Clopidogrel: review of bioanalytical methods, pharmacokinetics/pharmacodynamics, and update on recent trends in drug–drug interaction studies

Mullangi, Ramesh; Srinivas, Nuggehally R.

doi:10.1002/bmc.1128

Cited by 45 publications

(23 citation statements)

References 52 publications

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“…Код оштећења бубрега и јетре, иако неки аутори сугеришу да то није потребно, треба водити рачуна о висини прописане дозе клопидогрела и врши-ти њено прилагођавање 12 . На биорасположи-вост клопидогрела не утичу храна и антациди Зато се препоручује започињање лечења са ударном дозом од 300 или 600 mg (посебно битно код пацијената којима је уграђен стент, где ова ударна доза скраћује време до макси-малне инхибиције од 80% на само 5 сати), а онда наставити са дозом одржавања од 75 или 150 mg на дан у једној дневној дози 2,[15][16][17] . У случају почетног дозирања од 75 mg на дан, до постизања максималног одговора потребно је 3 до 7 дана .…”

Section: фармакокинетикаunclassified

Importance of pharmacogenetics for therapeutic use of clopidogrel

Nemanja¹,

Aleksandra²,

Viktorija³

2013

Racion ter

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СКРАЋЕНИЦЕADP -аденозин-дифосфат P2Y12 -пуринергички рецептор на тром-боцитној мембрани CYP-цитохром P450 PCI-перкутана коронарна интервенција RPA-Residual platelet activity LTA-Light transmittance aggregometry VASP -Vasodilatator-stimulated phosphoprotein САЖЕТАК Цереброваскуларна и кардиоваскуларна обољења су један од водећих узрока смрти широм света. Самим тим, њихова терапија има велики значај. Важно место у терапији заузима клопидогрел, самостално или у ком-бинацији са аспирином. Проблем који се јав-ља у лечењу јесте слабији одговор на стан-дардну терапију, а тиме и повећана стопа по-новних кардиоваскуларних догађаја. Овај слабији одговор на терапију клопидогрелом последица је пре свега фармакогенoмске мо-дификације ензима цитохрома P450, као и П-гликопротеина одговорних за апсорпцију и биорасположивост. Код пацијената који пока-зују слабији одговор на стандардну антиагре-гациону терапију препоручује се генетско те-стирање.Кључне речи: клопидогрел, резистенција, тромбоцити, интеракције лекова ABSTRACT Cerebrovascular and cardiovascular diseases are the worldwide leading causes of mortality. Therefore, therapy of these diseases is of great importance. Antiplatelet therapy with clopidogrel alone and in combination with aspirin has a prominent place. The major problem in clopidogrel therapy is patients` poor response to standard protocols of treatment, followed by increased rate of repeated cardiovascular events. Main cause of the poor response to antiplatelet clopidogrel therapy is pharmacogenomic modification of cytochrome P450 as well as P-glycoprotein, responsible for absorption and bioavailability. Genetic testing is recommended for patients who respond poorly to standard antiplatelet therapy.

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Section: фармакокинетикаunclassified

Importance of pharmacogenetics for therapeutic use of clopidogrel

Nemanja¹,

Aleksandra²,

Viktorija³

2013

Racion ter

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“…The pharmacokinetic properties of prasugrel and clopidogrel have been investigated in several studies and are summarized in Table 2. 12,[29][30][31][32][33][34][35][36][37][38][39][40][41][42] In contrast to clopidogrel, [43][44][45] genetic variants in CYP 2C19 genes have not been shown to affect the antiplatelet response to prasugrel. …”

Section: Current Recommendations For Thienopyridines As Add-on Antiplmentioning

confidence: 99%

“…55 This conclusion was derived from an analysis of pharmacy and medical claims in the Medco Solutions database for 9,862 patients who received a PPI, compared with 6,828 patients who did not receive a PPI following a percutaneous coronary intervention (PCI). The Society for Cardiovascular Angiography and Interventions issued a statement on May 6, [29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45]58 Prasugrel…”

Section: Clinical Profile Of Prasugrelmentioning

confidence: 99%

Review of Prasugrel for the Secondary Prevention of Atherothrombosis

Spinler

Rees²

2009

JMCP

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BACKGROUND: The role of platelets in atherothrombotic disease is well established, and antiplatelet therapy is now recommended for the shortand long-term management of patients with acute coronary syndromes (ACS), with and without percutaneous coronary intervention (PCI). The thienopyridine clopidogrel is accepted as a key component of antiplatelet management and is recommended in current treatment guidelines as addon therapy to aspirin in secondary prevention to reduce coronary risk in patients with ACS and/or following PCI. The FDA Cardiovascular and Renal Drugs Advisory Committee met on February 3, 2009, and recommended approval of prasugrel, but with guidance to physicians about increased risk in low-weight or elderly patients and avoidance of use (a) around coronary artery bypass graft (CABG) or other surgical or invasive procedures and (b) in patients with prior or current stroke or transient ischemic attack (TIA).OBJECTIVE: To review the published literature examining primarily the clinical efficacy and safety of prasugrel in ACS patients.METHODS: The PubMed database was searched for English language studies involving the use of prasugrel in human subjects published up to April 2009 using the keyword "prasugrel." The review focused on randomized, controlled trials with clinical end points. Abstracts from recent scientific meetings (up to November 2008) were also searched for relevant studies, as was the FDA briefing document prepared in advance of the advisory committee meeting on February 3, 2009. RESULTS: Of the 124 published papers identified, 28 pertained to research in human subjects: 21 on prasugrel pharmacology and 7 with clinical end points. In the Prasugrel in Comparison to Clopidogrel for Inhibition of Platelet Activation and Aggregation-Thrombolysis in Myocardial Infarction (PRINCIPLE-TIMI) 44 trial, a cross-over study of laboratory-determined platelet activity, prasugrel produced significantly greater inhibition of platelet aggregation than clopidogrel after both loading dose (74.8% vs. 31.8% at 6 hours, P < 0.001) and maintenance dose (day 14: 61.3% vs. 46.1%, P < 0.001) in patients with stable coronary artery disease (CAD). In the only end point outcomes study (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis in Myocardial Infarction [TRITON-TIMI 38]) there was a significant reduction in adverse cardiac outcomes in patients with ACS treated with prasugrel, 94% of whom received at least 1 coronary stent. The incidence of the primary composite end point of cardiovascular death, nonfatal MI, or nonfatal stroke was 9.9% in the prasugrel group versus 12.1% in the clopidogrel group (hazard ratio = 0.81, 95% CI = 0.73-0.90, P < 0.001). However, the risk of a major bleeding event was significantly greater with prasugrel versus clopidogrel, and prasugrel appeared to be of net clinical harm in patients with a history of stroke/TIA. The FDA reviewer recommended that prasugrel use be discouraged in patients aged 75 years or older o...

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“…Up to now, numerous HPLC assays for the determination of CLP and CLPM have been reported in the literature. Recently, a review was published comprising the methods used for the determination of CLP and its metabolites in biological fluids [10]. Mitakos and Panderi reported a non-stereospecific HPLC method with UV detection for the determination of CLP in oral dosage forms.…”

Section: Introductionmentioning

confidence: 99%