Abstract
Background
Inflammatory bowel disease (IBD), characterised by chronic intestinal inflammation, is hypothesised to arise from the interplay between susceptibility genes, the immune system, ...environmental factors, and gut microbiota. Akkermansia muciniphila is a symbiotic bacterium that accounts for 1-5% of the human fecal microbiota. This microbe has been hailed as a next-generation probiotic, principally with regard to its plethora of beneficial host interactions, including the ability to influence mucin secretion and strengthen the intestinal barrier.
Purpose
Though a clear-cut role and mechanism by which A. muciniphila influences inflammatory conditions is unknown, evidence indicates this microbe is depleted in IBD, suggesting it may have protective effects that are lost in these conditions. Here, we investigate the role and mechanism of A. muciniphila in intestinal inflammation and its influence on intestinal barrier function by utilizing barrier-disrupting models of colitis.
Method
Across several experimental models of intestinal inflammation including the chemically-induced dextran sulphate sodium (DSS) model, the parasitic-based model of Trichuris muris infection, and the spontaneous Muc2-/- model, A.muciniphila was administered by oral gavage. Disease activity index, macroscopic scoring and histological scoring were all performed to assess the severity of intestinal inflammation. Various pro- and anti-inflammatory cytokines were assessed within colonic tissue using commercially available ELISA kits.To investigate the effects that A. muciniphila has on barrier function in the context of colitis, reverse transcriptase qPCR was used to explore several factors, including several TJPs, AMPs, and mucins. To analyse the composition of the microbiota and changes in diversity with A. muciniphila supplementation, 16S rRNA sequencing of fecal samples was performed.
Result(s)
Though only minor benefits were derived from this microbe in germ-free mice, in specific pathogen-free (SPF) mice, administration of pasteurized A. muciniphila in a DSS recovery model ameliorated inflammation severity and promoted recovery compared to controls. When gavaged prior to DSS administration, both live and pasteurized A. muciniphila failed to diminish inflammatory markers indicating minimal preventative effects. T. muris-infected SPF mice treated with live A. muciniphila showed increased levels of Th2 and anti-inflammatory cytokines, decreased worm burden, and enhanced levels of the mucin, Muc5ac, compared with those receiving control broth or pasteurized bacteria. Further, both live and pasteurized A. muciniphila ameliorated the severity of inflammation in a mucin 2 deficient (Muc2-/-) mouse model of spontaneous colitis, indicating that these protective effects are Muc2-independent.
Conclusion(s)
These observations provide us not only with an enhanced understanding of the role A. muciniphila plays in the pathogenesis of intestinal inflammatory conditions but also may fuel novel avenues of treatment for those with IBD.
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CIHR
Disclosure of Interest
None Declared
Abstract
Background
Non-invasive assessment of Fontan Associated Liver Disease (FALD) is of interest, but studies have yielded inconsistent results about the correlation of severity of disease with ...laboratory values and imaging. Transient elastography (TE) is a non-invasive imaging modality used commonly for liver stiffness measurement (LSM) and in Fontan patients it is hypothesized to reflect not only liver fibrosis but also venous congestion.
Purpose
To better define the potential role of TE for non-invasive assessment of the severity of FALD.
Method
This was a retrospective study conducted on patients’ medical records at CHU Sainte-Justine Hospital. Patients less than 18 years of age with FALD who had at undergone at least one LSM by TE between 1998-2021 were included. The relationship between LSM and liver function tests, hepatic ultrasound findings (including a cirrhosis score), cardiac catheterization results and histological fibrosis scores were analyzed. The impact of interventions during cardiac catherization on LSM were also studied.
