Improving Medication Adherence in an ACO Primary Care Office With a Pharmacist-Led Clinic: A Report From the ACORN SEED.

BACKGROUND: As health care moves into the era of value-based medicine, both ambulatory and acute settings are being held accountable for the quality of care provided to patients. Previous studies have shown improved clinical outcomes through medication therapy management (MTM) due to improved medication adherence. OBJECTIVE: The purpose of this study is to assess the effects of a pharmacist-led MTM clinic in an accountable care organization (ACO) affiliated primary care office on adherence to renin-angiotensin system (RAS) antagonists, diabetic medications, and/or statin medications reported through Healthcare Effectiveness Data and Information Set (HEDIS) Medicare Star Ratings. METHODS: In this retrospective cohort study, data were collected via chart review of pharmacist-led MTM patient interviews and follow-ups between October 2015 and April 2017. Eligible patients were Humana HMO Medicare beneficiaries, with at least one chronic disease state, for which they were treated with a RAS antagonist, statin, or diabetic medication. The primary outcome of this investigation was a change in Star Rating scores for medication adherence to RAS antagonists, diabetic medications, and statins from pre- and postpharmacist MTM intervention. RESULTS: A total of 102 patients were referred to the MTM clinic. Out of these, 32 had a follow-up visit, resulting in a total of 25 interventions. One year prior to MTM clinic implementation, most Star Ratings were consistently 3 (out of 5) for RAS antagonists, diabetic medications, and statins. Postintervention, ratings increased to 4 or 5 across these categories. Conclusion: Implementing a pharmacist-led MTM clinic in the ACO primary care setting improves Medicare Star Ratings in patients with chronic conditions.

Third-year pharmacy students propose an interprofessional prediabetes educational programme: PreDiaMe (Prediabetes + Me).

The American Diabetes Association announced in 2012 that 86 million Americans were diagnosed with prediabetes compared to 79 million in 2010. Prediabetes + Me (PreDiaMe) is an innovative educational programme developed by pharmacy students at Nova Southeastern University College of Pharmacy, which provides collaborative interprofessional care for patients with prediabetes. A literature review using EBSCOhost, EMBASE, and MEDLINE databases searching the terms education, health services, interprofessional team, and prediabetes was conducted. Human studies published in English between 2006 and 2016 were included. Investigators interviewed a community pharmacist and a consultant pharmacist certified in diabetes education. Based on these interviews and the literature found, PreDiaMe was created to unite healthcare professionals through a three-step community outreach programme. The goal of PreDiaMe is to identify patients at risk of prediabetes, to decrease the prevalence of type 2 diabetes mellitus (T2DM), to reduce healthcare costs, and to improve the quality of life for patients with prediabetes. PreDiaMe benefits patients with prediabetes, the healthcare system, and pedagogy as it aims to decrease in the prevalence and economic burden and increase health outcomes of patients with prediabetes while being used as a tool to provide integrative education in health professional programmes.

NDFIP allows NEDD4/NEDD4L-induced AQP2 ubiquitination and degradation.

Regulation of our water homeostasis is fine-tuned by dynamic translocation of Aquaporin-2 (AQP2)-bearing vesicles to and from the plasma membrane of renal principal cells. Whereas binding of vasopressin to its type-2 receptor initiates a cAMP-protein kinase A cascade and AQP2 translocation to the apical membrane, this is counteracted by protein kinase C-activating hormones, resulting in ubiquitination-dependent internalization of AQP2. The proteins targeting AQP2 for ubiquitin-mediated degradation are unknown. In collecting duct mpkCCD cells, siRNA knockdown of NEDD4 and NEDD4L E3 ligases yielded increased AQP2 abundance, but they did not bind AQP2. Membrane Yeast Two-Hybrid assays using full-length AQP2 as bait, identified NEDD4 family interacting protein 2 (NDFIP2) to bind AQP2. NDFIP2 and its homologue NDFIP1 have PY motifs by which they bind NEDD4 family members and bring them close to target proteins. In HEK293 cells, NDFIP1 and NDFIP2 bound AQP2 and were essential for NEDD4/NEDD4L-mediated ubiquitination and degradation of AQP2, an effect not observed with PY-lacking NDFIP1/2 proteins. In mpkCCD cells, downregulation of NDFIP1, NEDD4 and NEDD4L, but not NDFIP2, increased AQP2 abundance. In mouse kidney, Ndfip1 and Ndfip2 mRNA distribution was similar and high in proximal tubules and collecting ducts, which was also found for NDFIP1 proteins. Our results reveal that NEDD4/NEDD4L mediate ubiquitination and degradation of AQP2, but that NDFIP proteins are needed to connect NEDD4/NEDD4L to AQP2. As NDFIP1/2 bind many NEDD4 family E3 ligases, which are implicated in several cellular processes, NDFIP1/2 may be the missing link for AQP2 ubiquitination and degradation from different subcellular locations.

Intravenous Immunoglobulin in Pediatric Rheumatology: When to Use It and What Is the Evidence.

Intravenous immunoglobulin (IVIG) is given to children with a variety of rheumatologic illnesses. The mechanism of action by which it exerts therapeutic effects is not well understood and likely differs in the medical conditions for which it is given. IVIG is approved by the US Food and Drug Administration and is the standard of care for Kawasaki disease, but most IVIG use in pediatric rheumatology is "off-label. " The literature supports the use of IVIG for juvenile dermatomyositis, although it is unclear whether its use should be limited to those children with more severe or refractory disease. It appears efficacious in the treatment of autoimmune thrombocytopenia secondary to lupus, but its use may be limited by transient responses. Treatment of other categories of pediatric rheumatologic diseases, such as juvenile idiopathic arthritis and non-Kawasaki vasculitides, is not well-established in the literature. This review focuses on current use of IVIG in the treatment of pediatric rheumatologic disorders. [Pediatr Ann. 2017;46(1):e19-e24.].

ß1-adrenoceptor Arg389Gly polymorphism confers differential ß-arrestin-binding tropism in cardiac myocytes.

AIM: The ß1-adrenergic receptor (AR) Arg389Gly polymorphism affects efficacy of its procontractile signaling in cardiomyocytes and carriers' responses to ß-blockers. To identify molecular mechanisms underlying functional differences between Arg389 and Gly389 ß1ARs, we examined their binding to ß-arrestins (ßarr-1 and -2), which mediate ß1AR signaling, in neonatal rat ventricular myocytes. METHODS: We tested the ß1AR-ßarr interaction via ß1AR immunoprecipitation followed by ßarr immunoblotting. RESULTS: ßarr1 binds both variants upon isoproterenol, carvedilol or metoprolol treatment in neonatal rat ventricular myocytes. Conversely, the potentially beneficial in the heart ßarr2 only interacts with the Arg389 receptor in response to isoproterenol or carvedilol. CONCLUSION: Arg389 confers unique ßarr2-interacting tropism to the ß1AR in cardiac myocytes, potentially underlying this variant's gain-of-function phenotype and better clinical responses to ß-blockers.