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What's up doc?" ] ] "contieneResumen" => array:2 [ "es" => true "en" => true ] "contieneTextoCompleto" => array:1 [ "es" => true ] "contienePdf" => array:1 [ "es" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0015" "etiqueta" => "Figura 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 765 "Ancho" => 1250 "Tamanyo" => 94937 ] ] "descripcion" => array:1 [ "es" => "<p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Paciente diagnosticado y tratado previamente entre 2004 y 2009; fue remitido en 2018 por gota refractaria a dosis altas de medicamentos reductores de uricemia. Se comprobó que la adherencia al tratamiento era del 11% respecto a la dosis prescrita con anterioridad. A) Radiografías simples iniciales, con enormes tofos (aumento de partes blandas) erosiones y daño articular establecido. B) Tras tratamiento desde el año 2018 al 2020 con una uricemia media <<span class="elsevierStyleHsp" style=""></span>2<span class="elsevierStyleHsp" style=""></span>mg/dl, el paciente queda sin ataques y con resolución de los tofos, pero con persistencia de las lesiones articulares destructivas.</p> <p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">Con permiso de ©PerezRuiz 2021.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Fernando Pérez Ruiz, Nuria Pérez Herrero, María Ángeles Gantes Pedraza" "autores" => array:3 [ 0 => array:2 [ "nombre" => "Fernando" "apellidos" => "Pérez Ruiz" ] 1 => array:2 [ "nombre" => "Nuria" "apellidos" => "Pérez Herrero" ] 2 => array:2 [ "nombre" => "María Ángeles" "apellidos" => "Gantes Pedraza" ] ] ] ] ] "idiomaDefecto" => "es" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S2387020622002492" "doi" => "10.1016/j.medcle.2022.01.006" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020622002492?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0025775322000033?idApp=UINPBA00004N" "url" => "/00257753/0000015800000012/v2_202206152104/S0025775322000033/v2_202206152104/es/main.assets" ] ] "itemSiguiente" => array:19 [ "pii" => "S2387020622002698" "issn" => "23870206" "doi" => "10.1016/j.medcle.2022.05.010" "estado" => "S300" "fechaPublicacion" => "2022-06-24" "aid" => "5894" "copyright" => "Elsevier España, S.L.U." 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RA: right atrium; LA: left atrium; CT angiography: computed tomography angiography; CBC: complete blood count; LBBB: left bundle branch block; CHD: congenital heart disease; RHC: right heart catheterization; CV: cardiovascular; DLCO: diffusing capacity of lung for CO; ECG: electrocardiogram; Echo: Echocardiogram; TOE: transoesophageal echocardiography; TTE: transthoracic echocardiogram; PVOD: pulmonary veno-occlusive disease; FEV1: <span class="elsevierStyleItalic">forced expiratory volume in one second</span>; RF: risk factor; CVRF: cardiovascular risk factors; CVF: <span class="elsevierStyleItalic">forced vital capacity</span>; BABG: basal arterial blood gas; PAH: pulmonary arterial hypertension; PCH: pulmonary capillary hemangiomatosis; PH: pulmonary hypertension; CTEPH: chronic thromboembolic pulmonary hypertension; LVH: left ventricular hypertrophy; PaCO2: partial pressure of carbon dioxide; CMRI: cardiac magnetic resonance imaging; NMR: nuclear magnetic resonance; HRCT: high-resolution computerized axial tomography; RV: right ventricle; VE/VCO2: ventilatory equivalent for carbon dioxide; HIV: human immunodeficiency virus.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Raquel Luna-López, Alicia Ruiz Martín, Pilar Escribano Subías" "autores" => array:3 [ 0 => array:2 [ "nombre" => "Raquel" "apellidos" => "Luna-López" ] 1 => array:2 [ "nombre" => "Alicia" "apellidos" => "Ruiz Martín" ] 2 => array:2 [ "nombre" => "Pilar" "apellidos" => "Escribano Subías" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0025775322000021" "doi" => "10.1016/j.medcli.2022.01.003" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0025775322000021?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020622002698?idApp=UINPBA00004N" "url" => "/23870206/0000015800000012/v1_202206230718/S2387020622002698/v1_202206230718/en/main.assets" ] "itemAnterior" => array:19 [ "pii" => "S238702062200273X" "issn" => "23870206" "doi" => "10.1016/j.medcle.2022.03.007" "estado" => "S300" "fechaPublicacion" => "2022-06-24" "aid" => "5935" "copyright" => "Elsevier España, S.L.U." 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What's up doc?" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "615" "paginaFinal" => "621" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Fernando Pérez Ruiz, Nuria Pérez Herrero, María Ángeles Gantes Pedraza" "autores" => array:3 [ 0 => array:4 [ "nombre" => "Fernando" "apellidos" => "Pérez Ruiz" "email" => array:1 [ 0 => "fperezruiz@telefonica.net" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "Nuria" "apellidos" => "Pérez Herrero" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 2 => array:3 [ "nombre" => "María Ángeles" "apellidos" => "Gantes Pedraza" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Servicio de Reumatología, Hospital Universitario Cruces, Osakidetza, OSI Enkarterri-Eskerraldea-Cruces, Grupo de Investigación en Artritis, Instituto de Investigación Biocruces-Bizkaia, Departamento de Medicina, Facultad de Medicina y Enfermería, Universidad del País Vasco, Baracaldo, Vizcaya, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Facultad de Medicina y Enfermería, Universidad del País Vasco" "etiqueta" => "b" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Servicio Extremeño de Salud, Hospital Virgen del Camino, Sección de Reumatología, Plasencia, Cáceres, Spain" "etiqueta" => "c" "identificador" => "aff0015" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Gota. ¿Qué hay de nuevo, doctor?" