Pilot study of an interactive voice response system to improve medication refill compliance

<p>Abstract</p> <p>Background</p> <p>Sub-optimal adherence to prescribed medications is well documented. Barriers to medication adherence include medication side effects, cost, and forgetting to take or refill medications. Interactive Voice Response (IVR) systems show promise as a tool for reminding individuals to take or refill medications. This pilot study evaluated the feasibility and acceptability of using an IVR system for prescription refill and daily medication reminders. We tested two novel features: personalized, medication-specific reminder messages and communication via voice recognition.</p> <p>Methods</p> <p>Patients enrolled in a study of electronic prescribing and medication management in Quebec, Canada who were taking chronic disease-related drugs were eligible to participate. Consenting patients had their demographic, telephone, and medication information transferred to an IVR system, which telephoned patients to remind them to take mediations and/or refill their prescriptions. Facilitators and barriers of the IVR system use and acceptability of the IVR system were assessed through a structured survey and open-ended questions administered by telephone interview.</p> <p>Results</p> <p>Of the 528 eligible patients who were contacted, 237 refused and 291 consented; 99 participants had started the pilot study when it was terminated because of physician and participant complaints. Thirty-eight participants completed the follow-up interview. The majority found the IVR system's voice acceptable, and did not have problems setting up the time and location of reminder calls. However, many participants experienced technical problems when called for reminders, such as incorrect time of calls and voice recognition difficulties. In addition, most participants had already refilled their prescriptions when they received the reminder calls, reporting that they did not have difficulties remembering to refill prescriptions on their own. Also, participants were not receptive to speaking to an automated voice system.</p> <p>Conclusion</p> <p>IVR systems designed to improve medication compliance must address key technical and performance issues and target those individuals with reported memory difficulties or complex medication regimens in order to improve the utility of the system. Future research should also identify characteristics of medication users who are more likely to be receptive to IVR technology.</p

Muc2 Protects against Lethal Infectious Colitis by Disassociating Pathogenic and Commensal Bacteria from the Colonic Mucosa

Despite recent advances in our understanding of the pathogenesis of attaching and effacing (A/E) Escherichia coli infections, the mechanisms by which the host defends against these microbes are unclear. The goal of this study was to determine the role of goblet cell-derived Muc2, the major intestinal secretory mucin and primary component of the mucus layer, in host protection against A/E pathogens. To assess the role of Muc2 during A/E bacterial infections, we inoculated Muc2 deficient (Muc2−/−) mice with Citrobacter rodentium, a murine A/E pathogen related to diarrheagenic A/E E. coli. Unlike wildtype (WT) mice, infected Muc2−/− mice exhibited rapid weight loss and suffered up to 90% mortality. Stool plating demonstrated 10–100 fold greater C. rodentium burdens in Muc2−/− vs. WT mice, most of which were found to be loosely adherent to the colonic mucosa. Histology of Muc2−/− mice revealed ulceration in the colon amid focal bacterial microcolonies. Metabolic labeling of secreted mucins in the large intestine demonstrated that mucin secretion was markedly increased in WT mice during infection compared to uninfected controls, suggesting that the host uses increased mucin release to flush pathogens from the mucosal surface. Muc2 also impacted host-commensal interactions during infection, as FISH analysis revealed C. rodentium microcolonies contained numerous commensal microbes, which was not observed in WT mice. Orally administered FITC-Dextran and FISH staining showed significantly worsened intestinal barrier disruption in Muc2−/− vs. WT mice, with overt pathogen and commensal translocation into the Muc2−/− colonic mucosa. Interestingly, commensal depletion enhanced C. rodentium colonization of Muc2−/− mice, although colonic pathology was not significantly altered. In conclusion, Muc2 production is critical for host protection during A/E bacterial infections, by limiting overall pathogen and commensal numbers associated with the colonic mucosal surface. Such actions limit tissue damage and translocation of pathogenic and commensal bacteria across the epithelium