Pharmacist Intervention for Blood Pressure Control in Patients with Diabetes and/or Chronic Kidney Disease.

OBJECTIVES: The objectives of this study were to determine if hypertensive patients with comorbid diabetes mellitus (DM) and/or chronic kidney disease (CKD) receiving a pharmacist intervention had a greater reduction in mean blood pressure (BP) and improved BP control at 9 months compared with those receiving usual care; and compare Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) guideline and 2014 guideline (JNC 8) BP control rates in patients with DM and/or CKD. METHODS: This cluster randomized trial included 32 medical offices in 15 states. Clinical pharmacists made treatment recommendations to physicians at intervention sites. This post hoc analysis evaluated mean BP and BP control rates in the intervention and control groups. MAIN RESULTS: The study included 335 patients (227 intervention, 108 control) when mean BP and control rates were evaluated by JNC 7 inclusion and control criteria. When JNC 8 inclusion and control criteria were applied, 241 patients (165 intervention, 76 control) remained and were included in the analysis. The pharmacist-intervention group had significantly greater mean systolic blood pressure reduction compared with usual care at 9 months (8.64 mm Hg; 95% confidence interval [CI] -12.8 to -4.49, p<0.001). The pharmacist-intervention group had significantly higher BP control at 9 months than usual care by either the JNC 7 or JNC 8 inclusion and control groups (adjusted odds ratio [OR] 1.97, 95% CI 1.01-3.86, p=0.0470 and OR 2.16, 95% CI 1.21-3.85, p=0.0102, respectively). PRINCIPAL CONCLUSIONS: This study demonstrated that a physician-pharmacist collaborative intervention was effective in reducing mean systolic BP and improving BP control in patients with uncontrolled hypertension with DM and/or CKD, regardless of which BP guidelines were used.

Physician-Pharmacist Collaborative Management: Narrowing the Socioeconomic Blood Pressure Gap.

Physician-pharmacist collaboration improves blood pressure, but there is little information on whether this model can reduce the gap in healthcare disparities. This trial involved 32 medical offices in 15 states. A clinical pharmacist was embedded within each office and made recommendations to physicians and patients in intervention offices. The purpose of the present analysis was to evaluate whether the pharmacist intervention could reduce healthcare disparities by improving blood pressure in high-risk racial and socioeconomic subjects compared with the control group. The analyses in minority subjects were prespecified secondary analyses, but all other comparisons were secondary, post hoc analyses. The 9-month visit was completed by 539 patients: 345 received the intervention, and 194 were in the control group. Following the intervention, mean systolic blood pressure was found to be 7.3 mm Hg (95% confidence interval 2.4, 12.3) lower in subjects from racial minority groups who received the intervention compared with the control group (P=0.0042). Subjects with ≤12 years of education in the intervention group had a systolic blood pressure 8.1 mm Hg (95% confidence interval 3.2, 13.1) lower than the control group with lower education (P=0.0001). Similar reductions in blood pressure occurred in patients with low incomes, those receiving Medicaid, or those without insurance. This study demonstrated that a pharmacist intervention reduced racial and socioeconomic disparities in the treatment of blood pressure. Although disparities in blood pressure were reduced by the intervention, there were still nonsignificant gaps in mean systolic blood pressure when compared with intervention subjects not at risk. CLINICAL TRIAL REGISTRATION: URL: http://clinicaltrials.gov. Unique identifier: NCT00935077.

Circulating FGF21 is liver derived and enhances glucose uptake during refeeding and overfeeding.

Fibroblast growth factor (FGF)21 is an endocrine hormone that is expressed in multiple tissues and functions physiologically to maintain energy homeostasis. FGF21 is being pursued as a therapeutic target for diabetes and obesity because of its rapid and potent effects on improving insulin sensitivity. However, whether FGF21 enhances insulin sensitivity under physiologic conditions remains unclear. Here, we show that liver-derived FGF21 enters the circulation during fasting but also remains present and functional during the early stage of refeeding. After a prolonged fast, FGF21 acts as an insulin sensitizer to overcome the peripheral insulin resistance induced by fasting, thereby maximizing glucose uptake. Likewise, FGF21 is produced from the liver during overfeeding and mitigates peripheral insulin resistance. DIO FGF21 liver-specific knockout, but not FGF21 adipose-specific knockout, mice have increased insulin resistance and decreased brown adipose tissue-mediated glucose disposal. These data are compatible with the concept that FGF21 functions physiologically as an insulin sensitizer under conditions of acute refeeding and overfeeding.