19 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

pharmacogenomics

These pubmed results were generated on 2019/02/08

PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

11 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

pharmacogenomics

These pubmed results were generated on 2019/02/07

PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

CCGG deletion (rs201074739) in CD33 results in premature termination codon and complete loss of CD33 expression: another key variant with potential impact on response to CD33-directed agents.

Leuk Lymphoma. 2019 Feb 05;:1-4

Authors: Papageorgiou I, Loken MR, Brodersen LE, Gbadamosi M, Uy GL, Meshinchi S, Lamba JK

PMID: 30721105 [PubMed - as supplied by publisher]

Antimicrobial and Antibiofilm Activity against Streptococcus mutans of Individual and Mixtures of the Main Polyphenolic Compounds Found in Chilean Propolis.

Biomed Res Int. 2019;2019:7602343

Authors: Veloz JJ, Alvear M, Salazar LA

Abstract
Dental caries is multifactorial disease and an important health problem worldwide. Streptococcus mutans is considered as a major cariogenic agent in oral cavity. This bacteria can synthetize soluble and insoluble glucans from sucrose by glucosyltransferases enzymes and generate stable biofilm on the tooth surface. Biological properties of Chilean propolis have been described and it includes antimicrobial, antifungal, and antibiofilm activities. The main goal of this study was to quantify the concentrations of main flavonoids presents in Chilean propolis and compare some biological properties such as antimicrobial and antibiofilm activity of individual compounds and the mixture of this compounds, against S. mutans cultures. Chilean propolis was studied and some polyphenols present in this extract were quantified by HPLC-DAD using commercial standards of apigenin, quercetin, pinocembrin, and caffeic acid phenethyl ester (CAPE). MIC for antimicrobial activity was determined by serial dilution method and biofilm thickness on S. mutans was quantified by confocal microscopy. Pinocembrin, apigenin, quercetin, and caffeic acid phenethyl ester (CAPE) are the most abundant compounds in Chilean propolis. These polyphenols have strong antimicrobial and antibiofilm potential at low concentrations. However, pinocembrin and apigenin have a greater contribution to this action. The effect of polyphenols on S. mutans is produced by a combination of mechanisms to decrease bacterial growth and affect biofilm proliferation due to changes in their architecture.

PMID: 30719447 [PubMed - in process]

Angiotensin Converting Enzyme Gene Insertion/Deletion Polymorphism Is Not Responsible for Antihypertensive Therapy Induced New Onset of Type 2 Diabetes in Essential Hypertension.

Clin Med Insights Endocrinol Diabetes. 2019;12:1179551418825037

Authors: Jhawat V, Gupta S, Agarwal BK, Roy P, Saini V

Abstract
Background: Antihypertensive drug therapies have been reported to be associated with new onset of type 2 diabetes mellitus in some hypertensive patients after prolonged use. Angiotensin converting enzyme (ACE) gene has been found to affect essential hypertension, response of antihypertensive therapies, and glycemic disturbances. Therefore, ACE gene I/D polymorphism may be associated with risk of new onset of type 2 diabetes via metabolic disturbances, glycemic dysregulation, and insulin resistance.
Aim: To assess the correlation between ACE gene I/D polymorphism and glycemic disturbance under influence of diuretic and other antihypertensive drug therapies.
Materials and methods: We recruited 270 normotensive patients as control (150 men and 120 women), 270 hypertensive patients (95 men and 175 women), and 240 hypertensive with new onset of diabetes patients (80 men and 160 women). All samples were genotyped for ACE gene polymorphic alleles and relationship between different genotypes and anthropometric and clinical parameters along with drug therapies was established and analyzed.
Results: Baseline clinical (systolic blood pressure, diastolic blood pressure, and fasting blood glucose level) and anthropometric parameters (height, weight, waist circumference, hip circumference, waist-hip ratio, and body mass index) of study populations were found highly statistically significant (P < .05) when compared among study groups. Furthermore, genotype wise comparison of all these parameters in essential hypertensive (EH) and essential hypertensive with onset of diabetes (EHNOD) patients found most of them nonsignificant and no variation was found with respect to different genotypes of ACE gene. The genotype wise comparison of clinical parameters among different antihypertensive drug therapy was found statistically nonsignificant in both EH and EHNOD patients.
Discussion: Anthropometric parameters can be taken as the risk indicator factors for hypertension and diabetes. However, ACE gene polymorphism may not be a risk factor for development of diabetes in hypertensive patients.
Conclusion: The present study suggested that ACE gene polymorphism did not show any significant association with the risk of new onset of diabetes in EH patients and more detailed studies with large population size are needed.

