mucosal outcomes at W52.

Disclosure

The study was funded by Bristol Myers Squibb, Princeton, NJ, USA.
WR: speaker for 4SC, Abbott Laboratories, AbbVie, Aesca, Aptalis, Astellas, Centocor, Celltrion, Danone Austria, Elan, Falk Pharma GmbH, Ferring, Immundiagnostik, Medice, Mitsubishi Tanabe Pharma Corporation, MSD, Otsuka, PDL, Pharmacosmos, PLS Education, Schering-Plough, Shire, Takeda, Therakos, Vifor, and Yakult; consulted for Abbott Laboratories, AbbVie, Aesca, Algernon, Amgen, AM Pharma, AMT, AOP Orphan, Arena, Astellas, AstraZeneca, Avaxia, Roland Berger GmbH, Bioclinica, Biogen IDEC, Boehringer Ingelheim, Bristol Myers Squibb, Calyx, Celgene, Cellerix, Celltrion, Centocor, ChemoCentryx, Covance, Danone Austria, DSM, Elan, Eli Lilly, Ernst & Young, Falk Pharma GmbH, Ferring, Galapagos, Gatehouse Bio, Genentech, Gilead, Grünenthal, ICON, Index Pharma, Inova, Intrinsic Imaging, Janssen, Johnson & Johnson, Kyowa Hakko Kirin Pharma, Landos, Lipid Therapeutics, LivaNova, Mallinckrodt, MedAhead, MedImmune, Millennium, Mitsubishi Tanabe Pharma, MSD, Nash Pharmaceuticals, Nestle, Nippon Kayaku, Novartis, Ocera, OMass, Otsuka, Parexel, PDL, Peri Consulting, Pharmacosmos, Philip Morris Institute, Pfizer, Procter & Gamble, Prometheus, Protagonist, Provention, Quell Therapeutics, Robarts Clinical Trial, Sandoz, Schering-Plough, Second Genome, Seres, Setpoint Medical, Sigmoid, Sublimity, Takeda, Teva, Therakos, Theravance, TiGenix, UCB, Vifor, Zealand, and Zyngenia; served as an advisory board member for 4SC, Abbott Laboratories, AbbVie, Aesca, Amgen, AM Pharma, Astellas, AstraZeneca, Avaxia, Biogen IDEC, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Cellerix, Celltrion, Centocor, ChemoCentryx, Danone Austria, DSM, Elan, Ferring, Galapagos, Genentech, Grünenthal, Inova, Janssen, Johnson & Johnson, Kyowa Hakko Kirin Pharma, Lipid Therapeutics, MedImmune, Millennium, Mitsubishi Tanabe Pharma, MSD, Nestle, Novartis, Ocera, Otsuka, PDL, Pharmacosmos, Pfizer, Procter & Gamble, Prometheus, Sandoz, Schering-Plough, Second Genome, Setpoint Medical, Takeda, Therakos, TiGenix, UCB, Zealand, and Zyngenia; received research funding from Abbott Laboratories, AbbVie, Aesca, Centocor, Falk Pharma GmbH, Immundiagnostik, Janssen, MSD, Sandoz, and Takeda.
AH: Consultant, advisory board member, or speaker for AbbVie, Atlantic, Bristol-Myers Squibb, Celltrion, Falk, Ferring, Janssen, MSD, Napp Pharmaceuticals, Pfizer, Pharmacosmos, Shire, and Takeda. Global Steering Committee for Genentech.
CS: served as a speaker for AbbVie, Bristol Myers Squibb, Janssen, Pfizer, Takeda, and UCB.
RKC: consulted for AbbVie, Bristol Myers Squibb, Janssen, LabCorp, Pfizer, Samsung Bioepis, and Takeda.
HAA, AJ, HW, and MTO: employees and/or shareholders of Bristol Myers Squibb.
RL: consulted for Bristol Myers Squibb and Pfizer.
JA: received consulting fees from AbbVie, BioFire Diagnostics, Janssen, and Pfizer; received research grants from BioFire Diagnostics.

Introduction

Inflammatory bowel diseases (IBD) are chronic systemic conditions that affect patients' lives in various ways. To date, there is a scarce evidence correlating fecal incontinence, sexual dysfunctions, disease activity, and quality of life (QoL) in these patients. This study aimed to evaluate the impact of fecal incontinence on sexual functions such as erectile and prostatic function in a cohort of IBD patients; and to analyse the relationship among fecal incontinence, sexual function and QoL.

