Framework for integrating electronic patient-reported data in routine cancer care: an Oncology Intake Questionnaire.

Objective: As part of ongoing implementation of electronic patient-reported outcome tools at the Dana-Farber Cancer Institute, here we describe the development of the electronic New Patient Intake Questionnaire. Materials and Methods: The original New Patient Intake Questionnaire includes a review of symptoms, oncology history, family history, health behaviors, health and social status, health literacy and numeracy, which was modified for integration into the EHR using content determination, build and configuration, implementation, analytics, and interventions. The engagement of key stakeholders, including patients, clinical staff, and providers, throughout the development and deployment of the electronic Questionnaire was crucial to producing a successful tool. Continual modifications based on input of stakeholders (such as mode of tool deployment) were made to ensure the utility and usability of the tool for both patients and providers. Results: Implementation of the EHR-integrated electronic New Patient Intake Questionnaire improved collection of the PRD by increasing questionnaire accessibility for patients, while also providing all available data to clinicians and researchers. Careful consideration of the content and configuration of the questionnaire allowed for a successful, institute-wide implementation of the tool. Discussion: This effort demonstrates the feasibility of implementation of a system-wide electronic questionnaire, emphasizing the importance of iterative refinement to create a tool that is both patient-centric and usable for clinicians. Conclusions: The electronic New Patient Intake Questionnaire allows for systematic collection of the PRD, which should benefit cancer care outcomes through innovative care delivery and healthcare interventions.

Corticosteroids prevent myofibroblast accumulation and airway remodeling in mice.

At present there are conflicting results from studies investigating the role of corticosteroids in inhibiting airway remodeling in asthma. We have used a mouse model to determine whether administration of corticosteroids prevents the development of allergen-induced structural features of airway remodeling. Mice treated with corticosteroids were subjected to repetitive ovalbumin (OVA) challenge for 3 mo, at which time levels of peribronchial fibrosis and the thickness of the peribronchial smooth muscle layer were assessed by immunohistology, levels of transforming growth factor (TGF)-beta1 by ELISA, and the number of alpha-smooth muscle actin+/Col-1+ peribronchial myofibroblasts by immunohistochemistry. Corticosteroids significantly reduced allergen-induced increases in peribronchial collagen deposition and levels of total lung collagen but did not reduce allergen-induced increases in the thickness of the peribronchial smooth muscle layer. Levels of lung TGF-beta1 were significantly reduced in mice treated with systemic corticosteroids, and this was associated with a significant decrease in the number of peribronchial inflammatory cells that expressed TGF-beta1, including eosinophils and mononuclear cells. Corticosteroids also significantly reduced the number of peribronchial myofibroblasts. Overall, these studies demonstrate that administration of corticosteroids significantly reduces levels of allergen-induced peribronchial fibrosis. The reduction in peribronchial fibrosis mediated by corticosteroids is likely to be due to several mechanisms including inhibition of expression of TGF-beta1, a reduction in the number of peribronchial inflammatory cells expressing TGF-beta1 (eosinophils, macrophages), as well as by corticosteroids reducing the accumulation of peribronchial myofibroblasts that contribute to collagen expression.