Difference in risk of gastrointestinal complications between users of enteric-coated and buffered low-dose aspirin

2014 ◽  
Vol 52 (03) ◽  
pp. 181-191 ◽  
Author(s):  
Mitsutaka Takada ◽  
Mai Fujimoto ◽  
Kouichi Hosomi
Keyword(s):  
Low Dose ◽  
Gastrointestinal Complications ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Enteric Coated

Risk of gastrointestinal complications associated to NSAIDs, low-dose aspirin and their combinations: Results of a pharmacovigilance reporting system

2016 ◽  
Vol 104 ◽  
pp. 108-114 ◽  
Author(s):  
Concetta Rafaniello ◽  
Carmen Ferrajolo ◽  
Maria Giuseppa Sullo ◽  
Maurizio Sessa ◽  
Liberata Sportiello ◽  
...  
Keyword(s):  
Low Dose ◽  
Reporting System ◽  
Gastrointestinal Complications ◽  
Dose Aspirin ◽  
Low Dose Aspirin

Aspirin-insensitive thromboxane biosynthesis in essential thrombocythemia is explained by accelerated renewal of the drug target

Blood ◽  
2012 ◽  
Vol 119 (15) ◽  
pp. 3595-3603 ◽  
Author(s):  
Silvia Pascale ◽  
Giovanna Petrucci ◽  
Alfredo Dragani ◽  
Aida Habib ◽  
Francesco Zaccardi ◽  
...  
Keyword(s):  
Platelet Count ◽  
Essential Thrombocythemia ◽  
Low Dose ◽  
Once Daily ◽  
Dosing Interval ◽  
Aspirin Dose ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Enteric Coated Aspirin ◽  
Enteric Coated

Abstract Essential thrombocythemia (ET) is characterized by enhanced platelet generation and thrombotic complications. Once-daily low-dose aspirin incompletely inhibits platelet thromboxane A2 (TXA2) in the majority of ET patients. In the present study, we investigated the determinants of aspirin-insensitive platelet TXA2 biosynthesis and whether it could be further suppressed by changing the aspirin dose, formulation, or dosing interval. In 41 aspirin-treated ET patients, the immature platelet count predicted serum TXB2 independently of platelet count, age, JAK-2 V617F mutation, or cytoreduction (β = 3.53, P = .001). Twenty-one aspirin-treated patients with serum TXB2 ≥ 4 ng/mL at 24 hours after dosing were randomized to the following 7-day regimens in a crossover design: enteric-coated aspirin 100 mg twice daily, enteric-coated aspirin 200 mg once daily, or plain aspirin 100 mg once daily. A twice-daily regimen caused a further 88% median (IQR, 78%-92%, P < .001) TXB2 reduction and normalized the functional platelet response to aspirin, as assessed by urinary 11-dehydro-TXB2 excretion and the VerifyNow Aspirin assay. Doubling the aspirin dose reduced serum TXB2 only partially by 39% median (IQR, 29%-54%, P < .05). We conclude that the abnormal megakaryopoiesis characterizing ET accounts for a shorter-lasting antiplatelet effect of low-dose aspirin through faster renewal of platelet cyclooxygenase-1, and impaired platelet inhibition can be rescued by modulating the aspirin dosing interval rather than the dose.

Effects of Non-Steroidal Anti-Inflammatory Drugs and COX-2 Inhibitors on Aspirin-Induced Platelet Inhibition.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 531-531
Author(s):  
Carol Sun ◽  
Angela Bergeron ◽  
Jennifer Wood ◽  
Jo Ellen Schweinle ◽  
Frank L. Lanza ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Naproxen Sodium ◽  
Low Dose ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Inflammatory Drugs ◽  
Cox 2 ◽  
Enteric Coated ◽  
Cox 2 Inhibitors ◽  
Initial Drug

Abstract Low dose aspirin has been widely used as a cardiac protective drug. It acts by inhibiting platelet activation and aggregation through the cyclooxygenase-1 pathway. However, such effects may be affected by short-term use of other drugs such as non-steroidal anti-inflammatory drugs (NSAIDs). We have conducted a multiple-dose, single-blind, parallel-group study to investigate the effects of over-the-counter NSAIDs and COX-2 inhibitors on arachidonic-induced platelet aggregation and thromboxane B2 (TxB2) production. We recruited 87 healthy individuals of 40-75 years of age, who met the inclusion and exclusion criteria by pretest screening. All subjects received 81 mg of aspirin (non-enteric coated and chewable) daily for eight days. Two hours after the 81 mg aspirin dose, the subjects received one of following drugs: acetaminophen (4 doses of 1000 mg daily), ibuprofen (3 doses of 400 mg daily), naproxen sodium (440 mg morning and 220 mg evening), a higher dose of aspirin (4 doses of 650 mg daily), celecoxib (2 doses of 200 mg daily) and rofecoxib (1 dose of 25 mg daily). Control individuals received only 81 mg of aspirin. Citrated blood was obtained before the treatment and at 2, 6, 12, and 24 hr during the first day and an identical schedule after 7 days of dosing (Day 8 of treatment). Platelet function was measured by arachidonic acid-induced platelet aggregation and serum levels of TxB2. We found that the maximal inhibitory effect (more than 85% reduction in aggregation) of 81 mg aspirin was reached more than 24 hr after initial drug intake; whereas it was observed within 6 hr in subjects receiving randomized 2600 mg of aspirin (but only took 1300 mg at time of blood draw). Similar to the higher dose of aspirin, both ibuprofen and naproxen sodium also significantly accelerated the inhibitory effects of low dose aspirin on platelet aggregation (Paired Student t test, p &lt; 0.01). In comparison, acetaminophen and two COX-2 inhibitors showed no additive effects with 81 mg of aspirin. Consistent with aggregation studies, the inhibition of TxB2 production was significantly greater than those with 81 mg of aspirin only at 6, 12, and 24 hr after initial drug intake for 2600 mg of aspirin, ibuprofen, and naproxen, but not for acetaminophen, celecoxib, and rofecoxib. Contrary to a report by Catella-Lawson et al, we found that ibuprofen did not interfere, but rather slightly enhanced, aspirin-induced inhibition of platelet aggregation. The reason for the discrepancy remains unknown, but may be attributed to the type of aspirin used (enteric-coated vs. non-enteric-coated) and different schedules of drug intakes between the two studies. Finally, it may also be due to the fact that our subjects were in their normal environments and not in a clinical research unit. In conclusion, we found that acetaminophen and COX-2 inhibitors did not affect the course of the low-dose aspirin action on platelets. Although ibuprofen and naproxen have had no additive effects, they accelerated the action of 81 mg of aspirin on platelet aggregation.

Difference between the frequencies of antisecretory drug prescriptions in users of buffered vs. enteric-coated low-dose aspirin therapies

2013 ◽  
Vol 51 (10) ◽  
pp. 807-815 ◽  
Author(s):  
Hiroko Hachiken ◽  
Ai Murai ◽  
Kyoichi Wada ◽  
Takeshi Kuwahara ◽  
Kouichi Hosomi ◽  
...  
Keyword(s):  
Low Dose ◽  
Drug Prescriptions ◽  
Dose Aspirin ◽  
Antisecretory Drug ◽  
Low Dose Aspirin ◽  
Enteric Coated
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