Aspirin interactions

In some individuals, ginkgo and aspirin interact to reduce the production of platelets, particles that are essential in the formation of blood clots, increasing the severity of bruising and bleeding. 

A systematic overview of major ACE inhibitor trials (CONSENSUS II, AIRE, TRACE, SMILE) found a trend toward less benefit from ACE inhibitors among aspirin users (109). Although the interaction was not statistically significant, the authors concluded that the data did not refute the hypothesis of a major aspirin interaction with ACE inhibitors, especially because patients taking aspirin had only 60% of the benefit seen in patients not taking it. 

WiUiams RL, Upton RA, Btrskin IN, Jones RM. Ketoprofen-aspirin interactions. Clin Pharmacol Ther 1981 30(2) 226-31. 

Brooks PM, Khoi TK Flurbiprofen-aspirin interaction a double-blind crossover stuity CurrMedRes 0pm (1977) 5,53-7. 

Williams RL, Upton RA, Bu in JN, Jones RM. Keteprofen-aspirin interactions. Clin Phar-macol Ther( 9Z ) 30,226-31. 

Segre EJ, Caplin H Forchielli E, Runkel R, Sevelius H. Naproxen-aspirin interactions in maa Clin Pharmacol Ther (1974) 15,374-9. 

Brool PH Walker JJ, Bell MA, Buchanan WW, Rhymer AR. Indomediacin—aspirin interaction a clinical appraisal. BMJ (1975) 3,69-71. 

Verzino E, Kaplan B, Ashley JV, Burdette M. Verapamil-aspirin interaction. Ann Pharma-co er 99A)2Z, 536-7. 

BasuTK. Vitamin C-aspirin interactions. IntJ Vitam NutrRes (y9 2) 23 (Suppl), 83-90. 

Das, N., and Nebioglu, S., 1992, Vitamin C aspirin interactions in laboratory animals, J. Clin. Pharm. Ther. 17 343-346. 

Continuum models of solvation treat the solute microscopically, and the surrounding solvent macroscopically, according to the above principles. The simplest treatment is the Onsager (1936) model, where aspirin in solution would be modelled according to Figure 15.4. The solute is embedded in a spherical cavity, whose radius can be estimated by calculating the molecular volume. A dipole in the solute molecule induces polarization in the solvent continuum, which in turn interacts with the solute dipole, leading to stabilization. 

Interactions with caffeine and aspirin can increase the effects of ephedrine. Norepinephrine works in part by increasing the levels of cyclic aminomethyl propanol (AMP) in cells. Caffeine inhibits the enzyme that breaks down cyclic AMP. Together, ephedrine makes more cyclic AMP, and caffeine prevents it from breaking down. Aspirin inhibits the receptors that turn off release of norepinephrine. 

As the solvent mixture also contained 225 mg of tetramethyl ammonium hydroxide pentahydrate per liter at a high water content (75%), the surface of the reverse phase would have been largely covered with the tetramethyl ammonium hydroxide pentahydrate. This would have acted as an adsorbed ion exchange stationary phase. It is clear that the free acids, salicylic acid, acetylsalicylic acid (aspirin) and benzoic acid were retained largely by ionic interactions with adsorbed basic ion exchanger and partly by dispersive interactions with the exposed reversed phase. The acetaminophen and the caffeine, on the other hand, being unionized substances, were retained only by dispersive interactions with the exposed reversed phase. 

This was largely influenced by the high-dose UFH group in 1ST (OR 1.38, 95% Cl 1.05-1.82). An interaction by UFH dose (p = 0.01) on recurrent stroke risk with combination UFH-aspirin therapy compared to aspirin monotherapy was observed, with a trend toward increased risk of recurrent stroke with high-dose UFH + aspirin (OR 1.22, 95% Cl 0.92-1.62) and a trend toward reduced risk with low-dose UFH + aspirin (OR 0.75, 95% Cl 0.56-1.03), equivalent to 10 fewer (95% Cl 0-20 fewer) recurrent strokes per 1000 patients treated. They found a small, but significant beneht of LMWH over aspirin in the prevention of symptomatic DVT, equivalent to 10 (95% Cl 0-30) fewer DVTs per 1000 patients treated. Compared with aspirin, anticoagulants were associated with nonsignificantly fewer symptomatic PEs (OR 0.85, 95% Cl 0.55-1.32). There were fewer PEs with the combination of UEH and aspirin (OR 0.58, 95% Cl 0.34—1.00), equivalent to 5 fewer (Cl 0-10) PEs per 1000 patients treated. However, the overall incidence of symptomatic DVT and PE was low (1.1% and 0.7%). 

Many dietary supplements have antiplatelet activity, which may increase the risk of bleeding when used concurrently with anticoagulants. Feverfew inhibits cyclooxygenase and phospholipase A2 and may interact with anticoagulants and potentiate the antiplatelet effect of aspirin. Other supplements that possess antiplatelet activity include but are not limited to garlic, ginkgo, vitamin E, vitamin A, and selenium. 

In many ways, the story of the discovery of aspirin is typical for the way in which new drugs are invented and developed in pharmaceutical research laboratories, where many individuals have to make a contribution and where it is often difficult to fathom completely what thought processes, suggestions and interactions lead to a successful new drug. 

For a drug to interact with a target, it has to be present in sufficient concentration in the fluid medium surrounding the cells with receptors. Pharmacokinetics (PK) is the study of the kinetics of absorption, distribution, metabolism, and excretion (ADME) of drugs. It analyzes the way the human body deals with a drug after it has been administered, and the transportation of the drug to the specihc site for drug-receptor interaction. For example, a person has a headache and takes an aspirin to abate the pain. How does the aspirin travel from our mouth to reach the site in the brain where the headache is and act to reduce the pain ... 

A contact dermatitis occurs infrequently. Because feverfew also inhibits human blood platelet aggregation, interactions are possible with antithrombotic medications such as aspirin or warfarin (Groenewegen and Heptinstall 1990). Abrupt discontinuation of feverfew by people taking it chronically for treatment of migraine can produce rebound withdrawal symptoms. These consist of migraines, anxiety, poor sleep patterns, and stiffness of the muscles and joints. 

Meune, C., et al. (2000). Interaction between angiotensin-converting enzyme inhibitors and aspirin, a review, Eur. J. Clin. Pharmacol., 56, 609-620. 

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