Outcomes of a pharmacist-managed glucose collaborative practice agreement.

PURPOSE: The impact of a pharmacist-managed glucose collaborative practice agreement (CPA) on glycemic control at a tertiary medical center was investigated. METHODS: A retrospective data analysis was performed on hospitalized, noncritically ill patients admitted between December 2012 and June 2014 who received at least one dose of subcutaneous insulin and experienced at least one blood glucose concentration of 140 mg/dL or higher. The study population was divided into cohorts based on admittance before versus after implementation of the CPA, as well as glucose management by pharmacist versus nonpharmacist provider. The primary endpoint of the study was glycemic control, defined as the percentage of total admitted days spent within a goal blood glucose range of 70-180 mg/dL. Secondary endpoints included the rate of hypoglycemia (less than 70 mg/dL), the rate of severe hypoglycemia (less than 40 mg/dL), the rate of severe hyperglycemia (greater than 300 mg/dL), the length of stay, and workload metrics. RESULTS: A total of 5146 patients were included in the study. There was no statistically significant difference in glycemic control across all cohorts (p > 0.05). Secondary outcomes showed no statistically significant differences in the rates of hypoglycemia, severe hypoglycemia, and severe hyperglycemia across all cohorts. There was a significantly longer length of stay in the pharmacist-managed cohort (p < 0.001). Workload metrics indicated a 25.8% increase in the number of pharmacist-managed glucose consults post-CPA implementation. CONCLUSION: Pharmacists at a tertiary medical center were able to provide an inpatient glucose management service that maintained similar glycemic control for patients with diabetes as nonpharmacist providers.

Delivery of celecoxib for treating diseases of the eye: influence of pigment and diabetes.

IMPORTANCE OF THE FIELD: Age-related macular degeneration (AMD) and diabetic retinopathy (DR) are two major causes of blindness. In these disorders, growth factors such as vascular endothelial growth factor (VEGF) are upregulated, leading to either enhanced vascular permeability or proliferation of endothelium. While corticosteroid therapies available at present suffer from side effects including cataracts and elevated intraocular pressure, anti-VEGF antibody therapies require frequent intravitreal injections, a procedure that can potentially lead to retinal detachment or endophthalmitis. Thus, there is a need to develop safe, sustained release therapeutic approaches for treating AMD and DR. AREAS COVERED IN THIS REVIEW: This review discusses the pharmacological basis for using celecoxib, an anti-inflammatory drug capable of selectively inhibiting cycloxygenase 2, in treating AMD and DR. In addition, this article discusses the safety, delivery advantage and efficacy of celecoxib by transscleral retinal delivery, a periocular delivery approach that is less invasive to the globe compared with intravitreal injections. WHAT THE READER WILL GAIN: The reader will gain insights into the development of a pharmacological agent and a sustained release delivery system for treating DR and AMD. Further, the reader will gain insights into the influence of eye physiology including pigmentation and disease states such as DR on retinal drug delivery. TAKE HOME MESSAGE: Transscleral sustained delivery of anti-inflammatory agents is a viable option for treating retinal disorders.

L-DOPA-induced activation of striatal p38MAPK and CREB in neonatal dopaminergic denervated rat: relevance to self-injurious behavior.

The destruction of nigrostriatal dopaminergic neurons with 6-hydroxydopamine (6OHDA) during the neonatal period results in dopamine (DA) loss and susceptibility for self-injurious behavior (SIB) when challenged with L-dihydroxyphenylalanine (L-DOPA), via a supersensitive D1 receptor-mediated mechanism. However, there are no changes in D1 receptor binding or mRNA levels, suggesting a potential postreceptor signaling mechanism(s). Here, we examined whether L-DOPA-induced SIB is associated with altered MAPK signaling (p38MAPK, ERK1/2, and JNK) and their nuclear target, CREB. Neonatal dopaminergic lesioned animals were challenged, as adults, with L-DOPA, observed for SIB for 6 hr, and then sacrificed. The data were grouped as follows: control, lesioned rats without SIB (SIB(-)), and lesioned rats that were positive for SIB (SIB(+)). HPLC analysis of striatal extracts revealed a more significant loss of DA and an increase of serotonin in the SIB(+) than in the SIB(-) group. The striatal levels of TH protein were severely decreased, but D1 receptor levels were unaltered in the lesioned groups. These results confirm and extend previous studies indicating that SIB is associated with a near-total loss of DA and TH, an increase in serotonin, and no change in D1 receptor levels. The present studies further revealed that the levels of active phosphorylated forms of p38MAPK and CREB were significantly higher in the SIB(+) group than in the SIB(-) group in the striatum, but not in cortex or olfactory tubercle. The results indicate an induction of striatal p38MAPK and an activation of its nuclear target, CREB, as additional mechanisms in the genesis of L-DOPA-induced SIB.