Basic & Clinical Pharmacology & Toxicology最新文献

{"title":"Pharmacology of Vitamin E","authors":"Maret G. Traber","doi":"10.1111/bcpt.70225","DOIUrl":"10.1111/bcpt.70225","url":null,"abstract":"<p>The mechanisms for the preferential α-tocopherol retention in the human body fall under the usual pharmacologic categories of absorption, disposition, metabolism and catabolism and excretion (ADME). Kinetic studies using α-tocopherol labelled with either radioactive or stable isotopes have been instrumental in our understanding of vitamin E trafficking and status. Additionally, different types of mathematical modelling have yielded novel information. Therefore, I will address each of these topics, what is currently known and not known, emphasizing what has been recently discovered and how the various mechanisms impact clinical disorders.</p>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"138 4","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bcpt.70225","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147484487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"6-Nitrodopamine Potentiates Catecholamine-Induced Ca2+i Release in Human Aortic Smooth Muscle and Modulates Vascular Smooth Muscle Contractility","authors":"José Britto-Júnior,&nbsp;Antonio Tiago Lima,&nbsp;Shuaihua Qiao,&nbsp;Hou Fong Tang,&nbsp;Valerie Cardenas,&nbsp;Edson Antunes,&nbsp;Gilberto De Nucci,&nbsp;Albert Ferro","doi":"10.1111/bcpt.70224","DOIUrl":"10.1111/bcpt.70224","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>In vascular smooth muscle, rises in intracellular calcium [Ca²⁺]_i drive contraction downstream of α₁-adrenoceptor activation via IP3. Endothelium-derived 6-nitrodopamine (6-ND) augments cardiac catecholamine actions; however, its effect on [Ca²⁺]_i is unknown. We hypothesized that 6-ND would increase intracellular [Ca²⁺]_i and potentiate catecholamine-induced [Ca²⁺]_i signalling in vascular smooth muscle cells, with resultant functional effects on vascular tone when measured in vitro.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Human aortic smooth muscle cells (HASMCs) were loaded with fura-2 AM (1 μM) and [Ca²⁺]_i measured using a CLARIOstar plate reader after addition of Hanks’ balanced salt solution. Rat thoracic aorta rings, with the endothelium removed, were mounted in Krebs–Henseleit baths, and isometric force was recorded via PowerLab.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>6-ND and classical catecholamines evoked concentration-dependent increases in HASMC Ca²⁺ flux, with 6-ND displaying the greatest potency. 6-ND potentiated the increases in HASMC Ca²⁺ flux induced by the classical catecholamines. Tetrodotoxin (TTX) caused a concentration-dependent inhibition of responses to 6-ND and dopamine but did not alter noradrenaline- or adrenaline-induced [Ca²⁺]_i rise. In endothelium-denuded aortic rings, 6-ND potentiated contractions elicited by catecholamines, and this potentiation was abolished by TTX.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>6-ND is a potent modulator of [Ca²⁺]_i in HASMCs and enhances catecholamine-driven vasoconstriction. Both effects are blocked by TTX, indicating that 6-ND modulates voltage-gated sodium channels upstream of Ca²⁺ entry/release in vascular smooth muscle cells.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"138 4","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12998412/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147472398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amantadine Enhances IL-10 Expressions to Maintain the Renal Functions Against Inflammation and Oxidative Stress via Increasing PI3K/AKT/HIF-1α Pathway and Decreasing AQP2–4 Signallings","authors":"Alim Kosar,&nbsp;Pinar Aslan Kosar,&nbsp;Muhammet Yusuf Tepebasi,&nbsp;Halil Asci,&nbsp;Ilter Ilhan,&nbsp;Esma Selcuk,&nbsp;Orhan Berk Imeci,&nbsp;Oznur Kolay,&nbsp;Ozlem Ozmen","doi":"10.1111/bcpt.70216","DOIUrl":"10.1111/bcpt.70216","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>This study aimed to show the beneficial effects of amantadine (AMA), used in antiviral medication and Parkinson's therapy, on the inflammatory response and apoptosis in a model of systemic inflammation induced renal damage by lipopolysaccharide (LPS).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Thirty-two wistar albino rats were divided into four equal groups: control, LPS (5 mg/kg), LPS + AMA (45 mg/kg) and AMA groups. Both drugs were administered intraperitoneally on the same day with a single dose. The rats were sacrificed 6 h after LPS administration. Renal tissues were collected for histopathological, immunohistochemical, biochemical and genetic analyses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Histopathological evaluation revealed a significant increase in all parameters (histological score, hyperemia, hemorrhage, inflammatory infiltration and degeneration/necrosis) in the LPS group compared to the control group (<i>p</i> &lt; 0.05, Kruskal-Wallis test). Dunn's post-hoc analysis showed that AMA treatment (LPS+AMA group) significantly reduced these increases. In the group treated with AMA alone, similar histological integrity was maintained compared to the control group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In this study, AMA treatment exhibited anti-inflammatory effects on kidney tissue via several different mechanisms. However, additional studies with varied doses and durations of AMA treatment, involving different pathways and detailed analyses, are necessary.