Result(s)
A total of 54 patients (36 boys and 18 girls) with FALD were studied. Median age at Fontan surgery was 4.6 years (IQR 4.0 ─ 5.4 years). Higher LSM values significantly correlated with longer time from Fontan, higher total and direct bilirubin and GGT levels, higher INR, longer APTT, lower Factor V, and lower absolute lymphocyte count. Greater LSM was also significantly associated with the presence of heterogenous parenchymal echogenicity, irregular liver contours and greater ultrasonographic cirrhosis scores. Higher TE values were significantly correlated with higher wedged hepatic venous pressure and Fontan pressure. After catherization interventions that addressed stenoses, there was a statistically significant reduction in mean LSM (24.9±3.63 kPa vs 15.8±4.6 kPa, p=0.005). After closure of significant pulmonary collaterals, mean LSM tended to increase, but this difference did not reach statistical significance (19.1±1.9 kPa vs 24.6±3.5 kPa, p=0.2). At liver biopsy, significant direct correlation was found between LSM and the grade of sinusoidal fibrosis and LSM. TE with values >20 kPa were found to have higher grades of sinusoidal fibrosis, while values <20kPa had higher grades of sinusoidal dilatation.
Conclusion(s)
This study showed that TE allows to identify patients with higher cholestatic parameters, more severe liver fibrosis at biopsy and sonographic signs suggestive of cirrhosis. Moreover, it confirmed that liver congestion significantly contributes to LSM values. Interestingly, catheter interventions addressing pulmonary stenoses led to the improvement of TE measurements, giving hope for the reduction of hepatic venous congestion in these patients, which might have an effect on their FALD. Finally, the LSM threshold of 20 kPa could be useful clinically as a value above which fibrosis is likely to be significant, while if below could indicate a greater contribution from hepatic congestion.
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None
Disclosure of Interest
None Declared
Abstract
Background
Canada is currently in the third epidemiological stage in the evolution of IBD: compounding prevalence. A high incidence of IBD, in conjunction with low mortality, leads to a ...steadily rising prevalence over time. By understanding historical epidemiological trends, we can forecast incidence and prevalence into the future to inform healthcare systems in Canada of the rising burden of IBD to society.
Purpose
To analyze past epidemiological trends in order to forecast the overall incidence and prevalence of IBD, Crohn’s disease (CD), and ulcerative colitis (UC) and stratified by age (<18, 18-64, 65+).
Method
Canadian population-based administrative data was acquired from: AB, BC, SK, MB, QC, and ON. Data were age and sex standardized to the matching year and provincial data aggregated into a representative sample of the Canadian population for prevalence (2002-2014) and incidence (2007-2014: 5-year washout period). Incidence and prevalence (per 100,000 persons) were calculated, with 95% confidence intervals (CI), using Canadian population estimates from Statistics Canada for IBD, CD, UC (IBD-unclassifiable+UC). Autoregressive Integrated Moving Average models were created, and rates forecasted from 2014 to 2035 with 95% prediction intervals (PI). Poisson (or negative binomial) for incidence and log binomial regression for prevalence estimated the Average Annual Percentage Change (AAPC), with 95% CIs, of the forecasted data.
Result(s)
The 2014 incidence of IBD in Canada was 28.4 per 100,000 (95%CI: 27.8, 29.0) and forecasted to significantly increase (AAPC: 0.58%; 95%CI: 0.04, 1.04) from 30.0 per 100,000 in 2023 to 32.1 (95%PI: 27.9, 36.3) in 2035. Pediatric onset IBD was 13.9 per 100,000 (95%CI: 13.0, 14.9) in 2014 and is forecasted to significantly increase to 18.0 per 100,000 (95%PI: 15.7, 20.2) in 2035 with an AAPC of 1.23% (95%CI: 0.76, 1.63). Adult and elderly onset incidence rates were forecasted to remain stable. Prevalence of IBD increased between 2002 (389 per 100,000) and 2014 (636 per 100,000) and is forecasted to continue to climb by an AAPC of 2.44% (95%CI: 2.34, 2.53). In 2023, the prevalence of IBD is 825 per 100,000. By 2035 prevalence is forecasted to climb to 1075 per 100,000 (95%PI: 1047, 1103) with 470,000 Canadians living with IBD. Prevalence across all age strata were forecasted to significantly increase. The highest AAPC was seen in the elderly (2.76%; 95%CI: 2.73, 2.79) with a prevalence of 841 per 100,000 (95%CI: 834, 849) in 2014 and forecasted to climb to 1534 per 100,000 (95%PI: 1519, 1550) in 2035.
