Clinical Decision Support to Address Racial Disparities in Hypertension Control in an Integrated Delivery System: Evaluation of a Natural Experiment.

INTRODUCTION: Effective, equity-promoting interventions implemented by health care systems are needed to address health care disparities and population-level health disparities. We evaluated the impact of a clinical decision support tool to improve evidence-based thiazide diuretic prescribing among Black patients to address racial disparities in hypertension control. METHODS: We employed an interrupted time series design and qualitative interviews to evaluate the implementation of the tool. Our primary outcome measure was the monthly rate of thiazide use among eligible patients before and after implementation of the tool (January 2013-December 2016). We modeled month-to-month changes in thiazide use for Black and White patients, overall, and by sex and medical center racial composition. We conducted key informant interviews to identify modifiable facilitators and barriers to implementation of the tool across medical centers. RESULTS: Of the 318,720 patients, 15.5% were Black. We observed no change in thiazide use or blood pressure control following the implementation of the tool in either racial subgroup. There was a slight but statistically significant reduction (2.32 percentage points, p < 0.01) in thiazide use among Black patients following the removal the tool that was not observed among White patients. Factors affecting the tool's implementation included physician and pharmacist resistance to thiazide use and a lack of ongoing promotion of the tool. DISCUSSION: The clinical decision support tool was insufficient to change prescribing practices and improve blood pressure control among Black patients. CONCLUSIONS: Future interventions should consider physician attitudes about thiazide prescribing and the importance of multilevel approaches to address hypertension disparities.

Population Health Management for Diabetes: Health Care System-Level Approaches for Improving Quality and Addressing Disparities.

PURPOSE OF REVIEW: Population care approaches for diabetes have the potential to improve the quality of care and decrease diabetes-related mortality and morbidity. Population care strategies are particularly relevant as accountable care organizations (ACOs), patient-centered medical homes (PCMH), and integrated delivery systems are increasingly focused on managing chronic disease care at the health system level. This review outlines the key elements of population care approaches for diabetes in the current health care environment. RECENT FINDINGS: Population care approaches proactively identify diabetes patients through disease registries and electronic health record data and utilize multidisciplinary care teams, personalized provider feedback, and decision support tools to target and care for patients at risk for poor outcomes. Existing evidence suggests that these strategies can improve care outcomes and potentially ameliorate existing race/ethnic disparities in health care. However, such strategies may be less effective for patients who are disengaged from the health care system. As population care for diabetes continues to evolve, future initiatives should consider ways to tailor population care to meet individual patient needs, while leveraging improvements in clinical information systems and care integration to optimally manage and prevent diabetes in the future.

Huntington's disease--like 2 is associated with CUG repeat-containing RNA foci.

OBJECTIVE: Huntington's disease-like 2 (HDL2) is caused by a CAG/CTG expansion mutation on chromosome 16q24.3. The repeat falls, in the CTG orientation, within a variably spliced exon of junctophilin-3 (JPH3). The existence of a JPH3 splice variant with the CTG repeat in 3' untranslated region suggested that transcripts containing an expanded CUG repeat could play a role in the pathogenesis of HDL2, similar to the proposed pathogenic role of expanded CUG repeats in myotonic dystrophy type 1 (DM1). The goal of this study, therefore, was to test the plausibility of an RNA gain-of-function component in the pathogenesis of HDL2. METHODS: The presence and composition of RNA foci in frontal cortex from HDL2, Huntington's disease, DM1, and control brains were investigated by in situ hybridization and immunohistochemistry. An untranslatable JPH3 transcript containing either a normal or an expanded CUG repeat was engineered and expressed in human embryonic kidney 293 and HT22 cells to further test the toxic RNA hypothesis. The formation of RNA foci and the extent of cell death were quantified. RESULTS: RNA foci resembling DM1 foci were detected in neurons in HDL2 cortex and other brain regions. Similar to DM1, the foci colocalize with muscleblind-like protein 1, and nuclear muscleblind-like protein 1 in HDL2 cortical neurons is decreased relative to controls. In cell experiments, expression of a JPH3 transcript with an expanded CUG repeat resulted in the formation of RNA foci that colocalized with muscleblind-like protein 1 and in cell toxicity. INTERPRETATION: These results imply that RNA toxicity may contribute to the pathogenesis of HDL2.