PMID: 30718967 [PubMed]

Targeted codelivery of doxorubicin and IL-36γ expression plasmid for an optimal chemo-gene combination therapy against cancer lung metastasis.

Nanomedicine. 2019 01;15(1):129-141

Authors: Chen Y, Sun J, Huang Y, Liu Y, Liang L, Yang D, Lu B, Li S

Abstract
Cancer metastasis is the main cause for the high mortality in breast cancer patients. In this work we developed a polymer POEG-st-Pmor for targeted co-delivery of IL-36γ expression plasmid and doxorubicin (Dox) to lung metastasis of breast cancer. The polymer readily formed micelles that were effective in loading Dox and simultaneously forming complexes with IL-36γ plasmid. Interestingly, particles co-loaded with Dox and plasmid was significantly smaller and more stable than the particles loaded with Dox only. Gene transfection in both lungs and s.c. tumors was significantly higher with our polymer compared to PEI. In addition, the Dox + IL-36γ/POEG-st-Pmor not only could bring improved anti-metastatic effect but synergistically enhance the type I immune response by increasing the IFN-γ positive CD4+ and CD8+ T cells and simultaneously decreasing the immunosuppressive myeloid-derived suppressor cells in the lung. POEG-st-Pmor may represent a simple and effective delivery system for an optimal chemo-gene combination therapy.

PMID: 30308300 [PubMed - indexed for MEDLINE]

13 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

pharmacogenomics

These pubmed results were generated on 2019/02/05

PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

13 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

pharmacogenomics

These pubmed results were generated on 2019/02/05

PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

Interpretation of the effect of CYP2C9, VKORC1 and CYP4F2 variants on warfarin dosing adjustment in Turkey.

Mol Biol Rep. 2019 Feb 02;:

Authors: Kocael A, Eronat AP, Tüzüner MB, Ekmekçi A, Orhan AL, İkizceli İ, Yılmaz-Aydoğan H, Öztürk O

Abstract
It was aimed to underline the importance and explain the meaning of genetic testing in warfarin dosing and investigate and evaluate the contributions of the CYP2C9, VKORC1, and CYP4F2 variants in a Turkish population. Two hundred patients were genotyped for CYP2C9 (rs1799853, rs1057910 and rs56165452), VKORC1 (rs9934438, rs8050894, rs9923231, rs7294 and rs2359612) and CYP4F2 (rs2108622), yet, only 127 patients were found suitable for further evaluation in terms of their personal response to warfarin due to long term usage and available INR and dose usage information. The DNA sequences were determined by the ABI PRISM 3100 Genetic Analyzer to 3130xl System (Applied Biosystems, Foster City, California). Warfarin dose application suggestions by warfaringdosing.org, FDA and MayoClinic were followed. Dose requirements in the Turkish population were found higher than the suggested doses by warfarindosing.org. The multivariate logistic regression analysis reveals the utilization of VCORC1 genetic evaluation is valuable in warfarin dosing (low and moderate vs. high) in this study (p < 0.001). The present study provides findings for clinicians to adapt the genetic data to the daily practice. We observed that the VKORC1 variant showed a more potent impact in warfarin dosing in this study.

PMID: 30712247 [PubMed - as supplied by publisher]

The tRNA-associated dysregulation in diabetes mellitus.

