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Hot Topics of the Day are picked by experts to capture the latest information and publications on public health genomics and precision health for various diseases and health topics. Sources include published scientific literature, reviews, blogs and popular press articles.

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24 hot topic(s) found with the query "Clopidogrel"

Implementation of pharmacogenomic clinical decision support for health systems: a cost-utility analysis
S Jiang et al, The PGX journal, April 1, 2022 (Posted: Apr 02, 2022 8AM)

We constructed a cost-effectiveness model to assess the clinical and economic value of a CDS alert program that provides pharmacogenomic (PGx) testing results, compared to no alert program in acute coronary syndrome (ACS) and atrial fibrillation (AF), from a health system perspective. We defaulted that 20% of 500,000 health-system members between the ages of 55 and 65 received PGx testing for CYP2C19 (ACS-clopidogrel) and CYP2C9, CYP4F2 and VKORC1 (AF-warfarin) annually. Clinical events, costs, and quality-adjusted life years (QALYs) were calculated over 20 years with an annual discount rate of 3%. In total, 3169 alerts would be fired. The CDS alert program would help avoid 16 major clinical events and 6 deaths for ACS; and 2 clinical events and 0.9 deaths for AF.


New genetic variants associated with major adverse cardiovascular events in patients with acute coronary syndromes and treated with clopidogrel and aspirin
X Liu et al, The Pharmacogenomics Journal, June 22, 2021 (Posted: Jun 23, 2021 8AM)

This study aims to identify new genetic variants associated with MACE end point during the 18-month follow-up period by a two-stage large-scale sequencing data, including high-depth whole exome sequencing of 168 patients in the discovery cohort and high-depth targeted sequencing of 1793 patients in the replication cohort. We discovered eight new genotypes and their genes associated with MACE in patients with ACS.


Ischemic stroke and myocardial ischemia in clopidogrel users and the association with CYP2C19 loss-of-function homozygocity: a real-world study
N Gronich et al, The PGX journal, March 1, 2021 (Posted: Mar 02, 2021 8AM)


The need of a multicomponent guiding approach to personalize clopidogrel treatment
C Valeria et al, Pharmacogenomics Journal, October 9, 2020 (Posted: Oct 10, 2020 7AM)

A systematic review of the controversies about the use of CYP2C19 pharmacogenetics and platelet function testing to personalize clopidogrel treatment. We assess literature with our findings concerning patients eligible for vascular surgery and treated with clopidogrel, in whom we used a combined management based on the CYP2C19 and ABCB1 pharmacogenetic testing.


Prediction Rule for Nonresponse to Clopidogrel: ABCD-GENE Score
ACC, March 3, 2020 (Posted: Mar 05, 2020 8AM)

The ABCD-GENE score, which encompasses a total of five variables: four clinical (age, body mass index, chronic kidney disease status, and diabetes mellitus) and one genetic (CYP2C19 loss-of-function alleles) showed reasonable discrimination in identifying patients with HPR status and predicted adverse clinical outcomes, including mortality.


Clopidogrel Pharmacogenetics - Why the Wait?
Roden Dan M et al. The New England journal of medicine 2019 10 (17) 1677-1678 (Posted: Oct 28, 2019 2PM)

We have known since time immemorial that every drug produces variable effects across populations, and we now understand the genetic basis for some of that variability. So why is CYP2C19 testing not the standard of care to guide antiplatelet therapy?


Systematic review of the evidence on the cost-effectiveness of pharmacogenomics-guided treatment for cardiovascular diseases
Ye Zhu, et al. Genetics in Medicine, October 8, 2019 (Posted: Oct 10, 2019 8AM)

The study conducted a systematic review using multiple databases from inception to 2018. The study found mixed evidence on the cost-effectiveness of PGx in CVD care. Supportive evidence exists for clopidogrel–CYP2C19 and warfarin–CYP2C9/VKORC1, but evidence is limited in other drug–gene combinations. Gaps persist, including unclear explanation of perspective and cost inputs, underreporting of study design elements.


Frequency and clinical outcomes of CYP2C19 genotype-guided escalation and de-escalation of antiplatelet therapy in a real-world clinical setting.
Martin Jesse et al. Genetics in medicine : official journal of the American College of Medical Genetics 2019 Jul (Posted: Jul 19, 2019 8AM)

The frequency of escalation (clopidogrel switched to prasugrel/ticagrelor) and de-escalation (prasugrel/ticagrelor switched to clopidogrel) was evaluated in 1063 PCI patients who underwent CYP2C19 genotyping. The study found that CYP2C19-guided escalation and de-escalation is common in a real-world setting. Continuation of clopidogrel in nonfunctional allele carriers is associated with adverse outcomes.


