Drug-related problems and satisfaction among patients receiving pharmacist-led consultations at the initiation of cardiovascular drugs.

BACKGROUND: Drug-related problems (DRPs) lead to substantial morbidity and mortality and increase healthcare costs. Several interventions have been developed to reduce DRPs and improve the outcome of drug therapy. OBJECTIVE: To investigate DRPs identified through a pharmacist-led intervention and to assess patient satisfaction with the intervention. METHODS: Patients received two pharmacist consultations 1-2 weeks and 3-5 weeks after collecting a new cardiovascular medicine. Information about patient characteristics, beliefs about medicines (BMQ), DRPs, and patient evaluations were collected using questionnaires. RESULTS: Pharmacists identified DRPs among 52.4% and 43.1% of the 633 patients at consultation 1 and 2, respectively. Of the DRPs reported in consultation 1, 43.7% were solved at consultation 2. Among patients with side effects, patients who received advice on managing these in consultation 1 where more likely to have solved problems at consultation 2 (61.2% vs. 42.6%, p = 0.008). Female gender, high BMQ concern and the number of new medicines were associated with DRPs. Patients were highly satisfied with the intervention. Predictors of satisfaction were female gender, older age, higher BMQ necessity, face-to-face consultations, longer duration of consultation 1, and solved problems in consultation 2. CONCLUSIONS: The results indicate that the pharmacist-led follow-up intervention can aid early identification and solving of DRPs in patients prescribed new cardiovascular drugs. Knowledge of factors associated with DRPs and patients' satisfaction may allow further improvement of the intervention.

Effect of a pharmacist-led intervention on adherence among patients with a first-time prescription for a cardiovascular medicine: a randomized controlled trial in Norwegian pharmacies.

OBJECTIVE: To examine whether a pharmacist-led intervention improves medication adherence among patients who have filled a first-time prescription for a cardiovascular medicine. METHODS: Design: Unblinded randomized controlled trial. SETTING: 67 Norwegian pharmacies, October 2014-June 2015. PARTICIPANTS: 1480 adults with a first-time prescription for a cardiovascular medicine. INTERVENTION: Participants in the intervention group received two consultations with a pharmacist 1-2 and 3-5 weeks after filling the prescription. Participants in the control group received care according to usual practice. MAIN OUTCOME MEASURE: The primary outcome was self-reported adherence as measured by the 8-item Morisky Medication Adherence Scale (MMAS-8), at 7 and 18 weeks after filling the prescription. Adherence from baseline to week 52 was estimated using data from the Norwegian Prescription Database (NPD). KEY FINDINGS: Data from MMAS-8 showed that 91.3% of the patients in the intervention group were adherent after 7 weeks versus 86.8% in the control group (4.5% difference, 95% CI 0.8-8.2, P = 0.017). The corresponding proportions were 88.7% versus 83.7% after 18 weeks (5.0% difference, 95% CI 0.8-9.2, P = 0.021). NPD data (n = 1294) showed no significant difference in adherence after 52 weeks (95% CI -2.0 to 7.8, P = 0.24). However, adherence among statin users (n = 182) was 66.5% in the intervention group versus 57.4% among new statin users in the general population (n = 1500) (difference 9.1%, 95% CI 1.5-16.0, P = 0.019). CONCLUSION: The main outcome measure indicates that a short, structured pharmacist-led intervention may increase medication adherence for patients starting on chronic cardiovascular medication. However, these findings could not be confirmed by the NPD data analysis.

High-affinity GABA uptake and GABA-metabolizing enzymes in pig forebrain white matter: a quantitative study.

