Non steroidal anti inflammatory patch

Major vascular events were increased by about a third by a coxib (rate ratio [RR] 1·37, 95% CI 1·14-1·66; p=0·0009) or diclofenac (1·41, 1·12-1·78; p=0·0036), chiefly due to an increase in major coronary events (coxibs 1·76, 1·31-2·37; p=0·0001; diclofenac 1·70, 1·19-2·41; p=0·0032). Ibuprofen also significantly increased major coronary events (2·22, 1·10-4·48; p=0·0253), but not major vascular events (1·44, 0·89-2·33). Compared with placebo, of 1000 patients allocated to a coxib or diclofenac for a year, three more had major vascular events, one of which was fatal. Naproxen did not significantly increase major vascular events (0·93, 0·69-1·27). Vascular death was increased significantly by coxibs (1·58, 99% CI 1·00-2·49; p=0·0103) and diclofenac (1·65, 0·95-2·85, p=0·0187), non-significantly by ibuprofen (1·90, 0·56-6·41; p=0·17), but not by naproxen (1·08, 0·48-2·47, p=0·80). The proportional effects on major vascular events were independent of baseline characteristics, including vascular risk. Heart failure risk was roughly doubled by all NSAIDs. All NSAID regimens increased upper gastrointestinal complications (coxibs 1·81, 1·17-2·81, p=0·0070; diclofenac 1·89, 1·16-3·09, p=0·0106; ibuprofen 3·97, 2·22-7·10, p<0·0001; and naproxen 4·22, 2·71-6·56, p<0·0001).

Two studies compared different types of non-selective NSAIDs, namely ibuprofen versus diclofenac and piroxicam versus indomethacin. The trials did not find any differences between these NSAID types, but both trials had small sample sizes. One trial reported no differences in pain intensity between treatment groups that used selective or non-selective NSAIDs. One other trial compared diflunisal with paracetamol and showed no difference in improvement from baseline on pain intensity score. One trial showed a better global improvement in favour of celecoxib versus tramadol.

NSAIDS have antipyretic activity and can be used to treat fever. [75] [76] Fever is caused by elevated levels of prostaglandin E2 , which alters the firing rate of neurons within the hypothalamus that control thermoregulation. [75] [77] Antipyretics work by inhibiting the enzyme COX, which causes the general inhibition of prostanoid biosynthesis ( PGE2 ) within the hypothalamus . [75] [76] PGE2 signals to the hypothalamus to increase the body's thermal set point. [76] [78] Ibuprofen has been shown more effective as an antipyretic than paracetamol (acetaminophen). [77] [79] Arachidonic acid is the precursor substrate for cyclooxygenase leading to the production of prostaglandins F, D & E.

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  • Citation tools Download this article to citation manager Arfè Andrea , Scotti Lorenza , Varas-Lorenzo Cristina , Nicotra Federica , Zambon Antonella , Kollhorst Bianca et al. Non-steroidal anti-inflammatory drugs and risk of heart failure in four European countries: nested case-control study BMJ 2016; 354 :i4857
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    Non steroidal anti inflammatory patch

    non steroidal anti inflammatory patch

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  • Citation tools Download this article to citation manager Arfè Andrea , Scotti Lorenza , Varas-Lorenzo Cristina , Nicotra Federica , Zambon Antonella , Kollhorst Bianca et al. Non-steroidal anti-inflammatory drugs and risk of heart failure in four European countries: nested case-control study BMJ 2016; 354 :i4857
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