P2Y12 Inhibitor Switching in Response to Routine Notification of CYP2C19 Clopidogrel Metabolizer Status Following Acute Coronary Syndromes.
Povsic Thomas J et al. JAMA cardiology 2019 May (Posted: May 31, 2019 10AM)


One Step Closer to Precision Medicine Strategies Based on Genetic Information-ABCB1 Polymorphisms in the CHANCE Trial-
BP George et al, JAMA Neurology, February 11, 2019 (Posted: Feb 13, 2019 8AM)


Association Between ABCB1 Polymorphisms and Outcomes of Clopidogrel Treatment in Patients With Minor Stroke or Transient Ischemic Attack- Secondary Analysis of a Randomized Clinical Trial
Y Pan et al, JAMA Neurology, February 11, 2019 (Posted: Feb 13, 2019 8AM)


Pharmacogenetics of Clopidogrel Therapy and Neurointerventional Procedures: We Need Precision Data for Precision Medicine.
Rakicevic Ljiljana et al. Clinical pharmacology and therapeutics 2018 Jun (Posted: Jun 20, 2018 9AM)


CYP2C19 or CYP3A5 Genotyping Does Not Predict Clinical Response to Clopidogrel.
Rodríguez-González Fayna et al. Journal of clinical pharmacology 2018 May (Posted: May 09, 2018 8AM)


Genome-wide and candidate gene approaches of clopidogrel efficacy using pharmacodynamic and clinical end points-Rationale and design of the International Clopidogrel Pharmacogenomics Consortium (ICPC).
Bergmeijer Thomas O et al. American heart journal 2018 Apr 198152-159 (Posted: Apr 18, 2018 10AM)


Clinical implementation of rapid CYP2C19 genotyping to guide antiplatelet therapy after percutaneous coronary intervention.
Cavallari Larisa H et al. Journal of translational medicine 2018 Apr 16(1) 92 (Posted: Apr 18, 2018 10AM)


Role of CYP2C19 genotype testing in clinical use of clopidogrel: is it really useful?
Zeb Irfan et al. Expert review of cardiovascular therapy 2018 Apr 1-9 (Posted: Apr 04, 2018 11AM)


CYP2C19 and ABCB1 genetic polymorphisms correlate with the recurrence of ischemic cardiovascular adverse events after clopidogrel treatment.
Hou Xumin et al. Journal of clinical laboratory analysis 2018 Feb (Posted: Feb 07, 2018 9AM)


Pharmacogenomic Impact of CYP2C19 Variation on Clopidogrel Therapy in Precision Cardiovascular Medicine.
Brown Sherry-Ann et al. Journal of personalized medicine 2018 Jan (1) (Posted: Feb 06, 2018 0PM)


Should We Perform Genetic Testing on Antiplatelet Therapy?
L Gross et al, American College of Cardiology, July 10, 2017 (Posted: Jul 11, 2017 10AM)


Optimizing clopidogrel dose response: a new clinical algorithm comprising CYP2C19 pharmacogenetics and drug interactions.
Saab Yolande B et al. Therapeutics and clinical risk management 2015 111421-7 (Posted: Apr 06, 2016 9AM)


Molecular diagnostic experience of whole-exome sequencing in adult patients.
Posey Jennifer E et al. Genetics in medicine : official journal of the American College of Medical Genetics 2015 Dec (Posted: Dec 09, 2015 9AM)


Physician perspectives of CYP2C19 and clopidogrel drug-gene interaction active clinical decision support alerts.
Nishimura Adam A et al. International journal of medical informatics 2015 Nov (Posted: Dec 09, 2015 9AM)


Effects of CYP2C19 and P2Y12 Gene Polymorphisms on Clinical Results of Patients Using Clopidogrel after Acute Ischemic Cerebrovascular Disease.
Sen H M et al. Balkan J. Med. Genet. 2014 Dec 17(2) 37-41 (Posted: May 06, 2015 10AM)


Thrombotic Thrombocytopenic Purpura
From NHLBI health topic site Brand (Posted: Jan 01, 2014 0AM)