GABA receptor activation in central nervous white matter may be protective during white matter hypoxia in the adult, and it may modify axonal conduction, especially in the developing brain. GABA uptake is important for the shaping of the GABA signal, but quantitative data are lacking for GABA uptake and GABA-metabolizing enzymes in central nervous white matter. We report that high-affinity uptake of GABA in adult pig corpus callosum, fimbria, subcortical pyramidal tracts, and occipital white matter is approximately 20% of that in temporal cortex gray matter. Tiagabine (0.1 microM), an antiepileptic drug that specifically inhibits the GAT-1 GABA transporter inhibited GABA uptake 50% in temporal cortex and 60-68% in white structures. This finding indicates that GAT-1 is an important GABA transporter in white matter and suggests that white matter GABA uptake is inhibited during tiagabine therapy. GABA transaminase activity in white structures was approximately 20% of neocortical values. Glutamate decarboxylase (GAD) activity in white structures was only 4% of that in neocortex (7-12 pmol/mg tissue x min(-1) versus approximately 200 pmol/mg tissue x min(-1)). Since white matter activity of citrate synthase of the tricarboxylic acid cycle was approximately 25% of neocortical values ( approximately 0.4 nmol/mg tissue x min(-1) versus approximately 1.5 nmol/mg tissue x min(-1)), the low GAD activity suggests a slower metabolic turnover of GABA in white than in gray matter.

High-affinity glycine and glutamate transport in pig forebrain white and gray matter: a quantitative study.

High-affinity uptake of glycine and glutamate modulates glutamatergic neurotransmission in gray matter. N-Methyl-D-aspartate (NMDA) receptors were recently described on white matter oligodendrocytes, therefore uptake of glutamate and glycine in white matter may also modulate NMDA receptor function. We found that glycine uptake in white structures of pig forebrain (corpus callosum, fimbria, subcortical pyramidal tracts, and occipital subcortical white matter) was similar to that in gray structures (frontal and temporal cortices and hippocampus), and that it was sensitive to sarcosine, a GLYT1 inhibitor (IC(50) 15 microM). Glutamate uptake in white matter was approximately 10% of that in gray; it was sensitive to dihydrokainate, an EAAT2 inhibitor. The levels of glycine and its precursor serine were similar in white and gray matter: approximately 2 and 1 nmol/mg tissue, respectively. The white matter level of glutamate was approximately 7.6 nmol/mg tissue, or approximately 74% of gray matter levels. The activity of serine hydroxymethyl transferase, which converts serine into glycine, was similar in white and gray matter (11-18 pmol/(mg tissue)min), whereas the white matter activity of phosphate-activated glutaminase, which converts glutamine into glutamate, was approximately 100 pmol/(mg tissue)min, or approximately 34% of gray matter activity. The white matter activity of glutamine synthetase, the glial enzyme that converts glutamate into glutamine, was 20-40 nmol/(mg tissue)min in neocortex and 5-6 nmol/(mg tissue)min in white matter. The data show that forebrain white matter is equipped to regulate extracellular levels of glycine and glutamate, functions that may modulate white matter NMDA receptor function.

Evidence for a higher glycolytic than oxidative metabolic activity in white matter of rat brain.

Different values exist for glucose metabolism in white matter; it appears higher when measured as accumulation of 2-deoxyglucose than when measured as formation of glutamate from isotopically labeled glucose, possibly because the two methods reflect glycolytic and tricarboxylic acid (TCA) cycle activities, respectively. We compared glycolytic and TCA cycle activity in rat white structures (corpus callosum, fimbria, and optic nerve) to activities in parietal cortex, which has a tight glycolytic-oxidative coupling. White structures had an uptake of [(3)H]2-deoxyglucose in vivo and activities of hexokinase, glucose-6-phosphate isomerase, and lactate dehydrogenase that were 40-50% of values in parietal cortex. In contrast, formation of aspartate from [U-(14)C]glucose in awake rats (which reflects the passage of (14)C through the whole TCA cycle) and activities of pyruvate dehydrogenase, citrate synthase, alpha-ketoglutarate dehydrogenase, and fumarase in white structures were 10-23% of cortical values, optic nerve showing the lowest values. The data suggest a higher glycolytic than oxidative metabolism in white matter, possibly leading to surplus formation of pyruvate or lactate. Phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, was similar in white structures and parietal cortex ( approximately 3 nmol/mg tissue/min), in spite of the lower glucose uptake in the former, suggesting that a larger fraction of glucose is converted into glucose-1-phosphate in white than in gray matter. However, the white matter glycogen synthase level was only 20-40% of that in cortex, suggesting that not all glucose-1-phosphate is destined for glycogen formation.