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 803 "Ancho" => 1500 "Tamanyo" => 148578 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0070" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Pathophysiology of gout, from asymptomatic deposits in cartilage (arthroscopic images in the left column, from top to bottom in increasing size), through gout attack (central panel, neutrophilic arthritis in synovial fluid and synovial biopsy) to chronic granulomatous synovitis (right column, from top to bottom, chronic synovial hypertrophy, articular tophi and bone lesion). The onset of attacks is only the clinical expression of an underlying chronic disease. (With permission from PerezRuiz, 2021.)</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Gout has been known for millennia and is therefore subject to the risk of so-called "clinical inertia", i.e., it is so well known, that tends to be underestimated, if not ignored.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> According to experts, gout can be considered a “curable disease”<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> and clinical practice audits show clear improvements in its management.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> However, the disease control rate is still not optimal, both in primary care and in specialised care.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">At the turn of the century, gout was considered an almost extinct field of research. The intention of this review article is to show readers interested in this disease the substantial changes that have occurred this century regarding its concept, pathophysiology, diagnosis and treatment. The <span class="elsevierStyleSmallCaps">XXI</span> century has seen a significant advance in both basic and cross-cutting knowledge of gout and the emergence of current clinical practice guidelines and recommendations.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Concepts</span><p id="par0015" class="elsevierStylePara elsevierViewall">Gout is a <span class="elsevierStyleItalic">disease caused by the deposition</span> of monosodium urate (MSU) monohydrate crystals. It is conceptually vital for an effective treatment approach<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> to consider the persistence of such deposits as persistence of disease and that their disappearance would lead to the absence of disease, or its "cure".<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">It has been considered a "metabolic disease", as it was presumed to be primarily caused by errors in purine metabolism, but this is far from the pathophysiological reality as we know it. It is currently considered a <span class="elsevierStyleItalic">“transportopathy”</span>,<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> since the primary mechanisms are basically renal or intestinal uric acid transport capacity anomalies, as we shall see.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Academically, gout has been classified into different states as "acute gout", "intercritical gout" and "chronic gout", based on the presence or absence of symptoms and its acute or chronic clinical features. This nomenclature has led to the perception that "acute gout" was a transient episode, "intercritical gout" was a temporary absence of disease and therefore did not require treatment and "chronic gout" something no longer curable.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> We have recently recommended a change in the nomenclature, based on preclinical, clinical and developmental states,<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> as shown in more detail in <a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>. Gout is the term that defines the whole disease (such as diabetes or hypertension) but understood as a condition that already has clinical manifestations.</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Epidemiology</span><p id="par0030" class="elsevierStylePara elsevierViewall">Although the incidence of gout does not seem to be increasing in developed countries, the prevalence has increased in relation to the increase in life expectancy and varies globally between 1 and 3%, except in ethnic groups with high incidence, such as Maori or Filipinos. The EPISER2016 study has shown for the first time that the <span class="elsevierStyleItalic">prevalence in Spain stands at</span> 2.4% of the adult population, being 4.55% in men and 0.38% in women, increasing in parallel with the increase in the age of the population.