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Genetic association analysis and frequency of NUDT15*3 with thiopurine-induced myelosuppression in patients with inflammatory bowel disease in a large Dutch cohort. 荷兰大型队列中炎症性肠病患者 NUDT15*3 与硫嘌呤诱导的骨髓抑制的遗传关联分析和频率。
IF 2.9 3区 医学 Q2 GENETICS & HEREDITY Pub Date : 2024-11-23 DOI: 10.1038/s41397-024-00358-7
Maarten J Deenen, Anouk J van Noordenburg, Joëlle Bouwens-Bijsterveld, Maarten A van Dijk, Janneke M Stapelbroek, Luc J J Derijks, Lennard P L Gilissen, Birgit A L M Deiman

Thiopurine drugs are cornerstone treatment for patients with inflammatory bowel disease (IBD). The most common adverse drug reaction is thiopurine-induced myelosuppression (TIM), that may partly be explained by the genetic polymorphism NUDT15*3. The aim of this retrospective study was to determine the NUDT15*3 polymorphism frequency and its association with TIM in an IBD patient population in the Netherlands. DNA from patients previously genotyped for TPMT was genotyped for NUDT15*3. In IBD patients treated with thiopurines association tests with TIM were conducted. Out of 988 included patients, 13 (1.3%) were heterozygous for NUDT15*3. Of all patients, 606 had IBD and received thiopurine treatment. In these patients, 8/606 (1.3%) were heterozygous polymorphic for NUDT15*3 of which 50.0% developed TIM compared to 2.3% in the wild type patients (p < 0.001). The study results show a clinically relevant prevalence of NUDT15*3 in the Dutch patient population. Its strong association with TIM suggests pre-therapeutic genotyping potentially clinically utile.

硫嘌呤类药物是治疗炎症性肠病(IBD)患者的基础药物。最常见的药物不良反应是硫嘌呤诱导的骨髓抑制(TIM),其部分原因可能与 NUDT15*3 基因多态性有关。这项回顾性研究旨在确定荷兰 IBD 患者中 NUDT15*3 多态性的频率及其与 TIM 的关系。对之前进行过 TPMT 基因分型的患者的 DNA 进行了 NUDT15*3 基因分型。对接受硫嘌呤治疗的 IBD 患者进行了与 TIM 的关联测试。在纳入的 988 名患者中,有 13 人(1.3%)是 NUDT15*3 的杂合子。在所有患者中,606 人患有 IBD 并接受了硫嘌呤治疗。在这些患者中,8/606(1.3%)人是 NUDT15*3 的多态杂合子,其中 50.0% 的患者出现了 TIM,而野生型患者中只有 2.3% 出现了 TIM(P<0.05)。
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引用次数: 0
Plasma concentrations of venetoclax and Pharmacogenetics correlated with drug efficacy in treatment naive leukemia patients: a retrospective study. 一项回顾性研究:Venetoclax 的血浆浓度和药物遗传学与治疗前白血病患者的疗效相关。
IF 2.9 3区 医学 Q2 GENETICS & HEREDITY Pub Date : 2024-11-22 DOI: 10.1038/s41397-024-00359-6
Yue Li, Qing Wan, Jiaqi Wan, Xiong Xiao, Jinfang Hu, Xintong Yang, Fancong Kong, Jieyu Wang, Baoquan Song, Zhentao Li, Fei Li, Simei Ren, Hongwei Peng

Venetoclax (VEN) was the only Bcl-2 inhibitor approved yet and showed large differences in clinical efficacy. The aim of the study was to explore the relationships between the plasma concentration and efficacy of VEN, and identify potential influencing factors. A retrospective cohort study was conducted and a total of 76 trough (C0h) and 91 6 h post-dose plasma concentration (C6h) blood concentrations of VEN were collected in 54 patients. C6h/D concentration of VEN was found to be significantly correlated with treatment efficacy (p = 0.006) in leukemia patients with good or intermediate prognosis stratification. A ROC curve was then established and the cut-off value was calculated as 0.2868 μg/ml (AUC = 0.7097, p = 0.1081). Besides, patients co-administered with triazoles or carrying CYP3A5 rs776746 AA/AG genotypes were prone to induce higher VEN plasma concentration regardless of whether VEN dosage was reduced or not. Through LASSO-logistic regression and nomogram analysis, chemotherapy regimens and neutrophil percentages were identified as the critical elements that may predict drug response. Above all, in addition to identify prognostic stratification, AML patients taken with VEN were suggested to test plasma concentration routinely so as to achieve desired efficacy, especially when co-administered with triazoles or carried with CYP3A5 rs776746 AA/AG.