Metabolism. 2019 Jan 31;:

Authors: Zhou Z, Sun B, Huang S, Jia W, Yu D

Abstract
Diabetes mellitus (DM) is a complex endocrine and metabolic disorder for human health and well-being. Deregulated glucose and lipid metabolism are the primary underlying manifestations associated with this disease. Transfer RNAs (tRNAs) are considered to mainly participate in protein translation and may contribute to complex human pathologies. Although the molecular mechanisms remain, for the most part, unknown, accumulating evidence indicates that tRNAs play a vital role in the pathogenesis of DM. This paper reviews different aspects of tRNA-associated dysregulation in DM, such as tRNA mutations, tRNA modifications, tRNA aminoacylation and tRNA derivatives, aiming at a better understanding of the pathogenesis of DM and providing new ideas for the personalized treatment of this metabolism-associated disease.

PMID: 30711570 [PubMed - as supplied by publisher]

Pandemrix-induced narcolepsy is associated with genes related to immunity and neuronal survival.

EBioMedicine. 2019 Jan 30;:

Authors: Hallberg P, Smedje H, Eriksson N, Kohnke H, Daniilidou M, Öhman I, Yue QY, Cavalli M, Wadelius C, Magnusson PKE, Landtblom AM, Wadelius M, Swedegene

Abstract
BACKGROUND: The incidence of narcolepsy rose sharply after the swine influenza A (H1N1) vaccination campaign with Pandemrix. Narcolepsy is an immune-related disorder with excessive daytime sleepiness. The most frequent form is strongly associated with HLA-DQB1*06:02, but only a minority of carriers develop narcolepsy. We aimed to identify genetic markers that predispose to Pandemrix-induced narcolepsy.
METHODS: We tested for genome-wide and candidate gene associations in 42 narcolepsy cases and 4981 controls. Genotyping was performed on Illumina arrays, HLA alleles were imputed using SNP2HLA, and single nucleotide polymorphisms were imputed using the haplotype reference consortium panel. The genome-wide significance threshold was p < 5 × 10-8, and the nominal threshold was p < 0.05. Results were replicated in 32 cases and 7125 controls. Chromatin data was used for functional annotation.
FINDINGS: Carrying HLA-DQB1*06:02 was significantly associated with narcolepsy, odds ratio (OR) 39.4 [95% confidence interval (CI) 11.3, 137], p = 7.9 × 10-9. After adjustment for HLA, GDNF-AS1 (rs62360233) was significantly associated, OR = 8.7 [95% CI 4.2, 17.5], p = 2.6 × 10-9, and this was replicated, OR = 3.4 [95% CI 1.2-9.6], p = 0.022. Functional analysis revealed variants in high LD with rs62360233 that might explain the detected association. The candidate immune-gene locus TRAJ (rs1154155) was nominally associated in both the discovery and replication cohorts, meta-analysis OR = 2.0 [95% CI 1.4, 2.8], p = 0.0002.
INTERPRETATION: We found a novel association between Pandemrix-induced narcolepsy and the non-coding RNA gene GDNF-AS1, which has been shown to regulate expression of the essential neurotrophic factor GDNF. Changes in regulation of GDNF have been associated with neurodegenerative diseases. This finding may increase the understanding of disease mechanisms underlying narcolepsy. Associations between Pandemrix-induced narcolepsy and immune-related genes were replicated.

PMID: 30711515 [PubMed - as supplied by publisher]

iPSC model of CHRFAM7A effect on α7 nicotinic acetylcholine receptor function in the human context.

Transl Psychiatry. 2019 Feb 01;9(1):59

Authors: Ihnatovych I, Nayak TK, Ouf A, Sule N, Birkaya B, Chaves L, Auerbach A, Szigeti K

Abstract
The α7 nicotinic acetylcholine receptor (α7nAChR) has been a promising target for diseases affecting cognition and higher cortical functions; however, the effect observed in animal models failed to translate into human clinical trials identifying a translational gap. CHRFAM7A is a human-specific fusion gene with properties that enable incorporation into the α7nAChR and, being human specific, CHRFAM7A effect was not accounted for in preclinical studies. We hypothesized that CHRFAM7A may account for this translational gap and understanding its function may offer novel insights when exploring α7nAChR as a drug target. CHRFAM7A is present in different copy number variations (CNV) in the human genome with high frequency. To study the functional consequences of the presence of the CHRFAM7A, two induced pluripotent stem cell (iPSC) lines (0 copy and 1 copy direct) were developed. The 0 copy line was rescued with CHRFAM7A transfection to control for genetic heterogeneity. As readouts for genotype-phenotype correlation, α7nAChR synaptic transmission and amyloid beta 1-42 (Aβ1-42) uptake were tested. Synaptic transmission in the presence of CHRFAM7A demonstrated that PNU-modulated desensitization of α7nAChR currents increased as a function of CHRFAM7A dosage. CHRFAM7A mitigated the dose response of Aβ1-42 uptake suggesting a protective effect beyond physiological concentrations. Furthermore, in the presence of CHRFAM7A Aβ1-42 uptake activated neuronal interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) without activating the canonical inflammasome pathway. Lead optimization may identify more potent molecules when the screen has a model harboring CHRFAM7A. Incorporating pharmacogenetics into clinical trials may enhance signals in efficacy measures.