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"138 4","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147466239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nintedanib Lacks Efficacy in a Spirometry-Confirmed and Bleomycin-Induced Mouse Model of Idiopathic Pulmonary Fibrosis","authors":"Jamal Bousamaki,&nbsp;Grzegorz Maciag,&nbsp;Asbjørn Graver Petersen,&nbsp;Stefanie H. Korntner,&nbsp;Stine Marie Jansen,&nbsp;Susanne E. Pors,&nbsp;Linn Salto Mamsen,&nbsp;Silas A. Rasmussen,&nbsp;Casper Gravesen Salinas,&nbsp;Louise Humle Kruse,&nbsp;Michael Feigh,&nbsp;Ulf Simonsen,&nbsp;Henrik H. Hansen","doi":"10.1111/bcpt.70220","DOIUrl":"10.1111/bcpt.70220","url":null,"abstract":"<p>Nintedanib, a multitargeted tyrosine kinase inhibitor, is approved for idiopathic pulmonary fibrosis (IPF) for its ability to slow lung function decline. This study systematically evaluated the effects of nintedanib across three independent treatment intervention studies in the single-dose bleomycin (BLEO) mouse model of IPF. In each study, male C57BL/6J mice received a single intratracheal instillation of BLEO (<i>n</i> = 15–18) or saline (<i>n</i> = 10). Animals were randomised and stratified by body weight, and treatment assignment was assessed using noninvasive whole-body plethysmography 6 days after BLEO administration. BLEO-IPF mice were administered (PO, BID) vehicle, nintedanib (50 or 60 mg/kg), or an activin receptor-like kinase 5 inhibitor (ALK5i, SB525334, 60 mg/kg) for up to 21 days. In all studies, nintedanib consistently failed to improve lung health, as evaluated by lung function tests, biochemistry, histology and RNA sequencing. Plasma concentrations of nintedanib showed no correlation to any efficacy endpoint applied. Lung transcriptome signatures in nintedanib-treated BLEO-IPF mice indicated upregulated mRNA expression of p-glycoprotein, a known nintedanib efflux transporter, suggesting limited lung exposure of nintedanib in the model. In comparison, ALK5i significantly improved lung function and exhibited robust antifibrotic efficacy. Collectively, these findings challenge the use of nintedanib as a benchmarking drug in the single-dose BLEO-IPF mouse model.</p>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"138 4","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12987715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147455455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Retrospective Analysis of Human Angiotensin II Receptor Blockers (ARB) Pharmacokinetics, Dosages and Cmax Values for the Experimental Modelling of Pleiotropic and Supratherapeutic Activities","authors":"Alexandria Evans,&nbsp;Pascal Bernatchez","doi":"10.1111/bcpt.70203","DOIUrl":"10.1111/bcpt.70203","url":null,"abstract":"<p>Angiotensin II (AngII) receptor blockers (ARBs) are medications that lower systolic blood pressure (BP) by antagonizing the AngII type 1 receptor (AT1). However, ARBs have documented or suspected therapeutic properties in diseases not caused by high BP including diabetes, muscular dystrophy, chronic obstructive pulmonary diseases (COPD) and Alzheimer's disease. ARBs have multiple pleiotropic properties; ‘<i>on-target</i>’ AT1-dependent pleiotropy can arise from blocking AngII-AT1 binding in non-BP-regulating cells or via inverse or biased ARB-AT1 agonism. In addition, activation of cells lacking AT1 by ARBs suggests the presence of AT1-independent ‘<i>off-target</i>’ pleiotropy, whereas supratherapeutic properties in the absence of further BP lowering have also been reported. Herein, to determine how ARB pleiotropy and supratherapeutic properties can be modelled in vitro or ex vivo, we perform a retrospective analysis of the literature that characterizes their maximal human plasma concentration, <i>C</i>_max, which is higher and more likely to trigger pleiotropy than their low nanomolar, AT1-blocking concentrations. Our findings suggest that <i>C</i>_max is variable and heterogeneous between ARBs, with upper range values as high as 13.6 micromolar in the case of valsartan and lower range values as low as 0.4 micromolar for candesartan. We propose that modelling of ARB pleiotropy be conducted at these concentrations, whereas higher concentrations will mimic supratherapeutic applications.