Venetoclax(VEN)是目前唯一获批的Bcl-2抑制剂,其临床疗效差异很大。该研究旨在探讨VEN的血浆浓度与疗效之间的关系,并找出潜在的影响因素。研究采用回顾性队列研究方法,共收集了54名患者的76份谷浓度(C0h)和91份给药后6小时血浆浓度(C6h)。研究发现,在预后分层为良好或中等的白血病患者中,VEN的C6h/D浓度与治疗效果明显相关(p = 0.006)。随后建立了 ROC 曲线,并计算出临界值为 0.2868 μg/ml(AUC = 0.7097,p = 0.1081)。此外,合用三唑类药物或携带 CYP3A5 rs776746 AA/AG 基因型的患者,无论是否减少 VEN 的剂量,均易诱发 VEN 血浆浓度升高。通过LASSO-逻辑回归和提名图分析,化疗方案和中性粒细胞百分比被确定为可能预测药物反应的关键因素。此外,除了确定预后分层外,还建议使用 VEN 的急性髓细胞白血病患者定期检测血浆浓度,以达到预期疗效,尤其是与三唑类药物合用或携带 CYP3A5 rs776746 AA/AG 时。
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引用次数: 0
Polygenic score analyses on antidepressant response in late-life depression, results from the IRL-GRey study. 晚年抑郁症患者抗抑郁反应的多基因评分分析,IRL-GRey 研究的结果。
IF 2.9 3区 医学 Q2 GENETICS & HEREDITY Pub Date : 2024-11-22 DOI: 10.1038/s41397-024-00351-0
Samar S M Elsheikh, Victoria S Marshe, Xiaoyu Men, Farhana Islam, Vanessa F Gonçalves, Guillaume Paré, Daniel Felsky, James L Kennedy, Benoit H Mulsant, Charles F Reynolds, Eric J Lenze, Daniel J Müller

Late-life depression (LLD) is often accompanied by medical comorbidities such as psychiatric disorders and cardiovascular diseases, posing challenges to antidepressant treatment. Recent studies highlighted significant associations between treatment-resistant depression (TRD) and polygenic risk score (PRS) for attention deficit hyperactivity disorder (ADHD) in adults as well as a negative association between antidepressant symptom improvement with both schizophrenia and bipolar. Here, we sought to validate these findings with symptom remission in LLD. We analyzed the Incomplete Response in Late Life Depression: Getting to Remission (IRL-GRey) sample consisting of adults aged 60+ with major depression (N = 342) treated with venlafaxine for 12 weeks. We constructed PRSs for ADHD, depression, schizophrenia, bipolar disorder, neuroticism, general intelligence, antidepressant symptom remission and antidepressant percentage symptom improvement using summary statistics from the Psychiatric Genomics Consortium and the GWAS Catalog. Logistic regression was used to test the association of PRSs with venlafaxine symptom remission and percentage symptom improvement, co-varying for the genomic principal components, age, sex and depressive symptoms severity at baseline. We found a nominal (i.e., p value ≤ 0.05) association between symptom remission and both PRS for ADHD and (OR = 1.36 [1.07, 1.73], p = 0.011) and PRS for bipolar disorder (OR = 0.75 [0.58, 0.97], p = 0.031), as well as between percentage symptom improvement and PRS for general intelligence (beta = 6.81 (SE = 3.122), p = 0.03). However, the ADHD association was in the opposite direction as expected, and both associations did not survive multiple testing corrections. Altogether, these findings suggest that previous findings regarding ADHD PRS and antidepressant response (measured with various outcomes) do not replicate in older adults.