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Conclusion(s)
Incidence of IBD continues to rise in Canada, driven by pediatric-onset IBD. In 2023, over 320,000 Canadians (0.83%) will be living with IBD. By 2035 prevalence will exceed 1% of the population with approximately 470,000 individuals in Canada with IBD. Future research should establish the environmental determinates of IBD that may influence temporal trends in the incidence of IBD, while healthcare systems adapt to the compounding prevalence of IBD.
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CIHR, Other
Please indicate your source of funding;
The Leona M. and Harry B. Helmsley Charitable Trust
Disclosure of Interest
S. Coward: None Declared, E. Benchimol Consultant of: Hoffman La-Roche Limited and Peabody & Arnold LLP for matters unrelated to medications used to treat inflammatory bowel disease and McKesson Canada and the Dairy Farmers of Ontario for matters unrelated to medications used to treat inflammatory bowel disease., C. Bernstein Grant / Research support from: Unrestricted educational grants from Abbvie Canada, Janssen Canada, Pfizer Canada, Bristol Myers Squibb Canada, and Takeda Canada. Has received research grants from Abbvie Canada, Amgen Canada, Pfizer Canada, and Sandoz Canada and contract grants from Janssen, Abbvie and Pfizer, Consultant of: Abbvie Canada, Amgen Canada, Bristol Myers Squibb Canada, JAMP Pharmaceuticals, Janssen Canada, Pfizer Canada, Sandoz Canada, and Takeda., Speakers bureau of: Abbvie Canada, Janssen Canada, Pfizer Canada and Takeda Canada, J. A. Avina-Zubieta: None Declared, A. Bitton: None Declared, L. Hracs: None Declared, J. Jones Consultant of: Janssen, Abbvie, Pfizer, Takeda, Speakers bureau of: Janssen, Abbvie, Pfizer, Takeda, E. Kuenzig: None Declared, L. Lu: None Declared, S. Murthy: None Declared, Z. Nugent: None Declared, A. Otley Grant / Research support from: Unrestricted educational grants from AbbVie Canada and Janssen Canada, Consultant of: Advisory boards of AbbVie Canada, Janssen Canada and Nestle, R. Panaccione Consultant of: Abbott, AbbVie, Alimentiv (formerly Robarts), Amgen, Arena Pharmaceuticals, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Celltrion, Cosmos Pharmaceuticals, Eisai, Elan, Eli Lilly, Ferring, Galapagos, Fresenius Kabi, Genentech, Gilead Sciences, Glaxo-Smith Kline, JAMP Bio, Janssen, Merck, Mylan, Novartis, Oppilan Pharma, Organon, Pandion Pharma, Pendopharm, Pfizer, Progenity, Protagonist Therapeutics, Roche, Sandoz, Satisfai Health, Shire, Sublimity Therapeutics, Takeda Pharmaceuticals, Theravance Biopharma, Trellus, Viatris, UCB. Advisory Boards for: AbbVie, Alimentiv (formerly Robarts), Amgen, Arena Pharmaceuticals, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Eli Lilly, Ferring, Fresenius Kabi, Genentech, Gilead Sciences, Glaxo-Smith Kline, JAMP Bio, Janssen, Merck, Mylan, Novartis, Oppilan Pharma, Organon, Pandion Pharma, Pfizer, Progenity, Protagonist Therapeutics, Roche, Sandoz Shire, Sublimity Therapeutics, Takeda Pharmaceuticals, Speakers bureau of: AbbVie, Amgen, Arena Pharmaceuticals, Bristol-Myers Squibb, Celgene, Eli Lilly, Ferring, Fresenius Kabi, Gilead Sciences, Janssen, Merck, Organon, Pfizer, Roche, Sandoz, Shire, Takeda Pharmaceuticals, J.-N. Pena-Sanchez: None Declared, H. Singh Consultant of: Pendopharm, Amgen Canada, Bristol Myers Squibb Canada, Roche Canada, Sandoz Canada, Takeda Canada, and Guardant Health, Inc., L. Targownik Grant / Research support from: Investigator initiated funding from Janssen Canada, Consultant of: Advisory board AbbVie Canada, Takeda Canada, Merck Canada, Pfizer Canada, Janssen Canada, Roche Canada, and Sandoz Canada, J. Windsor: None Declared, G. Kaplan Grant / Research support from: Ferring, Janssen, AbbVie, GlaxoSmith Kline, Merck, and Shire, Consultant of: Gilead, Speakers bureau of: AbbVie, Janssen, Pfizer, Amgen, and Takeda
Abstract
Background
The effectiveness of colonoscopy screening to prevent colorectal cancer (CRC) is directly linked to its procedural quality. An independent observer (Hawthorne effect) can improve ...colonoscopy procedural quality metrics, including adenoma detection rate (ADR). However, the results of studies are limited or controversial.
