Patient expectations and experiences of multiple sclerosis interferon β-1a treatment: a longitudinal, observational...

Premature discontinuation and poor treatment adherence are problems in chronic conditions, such as multiple sclerosis in which patients must take long-term treatment in order to receive maximum benefit from their medication. The Assessing needs In Multiple Sclerosis (AIMS) study explored factors related to premature treatment discontinuation and patients' experiences of subcutaneous (sc) interferon (IFN) β-1a treatment in the UK.

A questionnaire-based survey was integrated into the Bupa Home Healthcare patient-support program, which delivers sc IFN β-1a to patients in their home. Data were collected via patient questionnaires incorporated into routine clinical care and administered upon registration of a new patient by the coordinator, following initial delivery of treatment, prior to each delivery during therapy and at the end of treatment. Univariate and multivariate analyses were performed to identify factors associated with premature discontinuation.

Data were collected from 2,390 patients (1,267 new; 1,123 existing) from 59 UK prescribing centers (November 2006-April 2011). Following the first delivery of sc IFN β-1a, 94% (1,149/1,225) of patients had received training, and 73% (818/1,120) reported that they had no concerns. In total, 24% of new patients discontinued therapy by the end of the study. In the univariate model, none of the candidate variables tested were significant predictors of treatment discontinuation. The strongest predictors of discontinuation in multivariate analyses were lack of information prior to starting treatment and patients feeling unwell on treatment and geographic region (P<0.05 for each variable).

This study suggests that patients feeling well on treatment and provision of high-quality information are the main determinants of persistence with sc IFN β-1a therapy. A package of care that targets these issues should therefore be considered when initiating sc IFN β-1a therapy.