Pharmacokinetic interactions between arbaprostil and aspirin in humans

Hsyu, Poe‐Hirr; Cox, James H.; Pullen, Robert H.; Gee, Winnie L.; Euler, Arthur R.

doi:10.1002/bdd.2510100408

Cited by 7 publications

(2 citation statements)

References 15 publications

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“…When high dose aspirin (975mg 4 times a day for 6 days) was administered with arbaprostil (50llg) the pharmacokinetics of aspirin were not changed by arbaprostil. [69) But more data are needed to make clear conclusions on many of these interactions. !70] The studies reviewed here show that there is a lack of significant effects of sucralfate on the absorption of the NSAIDs that are frequently used in clinical practice.…”

Section: Sucralfate and Other Mucosal Protective Agentsmentioning

confidence: 98%

Pharmacokinetic-Pharmacodynamic Drug Interactions with Nonsteroidal Anti-Inflammatory Drugs

Brouwers¹,

Smet

1994

Clinical Pharmacokinetics

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The nonsteroidal anti-inflammatory drugs (NSAIDs) are very commonly prescribed, especially in the elderly population. In many countries more than 10 different NSAIDs are available. As the older pyrazole compounds like phenylbutazone, oxyphenbutazone and azapropazone are most prone to pharmacokinetic interactions, the use of these compounds should be avoided where possible. Acidic NSAIDs interact with bile acid-binding resins, resulting in decreased concentrations of NSAIDs in the blood. In earlier reports it was suggested that the absorption of NSAIDs was affected by antacids and sucralfate. More recently, it was shown that there is delayed absorption of these drugs, but there is no difference in the extent of absorption. Only salicylates had their urinary secretion enhanced by antacids, which increase the urinary pH to values > 7. Histamine H2-receptor antagonists can be combined safely with NSAIDs. The concomitant administration of probenecid increased the blood concentration of NSAIDs, so an enhanced anti-inflammatory effect can be expected when these 2 drugs are combined. More importantly, NSAIDs can cause pharmacokinetic drug-drug interactions with other drugs. As can be expected, interactions with drugs that have a small therapeutic window are most likely to be of clinical significance. For example, lithium, medium to high dose methotrexate and, to a lesser extent, cyclosporin may be affected by concomitant administration of an NSAID. Aspirin (acetylsalicylic acid) and/or pyrazoles interact with oral anticoagulants, oral antihyperglycaemic agents and the anticonvulsants phenytoin and valproic acid (sodium valproate). Elevation of blood concentrations of these agents can be potentially dangerous. Similarly, NSAIDs interact with digoxin. This interaction is most likely to occur in the elderly, in neonates or in patients with renal impairment. Indomethacin can influence the blood concentrations of aminoglycosides in neonates. Unfortunately, this effect seems unpredictable, so practical therapeutic recommendations cannot be made. When NSAIDs are combined with salicylates or diflunisal, the blood concentrations of the salicylate or diflunisal may increase. However, the clinical relevance of this increase in drug concentration seems to be of minor importance. Gastrointestinal bleeding caused by NSAIDs is the most dangerous when it results from a mixed pharmacokinetic/pharmacodynamic interaction; however, patients are also at risk when pharmacodynamic interactions only are involved.

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Section: Sucralfate and Other Mucosal Protective Agentsmentioning

confidence: 98%

Pharmacokinetic-Pharmacodynamic Drug Interactions with Nonsteroidal Anti-Inflammatory Drugs

Brouwers¹,

Smet

1994

Clinical Pharmacokinetics

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“…Arylesterase activity was expressed in units per liter. One unit is defined as 1 mmol phenyl acetate hydrolyzed per minute (Hsyu et al, 1989).…”

Section: Determination Of Arylesterase Activitymentioning

confidence: 99%

Effect of Glimepiride on Paraoxonase Activity

Demir

Nadaroğlu

Demir

2006

Pharmaceutical Biology

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In this study, the effect of glimepiride on serum paraoxonase activity (EC 3.1.8.1.) has been investigated in vitro. The inhibition and activation effects of this drug on serum paraoxonase activity was measured spectrophotometrically using paraoxon as the substrate. The phenotypic distribution of paraoxonase was determined using the dual substrate paraoxon and phenyl acetate as substrates. It was observed that glimepiride inhibited serum paraoxonase activity. In addition, an in vivo study was performed for glimepiride in Sprague-Dawley rats. It was demonstrated that paraoxonase in serum, liver, and heart of Sprague-Dawley rat was significantly inhibited.

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A review of interaction studies between non-steroidal anti-inflammatory drugs and H2-receptor antagonists or prostaglandin analogues

Dixon¹,

Page²

1992

Side-Effects of Anti-Inflammatory Drugs 3

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Pharmacokinetic interactions between arbaprostil and aspirin in humans

Cited by 7 publications

References 15 publications

Pharmacokinetic-Pharmacodynamic Drug Interactions with Nonsteroidal Anti-Inflammatory Drugs

Pharmacokinetic-Pharmacodynamic Drug Interactions with Nonsteroidal Anti-Inflammatory Drugs

Effect of Glimepiride on Paraoxonase Activity

A review of interaction studies between non-steroidal anti-inflammatory drugs and H2-receptor antagonists or prostaglandin analogues

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