PMID: 30710073 [PubMed - in process]

12 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

pharmacogenomics

These pubmed results were generated on 2019/02/02

PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

Sodium Channels in Human Pain Disorders: Genetics and Pharmacogenomics.

Annu Rev Neurosci. 2019 Jan 31;:

Authors: Dib-Hajj SD, Waxman SG

Abstract
Acute pain is adaptive, but chronic pain is a global challenge. Many chronic pain syndromes are peripheral in origin and reflect hyperactivity of peripheral pain-signaling neurons. Current treatments are ineffective or only partially effective and in some cases can be addictive, underscoring the need for better therapies. Molecular genetic studies have now linked multiple human pain disorders to voltage-gated sodium channels, including disorders characterized by insensitivity or reduced sensitivity to pain and others characterized by exaggerated pain in response to normally innocuous stimuli. Here, we review recent developments that have enhanced our understanding of pathophysiological mechanisms in human pain and advances in targeting sodium channels in peripheral neurons for the treatment of pain using novel and existing sodium channel blockers. Expected final online publication date for the Annual Review of Neuroscience Volume 42 is July 8, 2019. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

PMID: 30702961 [PubMed - as supplied by publisher]

Genome-wide association study of antidepressant treatment resistance in a population-based cohort using health service prescription data and meta-analysis with GENDEP.

Pharmacogenomics J. 2019 Jan 31;:

Authors: Wigmore EM, Hafferty JD, Hall LS, Howard DM, Clarke TK, Fabbri C, Lewis CM, Uher R, Navrady LB, Adams MJ, Zeng Y, Campbell A, Gibson J, Thomson PA, Hayward C, Smith BH, Hocking LJ, Padmanabhan S, Deary IJ, Porteous DJ, Mors O, Mattheisen M, Nicodemus KK, McIntosh AM

Abstract
Antidepressants demonstrate modest response rates in the treatment of major depressive disorder (MDD). Despite previous genome-wide association studies (GWAS) of antidepressant treatment response, the underlying genetic factors are unknown. Using prescription data in a population and family-based cohort (Generation Scotland: Scottish Family Health Study; GS:SFHS), we sought to define a measure of (a) antidepressant treatment resistance and (b) stages of antidepressant resistance by inferring antidepressant switching as non-response to treatment. GWAS were conducted separately for antidepressant treatment resistance in GS:SFHS and the Genome-based Therapeutic Drugs for Depression (GENDEP) study and then meta-analysed (meta-analysis n = 4213, cases = 358). For stages of antidepressant resistance, a GWAS on GS:SFHS only was performed (n = 3452). Additionally, we conducted gene-set enrichment, polygenic risk scoring (PRS) and genetic correlation analysis. We did not identify any significant loci, genes or gene sets associated with antidepressant treatment resistance or stages of resistance. Significant positive genetic correlations of antidepressant treatment resistance and stages of resistance with neuroticism, psychological distress, schizotypy and mood disorder traits were identified. These findings suggest that larger sample sizes are needed to identify the genetic architecture of antidepressant treatment response, and that population-based observational studies may provide a tractable approach to achieving the necessary statistical power.

PMID: 30700811 [PubMed - as supplied by publisher]

OPRM1 Gene Interaction with Sleep in Chronic Pain Patients Treated with Opioids.

