Journal of internal medicine
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Both laboratory studies in healthy volunteers and clinical studies have suggested adverse interactions between antiplatelet drugs and other commonly used medications. Interactions described include those between aspirin and ibuprofen, aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), and the thienopyridine, clopidogrel, and drugs inhibiting CYP2C19, notably the proton pump inhibitors (PPI) omeprazole and esomeprazole. Other interactions between thienopyridines and CYP3A4/5 have also been reported for statins and calcium channel blockers. ⋯ However, there is less good evidence to support the clinical importance of these interactions. Again, a reasonable strategy is to avoid the chronic use of drugs that inhibit CYP2C19, notably PPIs, in subjects taking clopidogrel and use high dose H2 antagonists instead. Finally, anti-platelet agents probably interact with other drugs that affect platelet function such as selective serotonin reuptake inhibitors, and clinicians should probably judge patients taking such combination therapies as at high risk for bleeding.
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Drug-drug interactions can lead to reduced efficacy of medical treatment. Therapeutic failure may for instance result from combined treatment with an inhibitor of the specific pathway that is responsible for the generation of pharmacologically active drug metabolites. ⋯ Several examples of drugs will be discussed -clopidogrel, losartan, tamoxifen and codeine - to illustrate differences in the potential impact on drug treatment in clinical practice. We conclude that the combined use of cytochrome P450-blocking serotonin reuptake inhibitors and tamoxifen or codeine should be avoided, whereas the situation is much more complex regarding the use of proton pump inhibitors together with clopidogrel, and the evidence regarding cytochrome P450 inhibitor-dependent activation of losartan is inconclusive.
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Multicenter Study
Interleukin family member ST2 and mortality in acute dyspnoea.
The study objective was to investigate the prognostic utility and patient-specific characteristics of ST2 (suppression of tumorigenicity 2), assessed with a novel sensitive assay. ⋯ In patients presenting to the ED with acute dyspnoea, ST2 is a strong and independent predictor of 30-day and 1-year mortality and might improve risk stratification already provided by BNP or NT-proBNP.
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Review
Type 2 transglutaminase in Huntington's disease: a double-edged sword with clinical potential.
Huntington's disease (HD) is a dominant genetic neurodegenerative disorder. The pathology affects principally neurons in the basal ganglia circuits and terminates invariably in death. There is compelling necessity for safe and effective therapeutic strategies to arrest, or even retard the progression of the pathogenesis. ⋯ Type 2 transglutaminase (TG2) plays an important role both in apoptosis and autophagy regulation, and accumulates at high levels in cells under stressful conditions. TG2 inhibition, achieved either via drug treatments or genetic approaches, has been shown to be beneficial for the treatment of HD in animal models. In this review we will discuss the relevance of TG2 to the pathogenesis of HD, in an effort to define novel therapeutic avenues.
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Matrix Gla protein (MGP) is a calcification inhibitor and alterations in circulating MGP have been observed in different populations characterized by vascular calcification. We hypothesized that patients with calcific valvular aortic stenosis (AS) would have dysregulated circulating MGP levels. ⋯ A dysregulated MGP system may have a role in the development of left ventricular dysfunction in patients with symptomatic AS.