Gout

@article{Dalbeth2016Gout,
  title={Gout},
  author={Nicola Dalbeth and Tony Raymond Merriman and Lisa K. Stamp},
  journal={The Lancet},
  year={2016},
  volume={388},
  pages={2039-2052}
}

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Osteoarthritis, which is thought to predispose patients to monosodium urate crystal deposition in their joints, is becoming more prevalent as a consequence of increased longevity.
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It is suggested that a reactive treat- to-avoid-symptoms approach may be a reasonable strategy with ULT instead of a proactive treat-to-target strategy because the latter has not been adequately tested.
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The main aim in gout is to lower serum uric acid levels to a pre-established target; there are different urate-lowering drugs (xanthine oxidase inhibitors, uricosurics and uricases) through which this can be achieved.
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Reactive oxygen species are essential for forming NETs and for allowing the resolution of inflammation in gout, since tophi are composed ofNETs and densely packed MSU crystals.
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Genetic data may inform assessment of disease prognosis in individuals with hyperuricaemia or established gout, personalised lifestyle advice, selection and dosing of urate-lowering therapy, and prevention of serious medication adverse effects.
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