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Concept: Non-steroidal anti-inflammatory drug


Objective To characterise the determinants, time course, and risks of acute myocardial infarction associated with use of oral non-steroidal anti-inflammatory drugs (NSAIDs).Design Systematic review followed by a one stage bayesian individual patient data meta-analysis.Data sources Studies from Canadian and European healthcare databases.Review methods Eligible studies were sourced from computerised drug prescription or medical databases, conducted in the general or an elderly population, documented acute myocardial infarction as specific outcome, studied selective cyclo-oxygenase-2 inhibitors (including rofecoxib) and traditional NSAIDs, compared risk of acute myocardial infarction in NSAID users with non-users, allowed for time dependent analyses, and minimised effects of confounding and misclassification bias. Exposure and outcomes Drug exposure was modelled as an indicator variable incorporating the specific NSAID, its recency, duration of use, and dose. The outcome measures were the summary adjusted odds ratios of first acute myocardial infarction after study entry for each category of NSAID use at index date (date of acute myocardial infarction for cases, matched date for controls) versus non-use in the preceding year and the posterior probability of acute myocardial infarction.Results A cohort of 446 763 individuals including 61 460 with acute myocardial infarction was acquired. Taking any dose of NSAIDs for one week, one month, or more than a month was associated with an increased risk of myocardial infarction. With use for one to seven days the probability of increased myocardial infarction risk (posterior probability of odds ratio >1.0) was 92% for celecoxib, 97% for ibuprofen, and 99% for diclofenac, naproxen, and rofecoxib. The corresponding odds ratios (95% credible intervals) were 1.24 (0.91 to 1.82) for celecoxib, 1.48 (1.00 to 2.26) for ibuprofen, 1.50 (1.06 to 2.04) for diclofenac, 1.53 (1.07 to 2.33) for naproxen, and 1.58 (1.07 to 2.17) for rofecoxib. Greater risk of myocardial infarction was documented for higher dose of NSAIDs. With use for longer than one month, risks did not appear to exceed those associated with shorter durations.Conclusions All NSAIDs, including naproxen, were found to be associated with an increased risk of acute myocardial infarction. Risk of myocardial infarction with celecoxib was comparable to that of traditional NSAIDS and was lower than for rofecoxib. Risk was greatest during the first month of NSAID use and with higher doses.

Concepts: Cyclooxygenase, Osteoarthritis, Non-steroidal anti-inflammatory drug, Paracetamol, Ibuprofen, Aspirin, Celecoxib, Naproxen



 To investigate the cardiovascular safety of non-steroidal anti-inflammatory drugs (NSAIDs) and estimate the risk of hospital admission for heart failure with use of individual NSAIDs.

Concepts: Hypertension, Glucocorticoid, Non-steroidal anti-inflammatory drug, Anti-inflammatory, Paracetamol, ACE inhibitor


Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used and have been associated with increased cardiovascular risk. Nonetheless, it remains unknown whether use of NSAIDs is associated with out-of-hospital cardiac arrest (OHCA).

Concepts: Non-steroidal anti-inflammatory drug, Anti-inflammatory, Paracetamol


Certain non-steroidal anti-inflammatory drugs (NSAIDs) (e.g., rofecoxib [Vioxx]) increase the risk of heart attack and stroke and should be avoided in patients at high risk of cardiovascular events. Rates of cardiovascular disease are high and rising in many low- and middle-income countries. We studied the extent to which evidence on cardiovascular risk with NSAIDs has translated into guidance and sales in 15 countries.

Concepts: Myocardial infarction, Atherosclerosis, Cardiovascular disease, Cyclooxygenase, Non-steroidal anti-inflammatory drug, Diclofenac, Celecoxib, Etoricoxib


The common non-steroidal anti-inflammatory drug ibuprofen has been associated with a reduced risk of some age-related pathologies. However, a general pro-longevity role for ibuprofen and its mechanistic basis remains unclear. Here we show that ibuprofen increased the lifespan of Saccharomyces cerevisiae, Caenorhabditis elegans and Drosophila melanogaster, indicative of conserved eukaryotic longevity effects. Studies in yeast indicate that ibuprofen destabilizes the Tat2p permease and inhibits tryptophan uptake. Loss of Tat2p increased replicative lifespan (RLS), but ibuprofen did not increase RLS when Tat2p was stabilized or in an already long-lived strain background impaired for aromatic amino acid uptake. Concomitant with lifespan extension, ibuprofen moderately reduced cell size at birth, leading to a delay in the G1 phase of the cell cycle. Similar changes in cell cycle progression were evident in a large dataset of replicatively long-lived yeast deletion strains. These results point to fundamental cell cycle signatures linked with longevity, implicate aromatic amino acid import in aging and identify a largely safe drug that extends lifespan across different kingdoms of life.