Aims & Methods

IBD patients were enrolled from IBD clinic of the Gastroenterology Unit of the University Hospital of Salerno. Demographic characteristics, anthropometric data, and usage of immunosuppressive drugs were collected. Patients underwent a physical examination, and laboratory tests, including C-reactive protein (CRP) and fecal calprotectin (FC). A standardized questionnaire was used to assess gastrointestinal (GI) symptoms such as abdominal pain and fecal incontinence. For the latter, we also used the Wexner score. Crohn's Disease Activity Index (CDAI) and Mayo score as well as FC levels, and endoscopic findings were used to classify IBD patients as in active or in remission phase. Patients with perianal manifestations were excluded. Hormonal values (FSH, LH, Prolactin, 17-betaestradiol, testosterone) were measured. Sexual function was evaluated using the International Index of Erectile Function (IIEF), Male Sexual Health Questionnaire (MSHQ), Ejaculatory Dysfuction (EjD), prostatic dysfunction using the National Institute of Health - Chronic Prostatitis Symptom Index (NIH-CPSI) and International Prostatic Symptoms Score (IPSS). QoL was assessed by FiQol domains (lifestyle, coping behaviour, self‐perception and depression, embarrassment).

Results

Eighty-five male IBD patients (47 Crohn's disease [CD] and 38 ulcerative colitis [UC]), were enrolled. Mean age was 43.7 ± 15.9 years; mean BMI was 36.4±25.5 Kg/m². Twenty-four CD patients had an active disease and 23 were in remission, while 20 UC patients had an active disease and 18 were in remission. UC patients showed significantly higher fecal incontinence and Wexner scores compared to CD patients (1.0±1.9 vs 0.4±1.2, p=0.05 and 2.84±4.2 vs 2.3±1.1, p=0.01, respectively). Only the Mayo score significantly correlated with Wexner score (Rs=0.578; p<0.001), and fecal incontinence (Rs=0.584; p<0.001). Sexual function, evaluated by erectile and prostatic scores, nicely correlated each other’s (p<0.05 in all cases). However, no association was found between fecal incontinence and all sexual function scores. The FiQol domain self‐perception and depression was significantly associated with IIEF (p=0.01).

Conclusion

This study highlighted the prevalence of fecal incontinence is higher in UC than CD patients. However, fecal incontinence did not impact on sexual function, evaluated by erectile and prostatic scores. QoL influenced erectile function.

Introduction

Microscopic colitis (MC) is an inflammatory gastrointestinal disease which typically presents with chronic watery diarrhea without blood. Despite a rising incidence over the last decades (1), studies on health economic outcomes are lacking.

Aims & Methods

In this cost-of-illness study, we estimate the societal economic burden of MC encompassing costs for healthcare, medications, and work loss, by the use of real-world data from Swedish health registers.
Through biopsy reports from Sweden’s 28 pathology departments, we identified 11,530 adult patients with MC as of January 1, 2017. Each patient was compared to up to 5 general-population comparators matched on date of birth, sex, and county of residence. Healthcare costs were based on prescription medications as well as non-primary outpatient visits and hospitalizations that included endoscopic procedures, while productivity losses were derived from work loss due to sick leave or disability leave. Mean differences were adjusted for age, sex, and education level. All costs were adjusted for inflation and converted from Swedish currency, SEK, to USD according to the annual average conversion rate in 2016 (1 USD = 8.5613 SEK or 0.9040 EUR).

Results

In 2016, patients with MC had a mean annual cost of $11,782 as compared with $6,170 in general-population comparators, corresponding to an annual excess cost of $5,615 per patient (adjusted mean difference $5,628 [95%CI: $5,278-$5,978], Table 1).
Even though less than half of the patients with MC were of working age (18-64 years, 42.5%), work loss was the largest cost component and accounted for more than half of the mean annual excess cost (57.7%). Excess costs related to hospitalizations accounted for 18.1%, whereas costs related to outpatient visits and medications accounted for 12.6% and 13.4% respectively. Although patients with MC had an increased use of MC-related medications such as local acting steroids (ATC code A07EA), these costs were comparatively small (mean annual cost, $106). Furthermore, MC-related healthcare costs such as colonoscopies, or outpatient visits and hospitalizations related to MC as defined by ICD code K.528, were negligible (mean annual cost, $68, $72 and $15 respectively).
The total annual societal cost of MC in Sweden was $135.9 million in 2016. By subtracting the baseline cost observed in general-population comparators, $64.7 million was found to be attributable to MC and MC-comorbidity.

Table 1. Use and cost of healthcare, prescription medications, and work loss in prevalent patients with microscopic colitis (MC) and general-population comparators in Sweden, 2016.

Conclusion

Patients with MC had an increased mean annual societal cost which was primarily driven by work loss. Healthcare costs specifically related to MC did not seem to be a major contributor to excess costs. Instead, excess healthcare costs in patients with MC are likely to be driven by concomitant disease. The societal economic burden of MC in Sweden was $135.9 million in 2016 with a population of 10.0 million and a prevalence of around 0.1%.

References

1. Bergman D, Clements MS, Khalili H, Agréus L, Hultcrantz R, Ludvigsson JF. A nationwide cohort study of the incidence of microscopic colitis in Sweden. Aliment Pharmacol Ther. 2019 Jun;49(11):1395-1400.

Disclosure

Dr Ludvigsson coordinates a study on behalf of the Swedish IBD quality register (SWIBREG). That study has received funding from the Janssen corporation. Dr Ludvigsson has also received financial support from MSD to develop a paper reviewing national healthcare registers in China.