晚年抑郁症(LLD)通常伴有精神障碍和心血管疾病等并发症,给抗抑郁治疗带来了挑战。最近的研究强调了治疗耐受性抑郁症(TRD)与成人注意缺陷多动障碍(ADHD)的多基因风险评分(PRS)之间的重要关联,以及抗抑郁剂症状改善与精神分裂症和双相情感障碍之间的负相关。在此,我们试图通过 LLD 的症状缓解来验证这些发现。我们分析了晚期抑郁症的不完全反应:Getting to Remission (IRL-GRey) 样本,该样本由 60 岁以上患有重度抑郁症的成年人组成(N = 342),他们接受了为期 12 周的文拉法辛治疗。我们利用精神疾病基因组学联盟和 GWAS Catalog 的汇总统计数据,构建了多动症、抑郁症、精神分裂症、双相情感障碍、神经质、一般智力、抗抑郁症状缓解和抗抑郁症状改善百分比的 PRSs。我们使用逻辑回归检验了PRSs与文拉法辛症状缓解和症状改善百分比之间的关系,并对基因组主成分、年龄、性别和基线抑郁症状严重程度进行了共同变量分析。我们发现,症状缓解与多动症和(OR = 1.36 [1.07, 1.73],p = 0.011)双相情感障碍 PRS(OR = 0.75 [0.58, 0.97],p = 0.031)PRS,以及症状改善百分比与一般智力 PRS(β = 6.81 (SE = 3.122),p = 0.03)之间存在名义上的(即 p 值小于 0.05)关联。然而,多动症的相关性与预期的方向相反,而且这两种相关性都没有通过多重测试校正。总之,这些研究结果表明,以前关于多动症PRS和抗抑郁药反应(用各种结果测量)的研究结果在老年人中并不适用。
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引用次数: 0
Implementation of pharmacogenetic testing in pediatric oncology: barriers and facilitators assessment at eight Canadian academic health centres. 在儿科肿瘤学中实施药物基因检测:加拿大八家学术健康中心的障碍和促进因素评估。
IF 2.9 3区 医学 Q2 GENETICS & HEREDITY Pub Date : 2024-11-19 DOI: 10.1038/s41397-024-00356-9
Jeanette Cooper, Joshua Pratt, Jamie Park, Christine Fahim, Jessica M Lovnicki, Gabriella S S Groeneweg, Bruce Carleton, Sharon Straus

Pharmacogenetic (PGx) testing can enhance drug safety, improve efficacy, and reduce the risk of toxicity. However, the implementation of PGx testing in Canadian pediatric oncology centers has been limited. To address this gap, the aim of this study was to assess the barriers and facilitators to implementing PGx testing for three oncology drugs in eight Canadian pediatric oncology centers and identify strategies that could be used to support PGx testing implementation. We used semi-structured interviews to identify barriers and facilitators to PGx testing and identified evidence-based strategies for PGx testing implementation through a mapping process that utilized the Theoretical Domains Framework, the Consolidated Framework for Implementation Research and the Behavior Change Wheel. We identified 38 facilitators and 26 barriers to implementation of PGx testing and mapped these to 6 implementation strategies.

药物基因学(PGx)测试可提高药物安全性、改善疗效并降低毒性风险。然而,加拿大儿科肿瘤中心实施 PGx 检测的程度有限。为弥补这一不足,本研究旨在评估在加拿大八家儿科肿瘤中心对三种肿瘤药物实施 PGx 检测的障碍和促进因素,并确定可用于支持 PGx 检测实施的策略。我们采用半结构式访谈来识别 PGx 检测的障碍和促进因素,并通过利用理论领域框架、实施研究综合框架和行为改变轮的映射过程来识别实施 PGx 检测的循证策略。我们确定了实施 PGx 检验的 38 个促进因素和 26 个障碍,并将这些因素与 6 个实施策略进行了映射。
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引用次数: 0
Correction to: A pharmacogenomic study on the pharmacokinetics of tacrolimus in healthy subjects using the DMETTM Plus platform. 更正:使用 DMETTM Plus 平台对健康受试者他克莫司药代动力学进行药物基因组学研究。
IF 2.9 3区 医学 Q2 GENETICS & HEREDITY Pub Date : 2024-11-18 DOI: 10.1038/s41397-024-00354-x
Y Choi, F Jiang, H An, H J Park, J H Choi, H Lee
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引用次数: 0
TMEM158, as plasma cfRNA marker, promotes proliferation and doxorubicin resistance in ovarian cancer. 作为血浆 cfRNA 标记的 TMEM158 可促进卵巢癌的增殖和多柔比星耐药性。
IF 2.9 3区 医学 Q2 GENETICS & HEREDITY Pub Date : 2024-11-15 DOI: 10.1038/s41397-024-00357-8
Xiaolin Zhu, Tongchao Liu, Xuexue Yin

