A Quality Improvement Initiative Is Associated With Reduced Time to Administer Biologics and Small Molecules and Emergency Room Visits in Inflammatory Bowel Disease.

BACKGROUND: Delays in biologic or small molecule medication administration are associated with increased adverse events, hospitalization, and surgery in inflammatory bowel disease (IBD). We evaluated the impact of a quality improvement (QI) intervention on the time to administration of biologics or small molecules (TABS) in IBD. METHODS: Data were retrospectively extracted for IBD patients prescribed biologics or small molecules from a convenience sample of providers participating in an accredited QI educational intervention (baseline cohort). Subsequent to the intervention, data were prospectively collected from patients prescribed these medications (postintervention cohort). Dates related to steps between a treatment decision to medication administration were collected. The primary outcome compared TABS in baseline and postintervention cohorts. RESULTS: Eighteen physicians provided survey and patient data for 200 patients in each cohort (n=400). The median time to medication administration (TABS) decreased from baseline to postintervention cohorts (30 vs. 26 d, P=0.04). Emergency room visits before medication administration also decreased (25.5% vs. 12.5%, P=0.001). Similar numerical TABS reductions were observed in subgroups limited to physicians providing patients to both cohorts and for individual medications prescribed. Primary contributors to delays included filling prescriptions subsequent to insurance approval and dispensation subsequent to this. CONCLUSIONS: A QI intervention successfully reduced medication administration times (TABS) by accelerating provider-dependent steps. This intervention was associated with reduced emergency room visits. We propose TABS as a quality metric to assess the effective delivery of therapies in IBD. Further evaluation of QI interventions, patient education on prescription drug insurance, and quality metrics are warranted.

IgA-coated E. coli enriched in Crohn's disease spondyloarthritis promote TH17-dependent inflammation.

Peripheral spondyloarthritis (SpA) is a common extraintestinal manifestation in patients with active inflammatory bowel disease (IBD) characterized by inflammatory enthesitis, dactylitis, or synovitis of nonaxial joints. However, a mechanistic understanding of the link between intestinal inflammation and SpA has yet to emerge. We evaluated and functionally characterized the fecal microbiome of IBD patients with or without peripheral SpA. Coupling the sorting of immunoglobulin A (IgA)-coated microbiota with 16S ribosomal RNA-based analysis (IgA-seq) revealed a selective enrichment in IgA-coated Escherichia coli in patients with Crohn's disease-associated SpA (CD-SpA) compared to CD alone. E. coli isolates from CD-SpA-derived IgA-coated bacteria were similar in genotype and phenotype to an adherent-invasive E. coli (AIEC) pathotype. In comparison to non-AIEC E. coli, colonization of germ-free mice with CD-SpA E. coli isolates induced T helper 17 cell (TH17) mucosal immunity, which required the virulence-associated metabolic enzyme propanediol dehydratase (pduC). Modeling the increase in mucosal and systemic TH17 immunity we observed in CD-SpA patients, colonization of interleukin-10-deficient or K/BxN mice with CD-SpA-derived E. coli lead to more severe colitis or inflammatory arthritis, respectively. Collectively, these data reveal the power of IgA-seq to identify immunoreactive resident pathosymbionts that link mucosal and systemic TH17-dependent inflammation and offer microbial and immunophenotype stratification of CD-SpA that may guide medical and biologic therapy.

The study of bone demineralization and its risk factors in an Afro-Caribbean subset of patients with inflammatory bowel disease.

INTRODUCTION: Bone demineralization has been increasingly recognized as a disease process concurrent with inflammatory bowel disease (IBD). Racial variation in osteoporosis in IBD patients has been poorly described. We sought to identify the risk factors for demineralization in Afro-Caribbeans (AC) with IBD. METHODS: A retrospective chart review was performed from a 10-year prospectively collected database of IBD patients seen at an urban medical center. Data on dual-energy X-ray absorptiometry (DXA) scanning, use of steroids, bisphosphonates, calcium, and vitamin D, as well as blood chemistries were collected. RESULTS: One hundred and fifteen charts of AC IBD patients were reviewed, of which 24 patients had undergone DXA scanning. Fourteen patients with a T-score of less than -1 were compared with 10 patients with DXA scores of more than -1. Two patients with T-scores of less than -1 had fractures, whereas none were observed in the comparison group (P=0.5). The mean BMI for those with T-scores of less than -1 was 23.9 kg/m compared with 31.5 kg/m in those with T-scores of more than -1 (P=0.0034). CONCLUSION: Screening for bone demineralization in ethnic populations with IBD is lacking as only 21% of AC IBD patients seen in our institution had undergone a DXA scan. Of those who were scanned, more than half of the patients had T-scores suggestive of bone demineralization. Although those who were obese did not have demineralization, our sample sizes were small and the results from this study should prompt further investigation to determine the prevalence and significance of bone demineralization in minority populations with IBD.