Purpose
We aimed to evaluate the colonoscopy quality metrics in a group of patients undergoing screening or diagnostic colonoscopies under stringent observer conditions.
Method
In a single-center, case–control study, consecutive patients undergoing routine screening or diagnostic colonoscopy were prospectively enrolled. In the case group, all procedural steps and quality metrics were observed and documented, and the procedure was video recorded by an independent research assistant. In the control group, colonoscopies were performed without independent observation. Colonoscopy quality metrics such as polyp, adenoma, serrated lesions, and advanced adenoma detection rates (PDR, ADR, SLDR, AADR), the mean number of adenomas detected per patient (MAP), and the mean number of adenomas and serrated lesions detected per patient (MASP) were compared. The probabilities of increased quality metrics were evaluated through regression analyses weighted by the inversed probability of observation during the procedure.
Result(s)
We included a total of 687 patients (327 cases and 360 controls) in the final analyses. The case group had significantly higher PDRs (62.4% vs. 53.1%) and ADRs (39.4% vs. 28.3%) compared with the control group. The SLDR was also higher in the case group than in the control group, but the difference was not significant (7.3% vs. 4.4%; P = 0.14). The AADR was not significantly increased. After adjusting for potential confounders, the ADR and SLDR were 50% (odds ratio OR 1.51; 95%CI 1.05–2.17) and more than twofold (OR 2.17; 95%CI 1.05–4.47) more likely to be higher in the case group than in the control group. The MAP and MASP were significantly increased in the case group compared with the control group (P < 0.001). The regression analyses for both metrics demonstrated the direct and significant association between the Hawthorne effect and elevated MAP/MASP.
Conclusion(s)
The presence of an independent observer documenting colonoscopy quality metrics and video recording the colonoscopy resulted in a significant increase in ADR and other quality metrics. The Hawthorne effect should be considered an alternative strategy to advanced devices to improve colonoscopy quality in routine practice.
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None
Disclosure of Interest
M. Taghiakbari: None Declared, D. Coman: None Declared, M. Takla: None Declared, A. N. Barkun: None Declared, M. Frija-Gruman: None Declared, M. Bouin: None Declared, S. Bouchard: None Declared, E. Deslandres: None Declared, S. Sidani: None Declared, D. von Renteln Grant / Research support from: ERBE, Ventage, Pendopharm, and Pentax, Consultant of: Boston Scientific and Pendopharm
Abstract
Background
Our gut microbiota plays an important role in protecting the gastrointestinal (GI) tract from invading enteric pathogens. Much of this colonization resistance is mediated by ...limiting nutrient availability, however, enteric pathogens have evolved strategies to subvert this competition, utilizing commensal metabolites to facilitate their infection. Access to nutrients is not only crucial for a pathogen’s metabolic fitness, but can also drive the expression of virulence factors, a process high in energy demands. In addition, enteric pathogens, such as the attaching and effacing (A/E) bacterium Citrobacter rodentium, must cross the colonic mucus layer that normally prevents their direct access to the underlying epithelium. Intestinal mucus is comprised of highly glycosylated mucins, with the sugar sialic acid frequently occupying the terminal position of their O-glycan side chains. We hypothesize that C. rodentium utilizes commensal-liberated mucin sugars, such as sialic acid, as nutrients and signals to promote its virulence.
