The prevalence of chronic medication therapy problems and pharmacists' interventions among hospitalized perioperative patients: a retrospective observational study.

BACKGROUND: Inadequate preoperative management of chronic medications can place perioperative patients at risk and cause unnecessary delays in surgical procedures. This study aims to investigate the prevalence of chronic medication therapy problems (CMTPs) in hospitalized perioperative patients and assess the relevance of pharmacists' interventions. METHODS: We conducted a retrospective study of pharmacist-led preoperative management of chronic medications in hospitalized adult patients from November 2018 to April 2019. The recorded drug-related problems (DRPs) were retrospectively reviewed and categorized according to the Pharmaceutical Care Network Europe classification V9.1 and were analyzed with a multinomial regression model to identify risk factors. RESULTS: A total of 254 DRPs were recorded, with an average of 0.52 DRPs per patient. Treatment safety (66.9%) was the most common DRP. The most frequent causes of perioperative DRPs and nonperioperative DRPs were drug selection (72.9%) and patient related (50.8%), respectively. Of the 292 documented interventions, 71.6% were fully accepted by the clinicians and patients. The majority (68.9%) of the recorded problems were completely resolved. The number of comorbidities (OR = 3.815) and the number of chronic medications taken (OR = 1.539) were risk factors for the occurrence of DRPs. CONCLUSION: The findings of this study suggest that pharmacist-led chronic medication therapy management in surgical wards may be an effective method to help reduce medication-related surgical risks and optimize the medication therapies used for the long-term treatment of chronic diseases.

Identification and analysis of hub genes and networks related to hypoxia preconditioning in mice (No 035215).

Hypoxia preconditioning is an effective strategy of intrinsic cell protection. An acute repetitive hypoxic mice model was developed. High-throughput microarray analysis was performed to explore the integrative alterations of gene expression in repetitive hypoxic mice. Data obtained was analyzed via multiple bioinformatics approaches to identify the hub genes, pathways and biological processes related to hypoxia preconditioning. The current study, for the first time, provides insights into the gene expression profiles in repetitive hypoxic mice. It was found that a total of 1175 genes expressed differentially between the hypoxic mice and normal mice. Overall, 113 significantly up-regulated and 138 significantly down-regulated functions were identified from the differentially expressed genes in repetitive hypoxic brains. Among them, at least fourteen of these genes were very associated with hypoxia preconditioning. The change trends of these genes were validated by reverse-transcription polymerase chain reaction and were found to be consistent with the microarray data. Combined the results of pathway and gene co-expression networks, we defined Plcb1, Cacna2d1, Atp2b4, Grin2a, Grin2b and Glra1 as the main hub genes tightly related with hypoxia preconditioning. The differential functions mainly included the mitogen-activated protein kinase pathway and ion or neurotransmitter transport. The multiple reactions in cell could be initiated by activating MAPK pathway to prevent hypoxia damage. Plcb1 was an important and hub gene and node in the hypoxia preconditioning signal networks. The findings in the hub genes and integrated gene networks provide very useful information for further exploring the molecular mechanisms of hypoxia preconditioning.

UPLC-HRMS based metabolomics reveals the sphingolipids with long fatty chains and olefinic bonds up-regulated in metabolic pathway for hypoxia preconditioning.

Hypoxia preconditioning (HPC) could protect cells, tissues, organs and systems from hypoxia injury, but the molecular mechanism still remained unclear. The ultra-high performance liquid chromatography coupled high resolution mass spectrometry (UPLC-HRMS) based metabolomics method was utilized to explore the key endogenous metabolites and metabolic pathways related to HPC. Our results clearly showed that the HPC mice model was established and refined, suggesting that there were significant differences between the control group and 6 × HPC group at the molecular levels. A serious of statistical analyses, including univariate analysis and multivariate analysis, were performed by the Progenesis QI software package and MetaboAnalyst web-server. The sphingolipid metabolic pathways were noticed due to the low p-value and high pathway impact calculated by the MetaboAnalyst and the pathways were altered under HPC condition. Especially, the sphingolipid compound sphingomyelin, ceramide, glucosylceramide, galactosylceramide and lactosylceramide were mapping in this metabolic pathway. Interestingly, these sphingolipid metabolites with olefinic bond in the long fatty chain were up-regulated, while those sphingolipids without olefinic bond were down-regulated. The results indicated that C24:1-Cers played a critical role in HPC and had potential in endogenous protective mechanism. Our data provided an insight to further reveal the protection mechanism of HPC.

Pharmacokinetic comparison of ketorolac after intracameral, intravitreal, and suprachoroidal administration in rabbits.

PURPOSE: To investigate the concentrations and pharmacokinetics of ketorolac in the rabbits by three different routes of administrations: a single intracameral, intravitreal, and suprachoroidal injection. METHODS: Fifty-four New Zealand white rabbits received ketorolac (250 µg/0.05 mL) in one eye by a single intracameral injection (group A, n = 18), single intravitreal injection (group B, n = 18), and single suprachoroidal injection (group C, n = 18). Drug concentrations in the vitreous, retina-choroid (RC), and plasma were determined by the methods of high-performance liquid chromatography at 0.5, 1, 2, 4, 8, and 24 hours after injection. The concentrations in the opposite eyes were also investigated. RESULTS: The mean maximum concentrations (Cmax) of ketorolac in the vitreous and RC were 0.378 ± 0.19 µg/mL and 3.15 ± 0.49 µg/g (at 0.5 hours), respectively, in group A; 156.2 ± 20.74 µg/mL (at 0.5 hours) and 208.0 ± 21.67 µg/g (at 1 hours), respectively, in group B; and 0.873 ± 0.34 µg/mL and 56.71 ± 22.64 µg/g (at 0.5 hours), respectively, in group C. In the RC, the area under the curve (AUC0-t) in group B (866.1 ± 52.67 µg/g·h) was higher (P < 0.01) than that in group C (77.10 ± 25.90 µg/g·h). The elimination half-life (t1/2) in group B (3.09 hours) was longer (P < 0.01) than that in group C (1.19 hours). In the control eyes, a drug level below 2 µg/g was detected in the RC in group C. Plasma concentrations were below 0.4 µg/mL in all 3 groups. Ketorolac was detectable in the RC till 24 hours after the intravitreal injection and 8 hours after the suprachoroidal injection. CONCLUSION: Intravitreal injection of ketorolac produced higher intraocular drug concentrations for a longer period compared with the other two routes. Suprachoroidal injection of ketorolac could reach an effective drug level in the RC with short half-lives and low drug levels in the vitreous. The plasma drug concentrations were low by all three routes.