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Objectives: Considerable international investment in hospital electronic prescribing (ePrescribing) systems has been made, but despite this, it is proving difficult for most organisations to realise safety, quality and efficiency gains in prescribing. The objective of this work is to develop policy-relevant insights into the optimisation of hospital ePrescribing systems in order to maximise the benefits and minimise the risks of these expensive digital health infrastructures.Methods: We undertook a systematic scoping review of the literature by searching Medline, Embase and CINAHL databases. We searched for primary studies reporting on ePrescribing optimisation strategies and independently screened and abstracted data until saturation was achieved. Findings were theoretically and thematically synthesised taking a medicines lifecycle perspective, incorporating consultative phases with domain experts. Results: We identified 23,609 potentially eligible studies from which 1,367 satisfied our inclusion criteria. Thematic synthesis was conducted on a dataset of 76 studies, of which 48 were based in the United States (US). Key approaches to optimisation included: stakeholder engagement, system or process redesign, technological innovations, and education and training packages. Single-component interventions (n=26) described technological optimisation strategies focusing on a single, specific step in the prescribing process. Multi-component interventions (n=50), employed a combination of optimisation strategies, typically targeting multiple steps in the medicines management process. Discussion: We identified numerous optimisation strategies for enhancing the performance of ePrescribing systems. Key considerations for ePrescribing optimisation include meaningful stakeholder engagement to re-conceptualise the service delivery model, and implementing technological innovations with supporting training packages to simultaneously impact on different facets of the medicines management process.

Many drugs have been reported to cause thrombotic microangiopathy (TMA), yet evidence supporting a direct association is often weak. In particular TMA has been reported in association with recombinant type I interferon therapies, with recent concern regarding the use of interferon in multiple sclerosis patients. However a causal association has yet to be demonstrated. Here we adopt a combined clinical and experimental approach to provide evidence of a such an association between type I interferon and TMA. We show the clinical phenotype of cases referred to a national centre is uniformly consistent with a direct dose-dependent drug-induced TMA. We then show that dose-dependent microvascular disease is seen in a transgenic mouse model of interferon toxicity. This includes specific microvascular pathological changes seen in patient biopsies, and is dependent on transcriptional activation of the interferon response through the type I interferon receptor (IFNAR). Together our clinical and experimental findings provide evidence of a causal link between type I interferon and thrombotic microangiopathy. As such, recombinant type I interferon therapies should be stopped at the earliest stage in patients who develop this complication, with implications for risk mitigation.

The menopause should be diagnosed based on age, menstrual history and clinical symptoms, and as such, follicle stimulating hormone testing may be considered inappropriate when diagnosing the menopause or peri-menopause in women aged 45 and over. As part of a demand optimisation programme, the number of follicle stimulating hormone tests requested to diagnose the menopause in this age group was quantified and educational interventions were implemented to reduce inappropriate testing. The number of follicle stimulating hormone tests requested to diagnose the menopause in women aged 45 and over was successfully and sustainably reduced.