Concepts: Genome, Chromosome, Fungus, Model organism, Cell cycle, Saccharomyces cerevisiae, Non-steroidal anti-inflammatory drug, Paracetamol


Folklore remedies for pain and inflammation in rheumatoid arthritis include the application of magnets and copper to the skin. Despite the popular use of devices containing magnets or copper for this purpose, little research has been conducted to evaluate the efficacy of such treatments.

Concepts: Inflammation, Clinical trial, Rheumatoid arthritis, Rheumatology, Pain, Non-steroidal anti-inflammatory drug, Anti-inflammatory, Acupuncture



Objective To investigate whether symptomatic treatment with non-steroidal anti-inflammatory drugs (NSAIDs) is non-inferior to antibiotics in the treatment of uncomplicated lower urinary tract infection (UTI) in women, thus offering an opportunity to reduce antibiotic use in ambulatory care.Design Randomised, double blind, non-inferiority trial.Setting 17 general practices in Switzerland.Participants 253 women with uncomplicated lower UTI were randomly assigned 1:1 to symptomatic treatment with the NSAID diclofenac (n=133) or antibiotic treatment with norfloxacin (n=120). The randomisation sequence was computer generated, stratified by practice, blocked, and concealed using sealed, sequentially numbered drug containers.Main outcome measures The primary outcome was resolution of symptoms at day 3 (72 hours after randomisation and 12 hours after intake of the last study drug). The prespecified principal secondary outcome was the use of any antibiotic (including norfloxacin and fosfomycin as trial drugs) up to day 30. Analysis was by intention to treat.Results 72/133 (54%) women assigned to diclofenac and 96/120 (80%) assigned to norfloxacin experienced symptom resolution at day 3 (risk difference 27%, 95% confidence interval 15% to 38%, P=0.98 for non-inferiority, P<0.001 for superiority). The median time until resolution of symptoms was four days in the diclofenac group and two days in the norfloxacin group. A total of 82 (62%) women in the diclofenac group and 118 (98%) in the norfloxacin group used antibiotics up to day 30 (risk difference 37%, 28% to 46%, P<0.001 for superiority). Six women in the diclofenac group (5%) but none in the norfloxacin group received a clinical diagnosis of pyelonephritis (P=0.03).Conclusion Diclofenac is inferior to norfloxacin for symptom relief of UTI and is likely to be associated with an increased risk of pyelonephritis, even though it reduces antibiotic use in women with uncomplicated lower UTI.Trial registration NCT01039545.

Concepts: Kidney, Urinary tract infection, Symptom, Symptomatic treatment, Non-steroidal anti-inflammatory drug, Diclofenac, Antibiotic, Ciprofloxacin


INTRODUCTION: Sweet’s syndrome is an acute neutrophilic dermatosis characterized by a diffuse dermal infiltrate of mature neutrophils. In most cases, it occurs as an isolated phenomenon (idiopathic Sweet’s syndrome) but it can be drug induced or associated with a variety of underlying diseases such as infections, neoplasms, and chronic inflammatory diseases. The association between Sweet’s syndrome and ankylosing spondylitis is rare. Only a few cases have been reported in the literature. We report a new case in which we describe an outbreak of acute neutrophilic dermatosis revealing ankylosing spondylitis. CASE PRESENTATION: A 33-year-old Moroccan man presented with large-joint polyarthralgia, inflammatory pain in his buttocks and lower lumbar spine, fever and skin lesions. On examination, the patient had a low-grade fever, six tender but not swollen joints, limitation of motion of the lumbar spine, and painful erythematous maculopapules over his face, neck, and hands. Laboratory tests showed hyperleukocytosis, and elevated erythrocyte sedimentation rate and C-reactive protein. The immunological tests and infectious disease markers were negative. Investigations for an underlying neoplastic disease remained negative. Magnetic resonance imaging showed a bilateral sacroiliitis. Skin biopsy findings were consistent with Sweet’s syndrome. The diagnosis of Sweet’s syndrome associated with ankylosing spondylitis was established. Nonsteroid anti-inflammatory drugs were started and the patient showed rapid clinical and biological improvement. CONCLUSION: Three observations of the association between Sweet’s syndrome and spondylarthropathy have been reported in the literature. The cause of this association remains unclear. Some hypotheses have been developed, but further studies are needed to confirm or refute them.

Concepts: Inflammation, Cancer, Infectious disease, Infection, Lumbar vertebrae, Rheumatoid arthritis, Non-steroidal anti-inflammatory drug, C-reactive protein