PubMed · 16368341
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Michel Carrier. 2006. Invited commentary.. https://doi.org/10.1016/j.athoracsur.2005.07.092
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The anhydrous sodium naproxen (ASN) can form several hydrated phases if maintained at different relative humidities (RH). The water uptake can promote crystallographic modifications, according to the amount of water. In a previous work, the authors showed that a dihydrated form could be obtained either by crystallization in water or by exposure of the anhydrous form to a RH of 55%. In the present work, the authors report about the formation and characterization of a new tetrahydrated form, obtained by exposing the ASN to RH >or= 75%. All the hydrated compounds were characterized by the combined use of several spectroscopic, thermal, and crystallographic techniques. The thermal stability of both the dihydrated and tetrahydrated compounds was also tested.
BACKGROUND: Gastrointestinal harm, known to occur with NSAIDs, is thought to be lower with NSAID and gastroprotective agent, and with inhibitors selective to cyclooxygenase-2 (coxibs) at usual plasma concentrations. We examine competing strategies for available evidence of reduced gastrointestinal bleeding in clinical trials and combine this evidence with evidence from clinical practice on whether the strategies work in the real world, whether guidance on appropriate prescribing is followed, and whether patients adhere to the strategies. METHODS: We used a series of systematic literature searches to find full publications of relevant studies for evidence about the efficacy of these different gastroprotection strategies in clinical trials, and for evidence that they worked and were adhered to in clinical practice--whether they were effective. We chose to use good quality systematic reviews and meta-analyses when they were available. RESULTS: Evidence of efficacy of coxibs compared to NSAIDs for upper gastrointestinal bleeding was strong, with consistent reductions in events of about 50% in large randomised trials (34,460 patients), meta-analyses of randomised trials (52,474 patients), and large observational studies in clinical practice (3,093 bleeding events). Evidence on the efficacy of NSAID plus gastroprotection with acid suppressants (proton pump inhibitors, PPIs, and histamine antagonists, H2As) was based mainly on the surrogate measure of endoscopic ulcers. The limited information on damage to the bowel suggested that NSAID plus PPI was more damaging than coxibs. Eleven observational studies studied 1.6 million patients, of whom 911,000 were NSAID users, and showed that 76% (range 65% to 90%) of patients with at least one gastrointestinal risk factor received no prescription for gastroprotective agent with an NSAID. The exception was a cohort of US veterans with previous gastrointestinal bleeding, where 75% had gastroprotection with an NSAID. When gastroprotection was prescribed, it was often described as inadequate. A single study suggested that patient adherence to prescribed gastroprotection was low. CONCLUSION: Evidence for efficacy of gastroprotection strategies with NSAIDs is limited. In clinical practice few patients who need gastroprotection get it, and those who get it may not take it. For coxibs, gastroprotection is inherent, although probably not complete.
Although considerable attention has been focused on elucidating the factors that drive inflammation, it is becoming clear that this "acceleration" state is offset by an internal "handbrake". A recent study has uncovered an essential component of this handbrake system, revealing that lipoxins trigger suppressors of cytokine signalling to dampen inflammatory responses to infection. This work bolsters the growing interest in understanding how inflammation is controlled from within and draws further attention to novel targets for drug development based on mimicking the actions of endogenous anti-inflammatory and pro-resolution signals.