The current study aimed to identify the potential biomarker for the diagnosis of ovarian cancer within plasma cell-free RNA (cfRNA) species and to characterize their oncogenic properties. cfRNAs were isolated from the peripheral blood of ovarian cancer patients and sequenced using an NGS platform. Principal component analysis (PCA) was performed using Salmon software. Gene ontology (GO) analysis was conducted with clusterProfiler. The relative abundance of TMEM158 transcripts was determined by real-time PCR. Cell viability and proliferation was monitored using the MTT and cell counting assays, respectively. The protein levels of TMEM158 and ABCG2 were quantified by immunoblotting. We observed a clear separation of cfRNAs between ovarian cancer patients and healthy individuals. Additionally, we identified TMEM158 as the most significantly differential gene in both peripheral blood and tumor tissues. Overexpression of TMEM158 stimulated cell viability and promoted cell proliferation in ovarian cancer cells. Notably, the aberrant upregulation of TMEM158 was closely associated with doxorubicin resistance in ovarian cancer. Mechanistically, we demonstrated that TMEM158 positively regulates ABCG2 expression, which consequently contributes to drug resistance. In summary, we identified cfRNA TMEM158 as a potential diagnostic biomarker for ovarian cancer and elucidated the critical involvement of TMEM158-ABCG2 signaling axis in the development of doxorubicin resistance.

本研究旨在确定血浆无细胞RNA(cfRNA)中诊断卵巢癌的潜在生物标记物,并描述其致癌特性。使用 Salmon 软件进行了主成分分析(PCA)。使用 clusterProfiler 进行了基因本体(GO)分析。通过实时 PCR 测定 TMEM158 转录本的相对丰度。分别使用 MTT 和细胞计数法监测细胞活力和增殖。免疫印迹法对 TMEM158 和 ABCG2 的蛋白水平进行了定量。我们观察到卵巢癌患者和健康人的 cfRNAs 有明显的差异。此外,我们还发现 TMEM158 是外周血和肿瘤组织中差异最大的基因。过表达 TMEM158 会刺激卵巢癌细胞的存活率并促进细胞增殖。值得注意的是,TMEM158的异常上调与卵巢癌的多柔比星耐药性密切相关。从机理上讲,我们证明了 TMEM158 能正向调节 ABCG2 的表达,从而导致耐药性。总之,我们发现了cfRNA TMEM158是一种潜在的卵巢癌诊断生物标记物,并阐明了TMEM158-ABCG2信号轴在多柔比星耐药性发生过程中的关键作用。
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引用次数: 0
The ZNF263/CPT1B axis regulates fatty acid β-oxidation to affect cisplatin resistance in lung adenocarcinoma. ZNF263/CPT1B轴调节脂肪酸β-氧化,从而影响肺腺癌的顺铂耐药性。
IF 2.9 3区 医学 Q2 GENETICS & HEREDITY Pub Date : 2024-11-05 DOI: 10.1038/s41397-024-00355-w
Renhe Yan, Caibin Zheng, Suting Qian, Kezhi Li, Xiangsheng Kong, Shunhang Liao

Cisplatin is widely used as a conventional chemotherapy drug for lung adenocarcinoma (LUAD) patients. However, the chemical resistance greatly limits its therapeutic potential. The study aimed to uncover the specific role and new mechanisms of CPT1B in the cisplatin resistance of LUAD. Bioinformatics analysis was utilized to analyze the expression level and enriched pathway of CPT1B in LUAD. The expression of CPT1B in LUAD cells was determined by utilizing quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot (WB). The cisplatin resistance in LUAD was measured with IC50 values obtained from the CCK-8 assay. We used the corresponding reagent kit and WB analysis to determine the levels of triglycerides, cholesterol, phospholipids, fatty acid β-oxidation (FAO) rate, and expression of lipid metabolism-related proteins. Finally, the regulation relationship between CPT1B and ZNF263 was confirmed through bioinformatics analysis, dual-luciferase, and chromatin immunoprecipitation assays. The present investigation revealed that CPT1B was upregulated in LUAD, participating in fatty acid metabolism pathways. In vitro studies have shown that upregulation of CPT1B promoted cisplatin resistance in LUAD cells. This promotion effect induced by the high expression of CPT1B on cisplatin resistance in LUAD was weakened after the addition of the FAO inhibitor Etomoxir. Mechanistically, ZNF263 was capable of binding to the promoter of CPT1B to activate its transcription, thereby enhancing FAO and promoting cisplatin resistance in LUAD cells. In summary, ZNF263 enhances cisplatin resistance in LUAD cells by upregulating CPT1B expression. This study enriches the molecular mechanisms of LUAD chemotherapy resistance and provides new directions for exploring therapeutic targets for LUAD.

