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001-es BibID:BIBFORM048954
Első szerző:Kovács Emese Gyöngyvér (kardiológus)
Cím:Evaluation of laboratory methods routinely used to detect the effect of aspirin against new reference methods / Emese G. Kovács, Éva Katona, Zsuzsanna Bereczky, Nóra Homoródi, László Balogh, Eszter Tóth, Hajna Péterfy, Róbert G. Kiss, István Édes, László Muszbek
Dátum:2014
ISSN:0049-3848
Megjegyzések:Background: Aspirin, a commonly used antiplatelet agent, blocks platelet thromboxane A2 (TXA2) formationfromarachidonic acid (AA) by acetylating platelet cyclooxygenase-1 (COX-1). Laboratory methods currently used todetect this antiplatelet effect of aspirin provide variable results. We have reported three methods that assessplatelet COX-1 acetylation (inactivation) by aspirin and its direct consequences. The first and second assaysuse monoclonal anti-human-COX-1 antibodies that only detect acetylated (inactivated) COX-1 and active(non-acetylated) COX-1, respectively. The third method measures platelet production of TXB2 (the stablemetabolite of TXA2) in vitro in response to AA. We compared the results of these three reference methodswith other routinely used methods for assessing the functional consequences aspirin treatment.Methods: 108 healthy volunteers were treated with low-dose aspirin for 7 days. On day 7 following aspirintreatment COX-1 in the platelets was fully acetylated whereas only non-acetylated COX-1 was present in theday 0 platelets. Further, TXB2 production by day 7 platelets was completely blocked. The following tests wereperformed on the samples obtained from study participants before and after seven days of aspirin treatment:PFA-100 closure time with collagen/epinephrine cartridge, VerifyNow? (VN) Aspirin Assay, platelet aggregationand ATP secretion using AA, ADP, epinephrine and collagen as agonists.Results: Comparing the pre-treatment and day 7 values, methods that use AA as platelet agonist (AA-inducedplatelet aggregation/secretion and VN Aspirin Assay) showed high discriminative power. In contrast, results ofthe other tests showed considerable overlap between day 7 and day 0 values.Conclusions: Only assays that clearly distinguish between acetylated and non-acetylated platelet COX-1 are usefulfor establishing the antiplatelet effect of aspirin. The other tests are not suitable for this purpose.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
aspirin
aspirin resistance
platelet aggregation
platelet secretion
reference method
thromboxane
Megjelenés:Thrombosis Research. - 133 : 5 (2014), p. 811-816. -
További szerzők:Katona Éva (1961-) (klinikai biokémikus) Bereczky Zsuzsanna (1974-) (orvosi laboratóriumi diagnosztika szakorvos) Homoródi Nóra (1974-) (kardiológus) Balogh László (1976-) (kardiológus) Tóth Eszter (1975-) (vegyész) Péterfy Hajna Kiss Róbert Gábor Édes István (1952-) (kardiológus) Muszbek László (1942-) (haematológus, kutató orvos)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM043389
Első szerző:Kovács Emese Gyöngyvér (kardiológus)
Cím:New direct and indirect methods for the detection of cyclooxygenase 1 acetylation by aspirin; the lack of aspirin resistance among healthy individuals / Emese G. Kovács, Éva Katona, Zsuzsanna Bereczky, Nóra Homoródi, László Balogh, Eszter Tóth, Hajna Péterfy, Róbert G. Kiss, István Édes, László Muszbek
Dátum:2013
ISSN:0049-3848
Megjegyzések:Background: Aspirin is widely used in the prevention of acute atherothrombotic complications. It acetylates Ser529 residue in cyclooxygenase-1 (COX-1) and prevents thromboxane A2 (TXA2) formation from arachidonic acid (AA) in platelets. Laboratory methods used for the detection of aspirin effect provide inconsistent results. Methods: Two new methods were developed for the direct and indirect detection of COX-1 acetylation by aspirin in 108 healthy volunteers treated daily with 100 mg enteric-coated aspirin for 7 days. Monoclonal antibodies were raised against acetylated and non-acetylated nonapeptides corresponding to the amino acid sequence of human COX-1 525-533 residues. Using Western blotting technique the antibodies clearly distinguished between acetylated and non-acetylated COX-1 in platelet lysate. The second method measures AA-induced TXB2 production of platelets in diluted platelet rich plasma. Results: No acetylated COX-1 was detected in platelets before aspirin treatment. At the same time antibodies raised against non-acetylated peptide gave intense reaction with COX-1 on the Western blot. In contrast, after 7 days of aspirin treatment, with a single exception, only acetylated COX-1 could be detected in the platelet lysate. The non-responding volunteer showed full response to aspirin after controlled drug intake. In parallel experiments aspirin treatment for 7 days practically completely inhibited AA-induced TXB2 production by platelets. Conclusions: Chemical ("true") aspirin resistance, if it exists, must be a rarity among healthy individuals. The new methods could be used for detecting the acetylation of COX-1 by aspirin in patients on preventive aspirin therapy and for evaluating methods routinely used for such purpose.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
aspirin
aspirin resistance
Doktori Iskola
Megjelenés:Thrombosis Research. - 131 : 4 (2013), p. 320-324. -
További szerzők:Katona Éva (1961-) (klinikai biokémikus) Bereczky Zsuzsanna (1974-) (orvosi laboratóriumi diagnosztika szakorvos) Homoródi Nóra (1974-) (kardiológus) Balogh László (1976-) (kardiológus) Tóth Eszter (1975-) (vegyész) Péterfy Hajna Kiss Róbert Gábor Édes István (1952-) (kardiológus) Muszbek László (1942-) (haematológus, kutató orvos)
Pályázati támogatás:TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
K 78386
OTKA
MTA11003
MTA
NKFP-07-A1-2008-0127
Egyéb
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Laki Kálmán Doktori Iskola
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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