Pain Physician. 2019 Jan;22(1):97-107

Authors: Margarit C, Ballester P, Inda MD, Roca R, Gomez L, Planelles B, Ajo R, Morales D, Peiro AM

Abstract
BACKGROUND: The experience of chronic non-cancer pain (CNCP) is one of the most common reasons individuals seek medical attention. Patients with CNCP frequently experience concomitant sleep-related problems.
OBJECTIVES: The aim was to evaluate sleep problems in opioid naïve CNCP patients, before and after opioid titration, analyzing the influence of OPRM1 gene variants.
STUDY DESIGN: A prospective, cohort, observational study.
SETTING: This study was performed at the Pain Unit of the Alicante University General Hospital.
METHODS: Pain and Medical Outcomes Study Sleep questionnaire (MOS-Sleep) were assessed at baseline and 3 months after opioid titration in 231 opioid naïve CNCP patients. Sleep data was compared with a matched-control group (n = 64). Morphine equivalent daily doses, adverse events, and drugs prescribed for pain were also registered. OPRM1 polymorphism rs1799971 was analyzed by RT-PCR. Ethics Committee approved the study and results were analyzed by R software.
RESULTS: After 3 months of opioid titration, patients with CNCP (63 ± 14 years, 64% female, VAS 74 ± 17 mm) significantly decreased pain intensity, anxiety and depression, and increased quality of life. Sleep problems were significantly more frequent in females (P = 0.002). Age, quality of life, anxiety, and depression all influenced sleep disturbances and problems indices, which were significantly different from the control group. Furthermore, the OPRM1 118-GG genotype was also associated with significantly lower sleep adequacy, and more sleep problems.
LIMITATIONS: Total number of subjects studied was relatively small and most patients were on other non-opioid centrally-acting medications.
CONCLUSIONS: Opioids decreased CNCP severity, improving patients' psychological areas, and quality of life. However, patients with OPRM1 118-GG genotype indicated an increase in sleep problems and worsening sleep pattern while taking opioids.
KEY WORDS: OPRM1, pharmacogenetics, MOS-Sleep, opioids, chronic noncancer pain, sleep related problems, sleep problem index SLP-6 and SLP-9.

PMID: 30700073 [PubMed - in process]

Nutraceuticals for major depressive disorder- more is not merrier: An 8-week double-blind, randomised, controlled trial.

J Affect Disord. 2019 Feb 15;245:1007-1015

Authors: Sarris J, Byrne GJ, Stough C, Bousman C, Mischoulon D, Murphy J, Macdonald P, Adams L, Nazareth S, Oliver G, Cribb L, Savage K, Menon R, Chamoli S, Berk M, Ng CH

Abstract
BACKGROUND: One of the most pressing questions in "Nutritional Psychiatry" is whether using combinations of different nutraceuticals with putative antidepressant activity may provide an enhanced synergistic antidepressant effect.
METHODS: A phase II/III, Australian multi-site, 8-week, double-blind, RCT involving 158 outpatients with a DSM-5 diagnosis of MDD. The intervention consisted of a nutraceutical combination: S-adenosyl methionine; Folinic acid; Omega-3 fatty acids; 5-HTP, Zinc picolinate, and relevant co-factors versus placebo. The primary outcome was change in MADRS score. Hypothesis-driven analyses of potential moderators of response involving key SNPs, and BDNF were also conducted.
RESULTS: Placebo was superior to the nutraceutical combination in reducing MADRS score (differential reduction -1.75 points), however a mixed linear model revealed a non-significant Group X Time interaction (p = 0.33). Response rates were 40% for the active intervention and 51% for the placebo; remission rates were 34% and 43% for active and placebo groups, respectively. No significant differences were found between groups on any other secondary depression, anxiety, psychosocial, or sleep outcome measures. Key SNPs and BDNF did not significantly moderate response. No significant differences occurred between groups for total adverse effects, aside from more nausea in the active group.
LIMITATIONS: Very high placebo response rates suggest a placebo run-in design may have been valuable.
INTERPRETATION: The adoption of a nutraceutical 'shotgun' approach to treating MDD was not supported, and appeared to be less effective than adding placebo to treatment as usual.

PMID: 30699842 [PubMed - in process]

CYP2C19 polymorphism in relation to the pharmacotherapy optimization of commonly used drugs.