What Is Thrombotic thrombocytopenic purpura (TTP) is a rare blood disorder. In TTP, blood clots form in small blood vessels throughout the body. The clots can limit or block the flow of oxygen-rich blood to the body's organs, such as the brain, kidneys, and heart. As a result, serious health problems can develop. The increased clotting that occurs in TTP also uses up platelets (PLATE-lets) in the blood. Platelets are blood cell fragments that help form blood clots. These cell fragments stick together to seal small cuts and breaks on blood vessel walls and stop bleeding. With fewer platelets available in the blood, bleeding problems can occur. People who have TTP may bleed inside their bodies, underneath the skin, or from the surface of the skin. When cut or injured, they also may bleed longer than normal. "Thrombotic" (throm-BOT-ik) refers to the blood clots that form. "Thrombocytopenic" (throm-bo-cy-toe-PEE-nick) means the blood has a lower than normal number of platelets. "Purpura" (PURR-purr-ah) refers to purple bruises caused by bleeding under the skin. Bleeding under the skin also can cause tiny red or purple dots on the skin. These pinpoint-sized dots are called petechiae (peh-TEE-kee-ay). Petechiae may look like a rash. Purpura and Petechiae The photograph shows purpura (bruises) and petechiae (red and purple dots) on the skin. The photograph shows purpura (bruises) and petechiae (red and purple dots) on the skin. Bleeding under the skin causes the purple, brown, and red color of the purpura and petechiae. TTP also can cause red blood cells to break apart faster than the body can replace them. This leads to hemolytic anemia (HEE-moh-lit-ick uh-NEE-me-uh)?a rare form of anemia. Anemia is a condition in which the body has a lower than normal number of red blood cells. A lack of activity in the ADAMTS13 enzyme (a type of protein in the blood) causes TTP. The ADAMTS13 gene controls the enzyme, which is involved in blood clotting. The enzyme breaks up a large protein called von Willebrand factor that clumps together with platelets to form blood clots. Types of Thrombotic Thrombocytopenic Purpura The two main types of TTP are inherited and acquired. "Inherited" means the condition is passed from parents to children through genes. This type of TTP mainly affects newborns and children. In inherited TTP, the ADAMTS13 gene is faulty and doesn't prompt the body to make a normal ADAMTS13 enzyme. As a result, enzyme activity is lacking or changed. Acquired TTP is the more common type of the disorder. "Acquired" means you aren't born with the disorder, but you develop it. This type of TTP mostly occurs in adults, but it can affect children. In acquired TTP, the ADAMTS13 gene isn't faulty. Instead, the body makes antibodies (proteins) that block the activity of the ADAMTS13 enzyme. It's not clear what triggers inherited and acquired TTP, but some factors may play a role. These factors may include: ?Some diseases and conditions, such as pregnancy, cancer, HIV, lupus, and infections ?Some medical procedures, such as surgery and blood and marrow stem cell transplant ?Some medicines, such as chemotherapy, ticlopidine, clopidogrel, cyclosporine A, and hormone therapy and estrogens ?Quinine, which is a substance often found in tonic water and nutritional health products If you have TTP, you may sometimes hear it referred to as TTP?HUS. HUS, or hemolytic-uremic syndrome, is a disorder that resembles TTP, but is more common in children. Kidney problems also tend to be worse in HUS. Although some researchers think TTP and HUS are two forms of a single syndrome, recent evidence suggests that each has different causes. Outlook TTP is a rare disorder. It can be fatal or cause lasting damage, such as brain damage or a stroke, if it's not treated right away. TTP usually occurs suddenly and lasts for days or weeks, but it can continue for months. Relapses (or flareups) can occur in up to 60 percent of people who have the acquired type of TTP. Many people who have inherited TTP have frequent flareups that need to be treated. Treatments for TTP include infusions of fresh frozen plasma and plasma exchange, also called plasmapheresis (PLAZ-ma-feh-RE-sis). These treatments have greatly improved the outlook of the disorder. Other Names Inherited Thrombotic Thrombocytopenic Purpura ?Familial thrombotic thrombocytopenic purpura ?Upshaw-Schulman syndrome (USS) Acquired Thrombotic Thrombocytopenic Purpura ?Moschcowitz disease ?Microangiopathic hemolytic anemia If you have TTP, you may sometimes hear it referred to as TTP?HUS. HUS, or hemolytic-uremic syndrome, is a disorder that resembles TTP, but is more common in children. Kidney problems also tend to be worse in HUS. Although some researchers think TTP and HUS are two forms of a single syndrome, recent evidence suggests that each has different causes.



Disclaimer: Articles listed in Hot Topics of the Day are selected by Public Health Genomics Branch to provide current awareness of the scientific literature and news. Inclusion in the update does not necessarily represent the views of the Centers for Disease Control and Prevention nor does it imply endorsement of the article's methods or findings. CDC and DHHS assume no responsibility for the factual accuracy of the items presented. The selection, omission, or content of items does not imply any endorsement or other position taken by CDC or DHHS. Opinion, findings and conclusions expressed by the original authors of items included in the Clips, or persons quoted therein, are strictly their own and are in no way meant to represent the opinion or views of CDC or DHHS. References to publications, news sources, and non-CDC Websites are provided solely for informational purposes and do not imply endorsement by CDC or DHHS.
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