ABSTRACT
The Centers for Disease Control and Prevention (CDC) Guidelines for Prescribing Opioids for Chronic Pain recommend co-prescribing naloxone as a harm reduction strategy when there is an increased risk of opioid overdose. Although naloxone co-prescribing is an important harm reduction strategy, many at risk patients are not prescribed naloxone. The objective was to assess the effectiveness of a pharmacist-driven protocol at increasing the number of patients co-prescribed naloxone according to CDC recommendations. The study design was a multi-center retrospective cohort to evaluate the outcomes of a quality improvement intervention at two primary care clinics which aimed to increase naloxone co-prescribing. The intervention used a two-pronged approach consisting of telephonic outreach to eligible patients by pharmacists and pharmacy interns related to naloxone education and recommendations for naloxone co-prescribing. Additionally, recommendations were sent to the primary care provider in the electronic medical record (EMR) for consideration and implementation. After the 3 month intervention, 57 of the 86 patients contacted were co-prescribed naloxone (66.3%). Most naloxone initiation occurred at the time of telephonic outreach as a new medication order (n = 36), however an additional 12 patients were co-prescribed naloxone at a subsequent primary care provider visit. The proportion of patients at each clinic with MME ≥ 50 co-prescribed naloxone significantly increased after implementation of the intervention (pre 25/64 vs. post 43/76, p = 0.043). Overall, telephonic outreach to patients with recommendations to primary care providers in the EMR were effective methods to increase the rate of naloxone co-prescribing in primary care based on this study.
ABSTRACT
One major aspect of the aging process is the onset of chronic, low-grade inflammation that is highly associated with age-related diseases. The molecular mechanisms that regulate these processes have not been fully elucidated. We have identified a spontaneous mutant mouse line, small with kinky tail (skt), that exhibits accelerated aging and age-related disease phenotypes including increased inflammation in the brain and retina, enhanced age-dependent retinal abnormalities including photoreceptor cell degeneration, neurodegeneration in the hippocampus, and reduced lifespan. By positional cloning, we identified a deletion in chondroitin sulfate synthase 1 (Chsy1) that is responsible for these phenotypes in skt mice. CHSY1 is a member of the chondroitin N-acetylgalactosaminyltransferase family that plays critical roles in the biosynthesis of chondroitin sulfate, a glycosaminoglycan (GAG) that is attached to the core protein to form the chondroitin sulfate proteoglycan (CSPG). Consistent with this function, the Chsy1 mutation dramatically decreases chondroitin sulfate GAGs in the retina and hippocampus. In addition, macrophage and neutrophil populations appear significantly altered in the bone marrow and spleen of skt mice, suggesting an important role for CHSY1 in the functioning of these immune cell types. Thus, our study reveals a previously unidentified impact of CHSY1 in the retina and hippocampus. Specifically, chondroitin sulfate (CS) modification of proteins by CHSY1 appears critical for proper regulation of immune cells of the myeloid lineage and for maintaining the integrity of neuronal tissues, since a defect in this gene results in increased inflammation and abnormal phenotypes associated with age-related diseases.