Purpose
This study investigates the mechanisms by which A/E pathogens reach the colonic mucosal surface, and the role played by commensal microbes in facilitating the infection.
Method
Expression of virulence factors secreted by C. rodentium in the presence or absence of sialic acid was analyzed by SDS-PAGE and mass spectrometry. Next, we infected specific-pathogen free (SPF), germfree (GF), and previously GF C57Bl/6 mice mono-colonized with Bacteroides thetaotaomicron, a mucus-degrading commensal, to examine their susceptibility to C. rodentium and to measure the levels of free sialic acid in their feces.
Result(s)
Sensing of sialic acid by C. rodentium, was found to induce the secretion of several key virulence proteins, enhancing the pathogen’s migration across the colonic mucus layer and adhesion to the underlying epithelium. Access to sialic acid within the gut environment was enhanced in the presence of microbiota, as the levels of free sialic acid were low in GF mice. Interestingly, despite GF mice carrying very high C. rodentium burdens, passage across the mucus layer and infection of their colonic epithelium was impaired as compared to SPF mice. Notably, B. thetaotaomicron was found to degrade whole mucus in vitro, facilitating its consumption by C. rodentium for growth, while B. thetaotaomicron mono-colonized GF mice showed increased susceptibility to colonic infection by C. rodentium.
Conclusion(s)
We demonstrate that although commensal microbes promote colonization resistance, as an A/E pathogen infection establishes, specific commensal bacteria accelerate infection in the GI tract by releasing an important nutrient, ie. sialic acid, from mucus. Access to sialic acid promotes C. rodentium virulence by inducing the key virulence factors that facilitate its translocation across the mucus layer as well as adhesion to the epithelium, thereby expediting disease progression.
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CCC, CIHR, Other
Please indicate your source of funding;
CH.I.L.D. Foundation
Disclosure of Interest
None Declared
Abstract
Background
Colorectal cancer is the second leading cause of cancer death in Canada. A major risk factor for the development of colorectal cancer is chronic inflammation leading to ...colitis-associated cancer (CAC). We previously described a CAC mouse model in which tumors arise from DCLK1+ tuft cells following loss of the tumor suppressor adenomatous polyposis coli (APC) and induction of colitis. Interestingly, both colitis and CAC display epigenetic changes that modulate gene expression. However, the impact of DNA methylation changes on colonic tumorigenesis is not known. Thus, we hypothesize that inhibition of DNA methylation in DCLK1+ tuft cells reduces colonic tumorigenesis.
Purpose
In this study, we aim to investigate the role of DNA methylation in CAC by inhibiting DNA methylation using genetic and pharmacologic means.
Method
Using a publicly available dataset (GSE75214) of gene expression data analyzed by microarray from colonic biopsies of patients with ulcerative colitis and Crohn’s Disease with active disease, we examined the expression of DNA methyltransferases (DNMTs). Expression of DNMTs in mice with colitis was additionally examined by RT-qPCR and global DNA methylation levels measured by 5-mC ELISA. In separate experiments, Dclk1-CreERT2/Apcf/f mice were crossed to DNMT1f/f mice to knock-out the DNA methyltransferase DNMT1 in DCLK1+ tuft cells. Dclk1/Apcf/f and Dclk1/Apcf/f/DNMT1f/f mice were then administered three doses of tamoxifen followed by 2.5% dextran sodium sulfate (DSS) for five days to induce colitis. Fourteen weeks later, we assessed colonic tumor number and size. In a separate cohort of Dclk1/Apcf/f mice, we induced colitis and treated the mice with six doses of the DNA de-methylating drug 5-AZA-2’-deoxycytidine (5-AZA) or vehicle, and assessed colonic tumor number. To examine DNA methylation changes, we then treated WT mice with 5-AZA and DSS and isolated intestinal epithelial cells. From the intestinal epithelial cell, we isolated DNA and ran the Infinium MouseMethylation BeadChip Array.
