Pharmacists' contribution to benzodiazepine deprescribing in older outpatients: a systematic review and meta-analysis.

BACKGROUND: Consolidated and reliable evidence regarding the effectiveness of pharmacist interventions for deprescribing benzodiazepines in older outpatients is lacking. AIM: This study evaluated and summarized the impact of pharmacist interventions on benzodiazepine deprescribing among older outpatients. METHOD: A literature search was conducted until August 2022 in PubMed, PsycINFO, and the Cochrane Central Register of Controlled Trials databases. The review included randomized controlled trials that assessed the impact of pharmacist interventions on deprescribing benzodiazepine in older outpatients. Two independent investigators conducted the study selection, data extraction, and risk of bias assessment. Meta-analyses were conducted using random-effect models in the RStudio software. RESULTS: A total of 893 records were identified. Five studies, including 3,879 patients, met the inclusion criteria and were included in the systematic review. All five studies used health education as an intervention strategy, and three also conducted medication reviews. There was no evidence of the pharmacist's authority to modify prescriptions during benzodiazepine deprescribing. One study was classified as having a low risk of bias, whereas the other had some concerns or a high risk of bias. Three studies were included in the meta-analysis and a significant impact of pharmacist interventions on benzodiazepines deprescribing rates in older outpatients was observed (RR = 2.75 [95%CI 1.29; 5.89]; p = 0.04; I2 = 69%; low certainty of evidence). CONCLUSION: Pharmacists may contribute to deprescribing benzodiazepines in older outpatients. Further studies are needed to increase the reliability of these findings. PROSPERO registration number: CRD42022358563.

Functional and morphologic dysfunctions in the airways of rats submitted to an experimental model of obesity-exacerbated asthma.

The obesity-exacerbated asthma phenotype is characterized by more severe asthma symptoms and glucocorticoid resistance. The aim of this study was to standardize an obesity-exacerbated asthma model by a high glycemic level index (HGLI) diet and ovalbumin (OVA) sensitization and challenges in Wistar rats. Animals were divided into groups: control (Ctrl), obese (Ob), asthmatic (Asth), obese asthmatic (Ob + Asth) and obese asthmatic treated with dexamethasone (Ob + Asth + Dexa), and in vivo and in vitro functional and morphological parameters were measured. After HGLI consumption, there was an increase in body weight, fasting blood glucose, abdominal circumferences, body mass index and adiposity index. Respiratory function showed a reduction in pulmonary tidal volume and ventilation. In isolated tracheas, carbachol showed an increase in contractile efficacy in the Ob, Ob + Asth and Ob + Asth + Dexa, but mostly on Ob + Asth. Histological analysis of lungs showed peribronchovascular inflammation and smooth muscle hypertrophy and extracellular remodeling on Ob + Asth and Ob + Asth + Dexa. An obesity-exacerbated asthma model was successfully established. Therefore, this model allows further molecular investigations and the search for new therapies for the treatment and relief of symptoms of patients with obesity-induced resistant asthma.