Therapeutic options for gout treatment

Giht je jedna od najčešćih reumatskih bolesti i njegova incidencija i prevalencija su u stalnom porastu. Iako je pozadina ove bolesti već odavno poznata, često se kasno dijagnosticira i nepravilno liječi što dovodi do smanjene kvalitete života i radne produktivnosti oboljelih te većih troškova zdravstvenog sustava. Giht nastaje kao posljedica odlaganja kristala mokraćne kiseline u zglobove i okolna tkiva što uzrokuje upalu i u konačnici strukturno oštećenje zglobova. Glavni rizični čimbenik za nastanak gihta je povećana razina mokraćne kiseline u serumu (hiperuricemija). Hiperuricemija može nastati zbog povećane sinteze ili smanjenog izlučivanja mokraćne kiseline koja je završni produkt metabolizma purina. Razlikujemo četiri klinička stadija gihta, a to su asimptomatska hiperuricemija, akutni napad gihta, asimptomatski period između dva napada te kronični giht s prisutnim tofima. Glavni ciljevi liječenja su ukloniti simptome akutnog napada, smanjiti rizik nastanka novih napada i sniziti razinu mokraćne kiseline u serumu. Lijekovi koji se najčešće koriste za smirivanje simptoma akutnog napada su nesteroidni protuupalni lijekovi, kolhicin i kortikosteroidi. Pacijenti koji imaju ponavljajuće akutne napade, bubrežne kamence ili tofe moraju uzimati kroničnu terapiju lijekovima koji snižavaju razinu mokraćne kiseline u serumu, a to su inhibitori ksantin oksidaze (alopurinol i febuksostat), urikozurici (probenecid, benzbromaron, sulfinpirazon) te rekombinantne urikaze (peglotikaza). Odnedavno su na tržištu dostupni i novi lijekovi kao što su IL-1β inhibitori za terapiju akutnog napada te lesinurad i topiroksostat za kroničnu terapiju gihta. Osim toga, u tijeku su brojna istraživanja za razvoj novih lijekova.Gout is one of the most common rheumatic diseases and its incidence and prevalence are constantly rising. Although the background of this disease has long been known, it is often late diagnosed and improperly treated which leads to impaired quality of life, loss of work productivity and higher costs of healthcare system. Gout is result of uric acid crystals deposition in joints and surrounding tissues which causes inflammation and ultimately structural joint damage. The main risk factor for gout is increased serum uric acid level (hyperuricemia). Uric acid is the final product of purine metabolism and hyperuricemia may occur due to increased synthesis or reduced secretion of uric acid. Gout has four clinical stages and there are defined as asymptomatic hyperuricemia, acute gout attack, asymptomatic period between two attacks and chronic tophaceous gout. The main aims of treatment are to remove the symptoms of an acute attack, decrease the risk of new attacks and lower serum uric acid levels. The most commonly used drugs for removing symptoms of acute attacks are nonsteroidal anti-inflammatory drugs, colchicine and corticosteroids. Patients with recurrent acute attacks, kidney stones or tophi need to take chronic therapy with drugs that reduce serum uric acid levels, such as xanthine oxidase inhibitors (allopurinol and febuxostat), uricosurics (probenecid, benzbromarone, sulfinpyrazone) and recombinant uricase (pegloticase). New drugs such as IL-1β inhibitors for acute attack therapy and lesinurad and topiroxostat for chronic gout therapy are recently available on the market. In addition, numerous researches for new drugs development are in progress