</p>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"138 4","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective Effects of Esketamine in Central Nervous System Disorders: Mechanisms and Cellular Targets","authors":"Chendi Zhao,&nbsp;Yan Wang,&nbsp;Jinglang Wu,&nbsp;Hong Cheng","doi":"10.1111/bcpt.70221","DOIUrl":"10.1111/bcpt.70221","url":null,"abstract":"<p>Esketamine (ESK), the dextrorotatory enantiomer of ketamine, is an antagonist of the N-methyl-D-aspartic acid (NMDA) receptor. ESK is considered an effective anesthetic because of its ability to mitigate postoperative pain and opioid use. Recently, it has attracted significant research attention for its fast-acting antidepressant effects. Given the advantages of ESK in both perioperative and postoperative contexts, foundational research into this molecule is progressively moving forward. Accumulating evidence suggests that ESK possesses anti-inflammatory, antiapoptotic and antioxidant characteristics in various diseases. This review summarizes the neuroprotective effects of ESK in central nervous system (CNS) disorders. ESK-mediated cellular processes, including neuronal apoptosis, microglial polarization and astrocytic functions, are also summarized. In addition, the underlying molecular mechanisms of ESK are discussed, with a focus on inflammatory pathways and signalling cascades in neurological disorders.</p>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"138 4","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bcpt.70221","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Supporting General Practitioners to Deprescribe Benzodiazepines and Z-Drugs in Primary Care: Findings From a Modified Delphi Study","authors":"Erin Oldenhof,&nbsp;Megan Pisegna,&nbsp;Mark Horowitz,&nbsp;Hester Wilson,&nbsp;Karen Gelb,&nbsp;Stephen Trumble,&nbsp;Catherine Andronis,&nbsp;Marguerite Tracy,&nbsp;Nicholas A. Zwar,&nbsp;Andrew Mau,&nbsp;Anna Chapman,&nbsp;Petra K. Staiger","doi":"10.1111/bcpt.70217","DOIUrl":"10.1111/bcpt.70217","url":null,"abstract":"<p>Long-term use of benzodiazepines and Z-drugs (collectively known as benzodiazepine receptor agonists; BZRAs) is associated with a range of adverse effects including dependence and withdrawal on stopping or reducing the dose. Deprescribing is recommended to improve patient outcomes and reduce medication-related harm, but its implementation in primary care is hindered by various barriers. This study aimed to identify the strategies that Australian general practitioners (GPs) agree were most useful in supporting them to deprescribe BZRAs. A modified Delphi was conducted online over three rounds with 38 Australian GPs. Participants were registered GPs with ≥ 10 years' experience in either addiction, mental health, sleep, pain management, or aged care. Participants rated and provided feedback on 61 implementation strategies over three rounds until they achieved either consensus or stability. Included strategies were mapped to the theoretical domains framework to understand their links to behaviour change mechanisms. Twenty-five strategies reached a consensus for inclusion indicating their importance to supporting GPs to deprescribe BZRAs. The most important strategies included extended consultation times, provision of clear deprescribing protocols and establishing practice-level agreement on deprescribing policies.</p><p>Findings provide a prioritised set of implementation strategies to address the barriers to BZRA deprescribing and offer a strong foundation for future research and policy to improve deprescribing in primary care.</p>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"138 4","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12964182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147363892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pregnane X Receptor Regulates Human Endocrine System by Inducing Sex Hormone–Binding Globulin Expression","authors":"Maria H. Ahonen,&nbsp;Anja Konzack,&nbsp;Tomas Smutny,&nbsp;Petr Pavek,&nbsp;Jukka Hakkola,&nbsp;Janne Hukkanen","doi":"10.1111/bcpt.70218","DOIUrl":"10.1111/bcpt.70218","url":null,"abstract":"<p>Sex hormone–binding globulin (SHBG) is a sex hormone carrier. We aimed to characterize the role of pregnane X receptor (PXR), a major regulator of drug metabolism, in SHBG regulation. Serum SHBG was measured in four clinical trials (<i>n</i> = 61) and expression in in vitro experiments in human 3D hepatocyte spheroids and HepG2 cells. We also analysed previously published chromatin immunoprecipitation sequencing data from cryopreserved human hepatocytes. One-week dosing of PXR ligand rifampicin increased SHBG in all but one healthy volunteer (geometric mean induction 2.0-fold; SHBG concentration 70.5 ± 34.1 nmol/L with rifampicin and 36.1 ± 19.0 nmol/L with control; <i>p</i> &lt; 0.0001; 95% confidence interval of the mean of differences between arms 31.9–42.0). In men, serum total testosterone increased and free androgen index decreased. In 3D human hepatocyte spheroids, rifampicin caused a clear induction of <i>SHBG</i> mRNA, while SPA70, a PXR antagonist, decreased both basal and rifampicin-induced <i>SHBG</i> mRNA expression. Analysis of ChIP-sequencing data identified a rifampicin-induced PXR binding site within the <i>SHBG</i> gene. These results show that PXR is a novel regulator of serum SHBG in humans. This mechanism may mediate effects of PXR-activating drugs and other chemicals on sex hormone balance and have implications for metabolic health.