顺铂被广泛用作肺腺癌(LUAD)患者的常规化疗药物。然而,耐药性极大地限制了其治疗潜力。本研究旨在揭示 CPT1B 在 LUAD 顺铂耐药性中的特殊作用和新机制。该研究利用生物信息学分析方法分析了CPT1B在LUAD中的表达水平和富集途径。利用定量反转录聚合酶链反应(qRT-PCR)和免疫印迹(WB)测定了CPT1B在LUAD细胞中的表达。LUAD的顺铂耐药性是通过CCK-8检测法获得的IC50值测定的。我们使用相应的试剂盒和 WB 分析测定了甘油三酯、胆固醇、磷脂、脂肪酸 β-氧化(FAO)率和脂代谢相关蛋白的表达水平。最后,通过生物信息学分析、双荧光素酶和染色质免疫沉淀实验证实了 CPT1B 和 ZNF263 之间的调控关系。本研究发现,CPT1B在LUAD中上调,参与脂肪酸代谢途径。体外研究表明,CPT1B的上调促进了LUAD细胞对顺铂的耐药性。在加入FAO抑制剂Etomoxir后,CPT1B的高表达对LUAD顺铂耐药性的促进作用减弱。从机制上看,ZNF263能够与CPT1B的启动子结合,激活其转录,从而增强FAO,促进LUAD细胞对顺铂的耐药性。综上所述,ZNF263通过上调CPT1B的表达增强了LUAD细胞的顺铂耐药性。这项研究丰富了LUAD化疗耐药的分子机制,为探索LUAD的治疗靶点提供了新的方向。
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引用次数: 0
Cost analysis of CYP2C19 genetic testing in percutaneous coronary intervention patients. 经皮冠状动脉介入治疗患者的 CYP2C19 基因检测成本分析。
IF 2.9 3区 医学 Q2 GENETICS & HEREDITY Pub Date : 2024-10-08 DOI: 10.1038/s41397-024-00353-y
Samuel Huxley, James Moriarty, Mark A Hlatky, Ryan Lennon, Kent Bailey, Malcolm Bell, Nancy Geller, Amir Lerman, Verghese Mathew, Yves Rosenberg, Michael Farkouh, Charanjit Rihal, Bijan Borah, Naveen L Pereira

CYP2C19 loss of function (LOF) carriers undergoing percutaneous coronary intervention (PCI) have an increased risk of ischemic events when treated with clopidogrel. PCI patients in TAILOR-PCI were randomized to clopidogrel or genotype-guided (GG) therapy in which LOF carriers received ticagrelor and non-carriers clopidogrel. Direct medical costs associated with a GG approach have not been described before. TAILOR-PCI participants for whom direct medical costs were available for the duration from the date of PCI to one-year post PCI were included. Primary cost estimates were obtained from the Mayo Clinic Cost Data Warehouse. There were no differences in direct medical costs between the GG and clopidogrel groups (mean $20,682 versus $19,747, p = 0.11) however total costs were greater in the GG group (mean $21,245 versus $19,891, p = 0.02) which was primarily driven by ticagrelor costs. In conclusion the increased expense of a GG strategy post PCI as compared to clopidogrel for all is primarily driven by the cost of ticagrelor.