Result(s)
Patients with IBD were found to have increased expression of DNMT1 compared to healthy controls. Mice treated with DSS similarly had increased DNMT1 expression, as well as, global methylation levels compared to controls. Deletion of DNMT1 in DCLK1+ cells significantly inhibited the number and size of colonic tumors. Treatment of mice with 5-AZA decreased global and gene specific DNA methylation levels, and significantly reduced both the number of mice with tumors, and the average colonic tumor number and size per mouse.
Conclusion(s)
Our findings demonstrate that colitis in both patients and mice is associated with DNA methylation. Furthermore, DNA hypomethylation by 5-AZA treatment or loss of DNMT1 reduces CAC formation suggesting that altered DNA methylation plays a critical role in colonic tumorigenesis.
Disclosure of Interest
None Declared
Abstract
Background
Liver transplantation is frequently lifesaving for people living with primary sclerosing cholangitis (PSC). However, patients are waitlisted for liver transplant (LT) according to ...the MELD-Na score, which may not accurately reflect the burden of living with PSC.
Purpose
We sought to describe and analyze the clinical trajectory for patients with PSC referred for LT, in a mixed deceased donor/live donor transplant programme.
Method
This was a retrospective cohort study from November 2012 to December 2019 including all patients with PSC referred for assessment at the University Health Network Liver Transplant Clinic. Patients who required multiorgan transplant or re-transplantation were excluded. Liver symptoms, hepatobiliary malignancy, MELD-Na progression, and death were abstracted from chart review. Competing Risk analysis was used for timing of LT, transplant type, and death.
Result(s)
Of 172 PSC patients assessed, 144 (84%) were listed, of whom 106/144 (74%) were transplanted. Mean age was 47.6 years and 66% were male. During follow-up through to 2021, 23/144 (16%) were removed from the waitlist due to infection, clinical deterioration, liver-related mortality or new cancer; 3 had clinical improvement. At the time of listing, 118/144 (81.95%) had a potential Living Donor (pLD) of whom 94 were transplanted: 64 live donor and 30 deceased donor. Patients with pLD had 79% lower mortality (p<0.001), and higher rates of transplantation (80% vs 46%). Exception points were granted to 13/172 (7.5%) patients.
Conclusion(s)
In a high-volume North American liver transplant centre, most patients with PSC assessed for transplant were listed and subsequently transplanted. However, this was a consequence of patients engaging in live donor transplantation. Our findings support the concern from patients with PSC that MELD-Na allocation does not adequately address their needs.
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CIHR, Other
Please indicate your source of funding;
This study was supported by PSC Partners Canada, Canadian Institutes of Health Research (CIHR), Toronto General and Western Hospital Foundation.
Disclosure of Interest
None Declared
Abstract
Background
The standard treatment of colorectal cancer (CRC) consists of a surgical resection of the colonic segment with the tumor, followed by a reconnection of the remaining bowel ends, ...or "anastomosis". The anastomosis may fail to heal in up to 20% of patients, which leads to anastomotic leak, a major complication that increases postoperative morbidity and mortality. This complication is unpredictable and its causes remain poorly understood.
Purpose
The objective of this study is to investigate the possible role of the gut microbiome in anastomotic healing after surgery in patients with CRC.
Method
We collected preoperative fecal samples and intraoperative mucosal samples from CRC patients undergoing surgery with anastomosis. The gut microbiota of patients with AL and of others that presented optimal healing after surgery was analyzed and compared using the Anchor 16S pipeline. To assess the role of the patients' microbiota in healing, fecal microbiota transplantation (FMT) was performed in mice using preoperative fecal samples from CRC patients with and without AL. Mice were then subjected to colonic surgery using a colonic anastomosis model. Six days after surgery, anastomotic healing was assessed macroscopically and microscopically. The gut barrier function was also assessed. The gut microbiota composition was compared between the groups colonized with samples from patients with and without AL to detect potential differences.
