Gouty Arthritis: Efficacy and safety of treatment

The maximum incidence of gouty arthritis is observed in the fifth decade of life; Although the disease predominantly affects men, the prevalence of gout increases in postmenopausal women with hypertension treated with diuretics or with renal failure.

Obesity, alcohol consumption, administration of diuretics, high intake of meat, seafood, high consumption of fructose in foods and beverages and renal dysfunction are factors associated with an increased risk of gout.

Likewise, patients with gout have reported an increased risk of cardiovascular disease, beyond that conferred by conventional cardiovascular risk factors. Symptoms of acute gouty arthritis appear rapidly, within 24 hours; The affected joints, most commonly the metatarsophalangeal joints, are edematous and inflamed and with intense pain.

According to the American College of Rheumatology Guidelines for Management of Gout 2012, non-steroidal anti-inflammatory drugs (NSAIDs) such as naproxen, indomethacin and sulindac, corticosteroids and oral colchicine represent the first-line treatment options for the treatment of acute gout; Some drug combinations can be used for severe or refractory episodes of gout.

Non-selective NSAIDs, however, are associated with significant gastrointestinal adverse effects, for example, perforations, ulcers and bleeding.

Etoricoxib is a highly selective inhibitor of cyclooxygenase (COX) 2, with anti-inflammatory, analgesic and antipyretic properties, associated with lower risk of gastrointestinal adverse effects, compared to traditional NSAIDs.

Indomethacin is considered the most potent non-selective NSAID, with greater inhibition of COX-1 than of COX-2. The aim of the present systematic review and meta-analysis was to compare the efficacy and safety of etoricoxib and indomethacin for the treatment of acute gout.

Prostaglandins (PG), derived from arachidonic acid by COX isoenzymes, play an essential role in the inflammation of various joint diseases, including gout.

COX-1 is constitutively expressed in most cells of the organism and intervenes in numerous physiological functions, such as cell epithelial protection, platelet aggregation and regulation of renal blood flow.

COX-2, on the other hand, is synthesized essentially in response to inflammatory stimuli; Even so, both isoforms participate in the acute inflammation process.

Gastrointestinal disorders are the most frequent adverse effects, in association with the use of etoricoxib and indomethacin. Gastric ulcer lesions induced by NSAIDs are a consequence of systemic effects-COX inhibition is associated with platelet inhibition and reduced synthesis of prostanoids-and mucosal injury.

Protective prostaglandins are mainly PGE2 and PGI2, and their inhibition through the use of NSAIDs may induce less secretion of mucus and bicarbonate, and reduce mucosal blood flow and epithelial proliferation, making the mucosa more susceptible To toxic factors, endogenous (acid) and exogenous (infection by Helicobacter pylori). In addition, NSAIDs are weak acids that can cause, per se, damage to the gastrointestinal mucosa.

PGE2 and PGI2 are vasodilators, so their inhibition could be associated with focal ischemia; In this scenario, selective COX-2 inhibitors do not decrease blood flow to the gastric mucosa. The reduction of thromboxane A2 synthesis, by means of the platelet inhibition of COX-1, increases the risk of bleeding in the presence of active gastrointestinal hemorrhage.

Both COX-1 and COX-2 are expressed in the kidneys; The inhibition of renal prostaglandin E2 induces sodium retention, edema and aggravation of arterial hypertension. Inhibition of renal synthesis of prostacyclines decreases renal blood flow and glomerular filtration rate.

The findings of the present meta-analysis suggest that etoricoxib and indomethacin exert similar efficacy for the relief of acute pain in gouty arthritis; however, etoricoxb is better tolerated since it is associated with lower risk of adverse effects, especially of gastrointestinal adverse effects.

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