Giht, suvremeni pogled na drevnu bolest = Gout, contemporary insight into an ancient disease / Nadica Laktašić Žerjavić, Nadia Hoteit, Dragica Soldo Jureša.
Sažetak

Giht je kronična metabolička, no istovremeno i upalna reumatska bolest koja nastaje kao posljedica hiperuricemije i taloženja kristala mononatrijeva urata. Glavni uzrok hiperuricemije je smanjeno bubrežno izlučivanje urata. U patogenezi upalnog odgovora na kristale urata važna je fagocitoza kristala od strane makrofaga koja dovodi do aktivacije inflamasoma NLRP3 i posljedičnog oslobađanja glavnog proupalnog citokina u gihtu interleukina 1β. Neadekvatno liječenje hiperuricemije dovodi do razvoja kroničnog gihta s tofima, značajnih strukturnih oštećenja zglobova s umanjenom funkcionalnom sposobnosti i kvalitetom života. Stoga je važno dugotrajno liječenje usmjereno k cilju održavanja koncentracije urata <350 umol/L, a u težem obliku bolesti s tofima <300 umol/L. Akutni artritis u gihtu i akutizaciju kroničnog gihta treba liječiti protuupalnim lijekovima: nesteroidnim antireumaticima, kolhicinom ili glukokortikoidima, uglavnom po monoterapijskom principu. Pacijente s gihtom treba pažljivo pratiti radi udruženih bolesti, posebice bubrežne bolesti, hipertenzije, metaboličkog sindroma i povišenog kardiovaskularnog rizika.; Gout is a chronic metabolic but at the same time inflammatory rheumatic disease which develops as a cosequence of increased urate concentration and deposites of monosodium urate crystals. The main cause of hyperuricaemia is renal urate underexcretion. In the pathogenesis of the inflammatory response to urate crystals, the phagocytosis of crystals by the macrophages is important, leading to activation of the NLRP3 inflammasome and the consequent release of the major proinflammatory cytokine interleukin 1β. Inadequate long-term treatment of hyperuricaemia leads to the development of chronic gout, which causes significant structural joint damage, disability and reduced quality of life. Therefore, long term urate lowering treatment aimed at maintaining urate concentrations <350 umol/L in early disease and <300 umol/L in chronic tophaceous disease is mandatory. Acute arthritis in gout, or a flaire in chronic arthritis should be treated with anti-inflammatory drugs: non-steroidal anti-inflammatory drugs, colchicine or glucocorticoids, mainly as a monotherapy. Patients with gout should be closely monitored for associated comorbidities, especially renal disease, hypertension, metabolic syndrome, and elevated cardiovascular risk.