</p>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"138 4","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12964185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147363945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vericiguat as a Novel Ferroptosis Inhibitor Alleviates Doxorubicin-Induced Cardiotoxicity","authors":"Huiwen Han,&nbsp;Tao Luo,&nbsp;Canzhao Liu,&nbsp;Wen Ou,&nbsp;Yu Zhang,&nbsp;Zhiyin Zhang,&nbsp;Shuwen Huang,&nbsp;Wenjun Luo,&nbsp;Jiahao Wen,&nbsp;Nan Wang,&nbsp;Ziwei Zhang,&nbsp;Haiqiong Liu,&nbsp;Xianbao Wang","doi":"10.1111/bcpt.70219","DOIUrl":"10.1111/bcpt.70219","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Purpose</h3>\u0000 \u0000 <p>Doxorubicin is a widely used chemotherapy drug, but its clinical application is limited by dose-dependent cardiotoxicity, known as doxorubicin-induced cardiomyopathy (DIC), for which no specific therapies currently exist. Vericiguat, a soluble guanylate cyclase agonist, has shown significant cardiovascular protective effects. However, its role and the underlying molecular mechanisms in DIC remain unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Experimental Approach</h3>\u0000 \u0000 <p>We established both in vivo and in vitro models of DIC. In the in vivo experiments, cardiac function in male wild-type C57BL/6 mice was evaluated through echocardiography, measurement of serum CK-MB and cTnT, and histological examinations. For the in vitro studies, cardiomyocyte viability was assessed by CCK-8 assay and PI/Hoechst staining. To evaluate ferroptosis, the accumulation levels of iron, reactive oxygen species (ROS), and lipid peroxides in cardiomyocytes were assessed using FerroOrange staining, DCFH-DA fluorescent probe, and MDA content measurement, respectively. The expression levels of ferroptosis-related markers SLC7A11 and GPX4 were examined by Western blot.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Key Results</h3>\u0000 \u0000 <p>Vericiguat significantly alleviated cardiac injury induced by doxorubicin by lowering oxidative stress and inhibiting ferroptosis and directly counteracted cardiomyocyte injury induced by the ferroptosis activator erastin.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion and Implications</h3>\u0000 \u0000 <p>These findings indicate that vericiguat protects against doxorubicin-induced myocardial ferroptosis, positioning it as a promising therapeutic candidate for DIC and a novel ferroptosis inhibitor.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"138 4","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147353556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Patients' Perspectives on Antidepressant Discontinuation and the Pharmacists' Role","authors":"Samah Bouarfa,&nbsp;Wilma Göttgens,&nbsp;Suzanne A. Ligthart,&nbsp;Otto R. Maarsingh,&nbsp;Marcel J. Kooij,&nbsp;Pierre M. Bet,&nbsp;Jacqueline G. Hugtenburg","doi":"10.1111/bcpt.70207","DOIUrl":"10.1111/bcpt.70207","url":null,"abstract":"<p>Antidepressant (AD) discontinuation care asks for tailored support and alignment with patients' expectations, needs and wishes. However, studies on patients' experiences and perspectives regarding the contribution of the pharmacist to AD discontinuation care are limited. The aim was to gain a deeper understanding of patients' perspectives regarding guidance during AD discontinuation and patients' views on the contribution of the pharmacist. A qualitative, explorative study was conducted with 15 semistructured face-to-face and video call interviews. Inclusion criteria were age ≥ 18 years and current or past use of ADs. The audiotapes were transcribed verbatim, coded and analysed by two researchers. The following four themes were identified: (1) experiences with <span>ad</span> use and discontinuation, (2) attitudes and behaviour towards AD discontinuation, (3) expectations and perceptions towards AD discontinuation and (4) needs regarding AD discontinuation. False beliefs about ADs and past negative experiences with AD discontinuation shape beliefs of patients that amount to a reluctance to discontinue ADs. The most urgent needs of patients were timely receiving guidance, including clear and relevant information from accessible, knowledgeable and trustable healthcare providers (HCPs). Pharmacists' easy accessibility, pharmacotherapeutic knowledge, expertise and capabilities should be put to use, as they may help meeting patients' needs on AD discontinuation.</p>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"138 4","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12950625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147324588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}