Result(s)
Mice colonized by FMT with the microbiota of donors with AL displayed poor anastomotic healing macroscopically, and a weaker wound microscopically. These same mice displayed a weaker gut barrier, as objectified by higher bacterial translocation to the spleen. The anastomoses of mice receiving the microbiota of AL donors displayed lower concentrations of collagen and fibronectin and higher inflammatory cytokines and collagenolytic enzymes, indicating poor extracellular matrix formation and collagen degradation locally.The beta-diversity of the gut microbiota was significantly different between mice receiving the microbiota of donors with and without AL, and several bacterial species were differentially abundant between the two groups.
Conclusion(s)
The preoperative gut microbiota in CRC patients who experience anastomotic leak after surgery induces poor anastomotic healing in mice and a weaker gut barrier after colonic surgery. Several bacterial species were found to be associated with the healing process.
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CIHR, Other
Please indicate your source of funding;
NSERC, FRQS, New Frontiers in Research, Montreal Cancer Institute.
Disclosure of Interest
None Declared
In recent years growing sociological interest in new forms of cultural distinction has led some to argue that the advantages previously conveyed by the consumption of ‘high’ culture ‘or ...‘omnivorousness’ are being overwritten by the possession of what has been termed ‘emerging cultural capital’. So far, though, this term has only been discussed in passing within empirical work and remains in need of further analytical specification. This special issue seeks to both critically interrogate and develop this concept by bringing together the work of leading cultural sociologists around four key themes: the role of age and generation in the formation of cultural capital; the power of visual display for distinction; the significance of new elite cultures; and the need for methodological pluralism to apprehend the expressions and mechanisms of distinction. This editorial introduction outlines the descriptive terrain on which the concept of emerging cultural capital has rested until now before exploring the common themes that sit across all five papers in the special issue.
Abstract
Background
The COVID-19 pandemic drastically impacted workflows in gastroenterology practice. Physicians managing immune-mediated diseases (IMDs) must complete special authorization (SA) and ...prescription renewal (Rx) forms for patients on biologic therapy. This adds significant administrative burden potentially leading to delays in therapy initiation and care continuity. Historically, document completion has largely been paper-based, with forms faxed between patient support programs (PSPs) and physician offices. Disruption of normal office processes during the pandemic necessitated the movement of existing paper-based workflows online. The use of secure electronic document signing (SEDS) platforms has allowed physicians to receive and complete documents digitally.
Aims
To evaluate the impact of SEDS-based biologic documentation on clinical practice. Objectives were 1) to determine if the use of SEDS platforms increased timeliness of document returns compared to traditional workflows 2) assess whether SEDS usage is acceptable and sustainable and 3) assess MD satisfaction with SEDS platforms.
Methods
This was a retrospective audit of SEDS and paper-based biologic document workflows from a single PSP (Abbvie Care). Outcomes of interest were the number of documents completed monthly using SEDS, new monthly users, and the number of active monthly users between April 1, 2020-March 31, 2021. Time (days) to SEDS completion (vs. paper process) was determined by reviewing timepoint data for SA and Rx documents from May 2019-January 2020 (‘pre- SEDS’) and for SEDS documents from May 2020-January 2021(‘SEDS’). The return time (RT) was defined as the time between date sent to a physician’s office by the PSP to the date returned to the PSP. Documents in the pre-SEDS cohort with a RT exceeding 30 days were excluded
Results
In totality, 5573 SA and Rx documents were completed by 383 physicians using the SEDS platform from April 2020-March 2021. A mean of 14.6 (sd 21.8) documents were signed per physician. The number of monthly electronic documents processed increased from 104 in April 2020 to 800 in March 2021. Active monthly users increased from 24 in April 2020 to 213 in March 2021 (31 new users monthly). A total of 19,387 paper documents were processed during the ‘pre-SEDS’ period and 3,317 electronic documents processed in the ‘SEDS’ period. The mean RT in the ‘pre-SEDS’ period was 8.03 days (Sd 8.2) and the ‘SEDS’ period was 1.11 days (sd 2.6).
Conclusions
This data demonstrates acceptability, appropriateness, and improved processing efficiency of a SEDS platform improving timeliness of patient care. Next steps in this research include surveying physicians to understand the work-flow impact of SEDS, functionality, long-term sustainability, satisfaction and impacts on disease related outcomes.
Funding Agencies
None
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