Pharmazie. 2018 11 01;73(11):619-624

Authors: Sienkiewicz-Oleszkiewicz B, Wiela-Hojeńska A

Abstract
Purpose: The CYP2C19 isoenzyme plays an important role in the efficacy and safe use of many drugs. The aim of this review is to demonstrate how CYP2C19 mutations influence everyday patient treatment, leading to adverse drug reactions or therapy failure in many common diseases. Methods: A PubMed literature search was performed on clinical publications evaluating the impact of CYP2C19 on pharmacotherapy outcome. Main fields of medicine with strong outcome dependency on the CYP2C19 genotype were selected. We also focused on clinical recommendations for the use of drugs referring to CYP2C19 polymorphism. Results: The fields of medicine where clinical outcome particularly depends on CYP2C19 polymorphism are gastroenterology, cardiology, psychiatry, mycology and oncology. CYP2C19 is involved in proton pump inhibitors metabolism, thus it can influence reflux therapy, ulcer prevention and Helicobacter pylori eradication treatment. The CYP2C19 enzyme plays also a vital role in the two bioactivation steps of clopidogrel leading to lower (CYP2C19*17 carriers) or higher (CYP2C19*2 carriers) risk of major adverse cardiovascular events. It affects the antidepressant treatment and methadone replacement therapy as well as voriconazole prophylaxis. The presence of a *2 allele is associated with longer relapse-free time or better survival, and the *17 allele with more favorable outcomes in breast cancer patients treated with tamoxifen. Conclusions: Knowledge of the CYP2C19 polymorphism could positively affect individual treatment and lead to better patient outcomes in many cases. The introduction of pharmacogenetic testing into medical practice would be a good way to minimize negative outcomes of therapy, and to reduce unnecessary medical costs.

PMID: 30396378 [PubMed - indexed for MEDLINE]

Harnessing the biological complexity of Big Data from LINCS gene expression signatures.

PLoS One. 2018;13(8):e0201937

Authors: Musa A, Tripathi S, Kandhavelu M, Dehmer M, Emmert-Streib F

Abstract
Gene expression profiling using transcriptional drug perturbations are useful for many biomedical discovery studies including drug repurposing and elucidation of drug mechanisms (MoA) and many other pharmacogenomic applications. However, limited data availability across cell types has severely hindered our capacity to progress in these areas. To fill this gap, recently, the LINCS program generated almost 1.3 million profiles for over 40,000 drug and genetic perturbations for over 70 different human cell types, including meta information about the experimental conditions and cell lines. Unfortunately, Big Data like the ones generated from the ongoing LINCS program do not enable easy insights from the data but possess considerable challenges toward their analysis. In this paper, we address some of these challenges. Specifically, first, we study the gene expression signature profiles from all cell lines and their perturbagents in order to obtain insights in the distributional characteristics of available conditions. Second, we investigate the differential expression of genes for all cell lines obtaining an understanding of condition dependent differential expression manifesting the biological complexity of perturbagents. As a result, our analysis helps the experimental design of follow-up studies, e.g., by selecting appropriate cell lines.

PMID: 30157183 [PubMed - indexed for MEDLINE]

Using Pharmacogenetic Testing or Platelet Reactivity Testing to Tailor Antiplatelet Therapy: Are Asians different from Caucasians?

Eur Cardiol. 2018 Dec;13(2):112-114

Authors: Su-Yin DT

Abstract
All studies to date involving platelet reactivity and gene testing document singular interventions and their associations with outcomes. The East Asian paradox has been well documented - Asians who have had a percutaneous coronary intervention (PCI) are at a lower risk of ischaemic events even though they have a higher platelet reactivity. Asians who have had a PCI also have a higher risk of bleeding. This article covers the differences in outcomes between Caucasians and Asians, and explores the impact of outcomes, highlighting differences between the two patient populations. Given the high prevalence of loss-of-function alleles in Asia, treatment strategies will differ for different populations. It is plausible that both platelet reactivity and gene testing should be used to inform holistic decision-making for all patients - Caucasian or Asian - with acute coronary syndrome who are undergoing PCI.

PMID: 30697355 [PubMed]