BackgroundOpioid over‐prescription following surgery is a significant public health issue in most developed countries. Multiple studies have been conducted in the USA demonstrating and investigating the issue; however, there is a lack of literature addressing this topic in the Australian setting. The aim of this study is to review prescribing practices at an Australian tertiary referral hospital on discharge in patients having undergone laparoscopic cholecystectomy (LC) or laparoscopic appendicetomy (LA). Additionally, to identify potential factors which influence medical officer prescribing practices.MethodsA retrospective observational study on opioid prescribing practice on all patients who underwent LC or LA over a 12‐month period at an Australian tertiary referral hospital.ResultsA total of 435 patients (223 LC, 214 LA) were prescribed a mean opioid dose on discharge of 25 oral morphine milli‐equivalents (range 0–180 morphine milli‐equivalents). Less opioids were prescribed following elective procedures (42% versus 10%, P < 0.001). There is a downward trend of opioid prescribing on discharge as the Junior Medical Officer clinical year progresses (P < 0.001).ConclusionsThis study demonstrates a lower rate of opiate prescription on discharge for LC and LA in an Australian setting when compared to the US data. There is a wide diversity of prescribing demonstrated. This indicates the need for better training of opioid prescribers to reduce over‐prescribing.

Background Activation of the YAP (Yes‐associated protein) pathway has been demonstrated to be related to smooth muscle cells ( SMC s) phenotypic modulation and vessel restenosis. The aim of this study was to illustrate the molecular mechanisms that regulate the expression of YAP during the process of SMC s phenotypic switch. Whether the molecular basis identified in the study could be a potential therapeutic target for drug‐eluting stents is further tested. Methods and Results In cell culture and in rat carotid arterial injury models, Sp‐1 (specificity protein 1) expression was significantly induced, and correlated with SMC s proliferative phenotype. Overexpression of Sp‐1 promoted SMC s proliferation and migration. Conversely, siSp‐1 transfection or Sp‐1 inhibitor Mithramycin A treatment attenuates SMC proliferation and migration. Through gain‐ and loss‐function assays, we demonstrated that YAP was involved in Sp‐1‐mediated SMC phenotypic switch. Mechanistically, activated Sp‐1 regulated YAP transcriptional expression through binding to its promoter. Moreover, we fabricated a Sp‐1 inhibitor Mithramycin A‐eluting stent and further tested it. In the rabbit carotid model, Mithramycin A‐eluting stent inhibited YAP transcription and attenuated in‐stent restenosis through regulating YAP ‐mediated SMC phenotypic switch. Conclusions Sp‐1 controls phenotypic modulation of SMC by regulating transcription factor YAP . Drug‐eluting stent targeting Sp‐1 might represent a novel therapeutic strategy to prevent in‐stent restenosis.

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