接受经皮冠状动脉介入治疗(PCI)的CYP2C19功能缺失(LOF)携带者在接受氯吡格雷治疗时发生缺血性事件的风险会增加。TAILOR-PCI中的PCI患者随机接受氯吡格雷或基因型指导(GG)疗法,其中LOF携带者接受替卡格雷治疗,非携带者接受氯吡格雷治疗。与 GG 方法相关的直接医疗成本以前从未描述过。TAILOR-PCI的参与者从PCI之日起至PCI术后一年内的直接医疗费用均可获得。主要成本估算来自梅奥诊所成本数据仓库。GG组和氯吡格雷组的直接医疗费用没有差异(平均为20,682美元对19,747美元,P = 0.11),但GG组的总费用更高(平均为21,245美元对19,891美元,P = 0.02),这主要是由替卡格雷费用引起的。总之,与氯吡格雷相比,PCI 后 GG 策略的费用增加主要是由替卡格雷的费用造成的。
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引用次数: 0
Effects and interaction of single nucleotide polymorphisms at the pharmacokinetic/pharmacodynamic site: insights from the Rotterdam study into metformin clinical response and dose titration. 单核苷酸多态性在药代动力学/药效学部位的影响和相互作用:鹿特丹研究对二甲双胍临床反应和剂量滴定的启示。
IF 2.9 3区 医学 Q2 GENETICS & HEREDITY Pub Date : 2024-10-07 DOI: 10.1038/s41397-024-00352-z
Soroush Mohammadi Jouabadi, Payam Peymani, Mitra Nekouei Shahraki, Jeroen G J van Rooij, Linda Broer, Anton J M Roks, Bruno H Stricker, Fariba Ahmadizar

Our study investigated the impact of genetic variations on metformin glycemic response in a cohort from the Rotterdam Study, comprising 14,926 individuals followed for up to 27 years. Among 1285 metformin users of European ancestry, using linear mixed models, we analyzed the association of single nucleotide polymorphisms (SNPs) and a Polygenic Risk Score (PRS) with glycemic response, measured by changes in metformin dosage or HbA1c levels. While individual genetic variants showed no significant association, rs622342 on SLC2A1 correlated with increased glycemic response only in metformin monotherapy patients (β = -2.09, P-value < 0.001). The collective effect of variants, as represented by PRS, weakly correlated with changes in metformin dosage (β = 0.023, P-value = 0.027). Synergistic interaction was observed between rs7124355 and rs8192675. Our findings suggest that while higher PRS correlates with increased metformin dosage, its modest effect size limits clinical utility, emphasizing the need for future research in diverse populations to refine genetic risk models.

我们的研究调查了鹿特丹研究队列中基因变异对二甲双胍血糖反应的影响,该队列由 14926 人组成,随访时间长达 27 年。在 1285 名欧洲血统的二甲双胍使用者中,我们使用线性混合模型分析了单核苷酸多态性(SNPs)和多基因风险评分(PRS)与血糖反应的关系,血糖反应通过二甲双胍剂量或 HbA1c 水平的变化来衡量。虽然单个基因变异没有显示出明显的相关性,但 SLC2A1 上的 rs622342 仅与二甲双胍单药治疗患者的血糖反应增加相关(β = -2.09,P 值为 0.05)。
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引用次数: 0
Clinical and economic outcomes of a pharmacogenomics-enriched comprehensive medication management program in a self-insured employee population 在自保员工群体中开展药物基因组学强化综合用药管理项目的临床和经济效果。
IF 2.9 3区 医学 Q2 GENETICS & HEREDITY Pub Date : 2024-10-02 DOI: 10.1038/s41397-024-00350-1
Maren S. Fragala, Murray Keogh, Steven E. Goldberg, Raymond A. Lorenz, Jeffrey A. Shaman
Clinical and economic outcomes from a pharmacogenomics-enriched comprehensive medication management program were evaluated over 26 months in a self-insured U.S. employee population (n = 452 participants; n = 1500 controls) using propensity matched pre-post design with adjusted negative binomial and linear regression models. After adjusting for baseline covariates, program participation was associated with 39% fewer inpatient (p = 0.05) and 39% fewer emergency department (p = 0.002) visits, and with 21% more outpatient visits (p < 0.001) in the follow-up period compared to the control group. Results show pharmacogenomics-enriched comprehensive medication management can favorably impact healthcare utilization in a self-insured employer population by reducing emergency department and inpatient visits and can offer the potential for cost savings. Self-insured employers may consider implementing pharmacogenomics-enriched comprehensive medication management to improve the healthcare of their employees.
我们采用倾向匹配前-后设计,并使用调整后的负二项式和线性回归模型,对美国自保员工群体(n = 452 名参与者;n = 1500 名对照组)在 26 个月内参加药物基因组学强化综合用药管理项目的临床和经济效果进行了评估。在对基线协变量进行调整后,参与该计划与住院病人减少 39% (p = 0.05)和急诊就诊次数减少 39% (p = 0.002)以及门诊就诊次数增加 21% (p = 0.003)相关。
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引用次数: 0
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Pharmacogenomics Journal
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