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a></p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Pathophysiology</span><p id="par0035" class="elsevierStylePara elsevierViewall">Gout is the disease caused by <span class="elsevierStyleItalic">inflammation induced by MSU</span> crystals in the tissues as a result of their nucleation, growth and apposition due to the <span class="elsevierStyleItalic">persistence of a state of hyperuricaemia.</span> This is defined as uricemia above the physicochemical saturation point of urate under physiological conditions.</p><p id="par0040" class="elsevierStylePara elsevierViewall">It has been typically associated with a type of dietary transgression, when only one third of the purines come from exogenous sources. Recent studies show that the effect of diet on hyperuricemia is less than that of body mass index (presumably mediated by peripheral insulin resistance),<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> or genetic predisposition, since it is the latter that shows the greatest effect on blood uric acid levels.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Since the beginning of this century, we have known that the mechanisms involved in hyperuricaemia are mostly, with the exception of impaired glomerular filtration in patients with chronic kidney disease, primary or drug-induced abnormalities in renal (mainly renal transporters URAT1 and Glut9) or intestinal (mainly transporter ABCG2) transport. The genetic component is the strongest factor<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> and appears to be even stronger in early onset gout.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> In contrast, the burden of comorbidity (kidney disease, medication use, underlying osteoarthritis) is an important component in the development of gout in women.</p><p id="par0050" class="elsevierStylePara elsevierViewall">Transcellular transport of uric acid is a complex mechanism in which proteins such as PDZK1 or SMCT1 and SMCT2<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> interact with uric acid transporters, forming a functional complex called 'transportome'. The structural and functional identification of transporters and associated proteins is allowing the establishment of new therapeutic targets for the development of new drugs.</p><p id="par0055" class="elsevierStylePara elsevierViewall">The formation, apposition and aggregation of MSU crystals initially occurs in the <span class="elsevierStyleItalic">hyaline cartilage surface</span>, where they are immunologically inert.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> Contrary to the belief that crystals form instantaneously in the joint structures before a gout attack, a significant accumulation of crystals can be present even before the first clinical manifestation (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>).</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0060" class="elsevierStylePara elsevierViewall">Their release from the deposit on the cartilage surface by various factors, such as overloading, local trauma, cartilage abrasion or sudden changes in blood uric acid levels due to other processes and their uptake by resident cells induces an acute self-limiting inflammatory phenomenon mediated by <span class="elsevierStyleItalic">inflammasome and interleukin-1 (IL-1)</span> and neutrophilic response, known as gout attack.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> Therefore, gout can be considered an autoinflammatory disease.</p><p id="par0065" class="elsevierStylePara elsevierViewall">The released crystals are deposited in the synovial membrane, where they aggregate and induce a <span class="elsevierStyleItalic">foreign body type chronic inflammatory phenomenon</span> leading to erosion and subsequent destruction of joint structures.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Clinical signs and symptoms</span><p id="par0070" class="elsevierStylePara elsevierViewall">Gout has been considered to be an intermittently acute but generally mild disease rather than a chronic disease with initially intermittent and eventually persistent manifestations.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> However, an analysis of the natural history of gout using data from the second half of the <span class="elsevierStyleSmallCaps">XX</span> century, when no effective drugs for the reduction of blood uric acid levels were available, shows that, after 20 years from the onset of symptoms, around 70% <span class="elsevierStyleItalic">of patients had developed erosive</span> radiographic gout, i.e. showing structural lesions due to joint deposits that induce inflammation and bone resorption, as well as a progression of clinical manifestations.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">The presence of tophi is not only associated with an increased risk of disability due to damage to joint structures but has been shown to be independently associated with an <span class="elsevierStyleItalic">increased risk of premature</span> mortality,<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a> presumably through the presence of subclinical inflammation.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a></p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Diagnosis</span><p id="par0080" class="elsevierStylePara elsevierViewall">The <span class="elsevierStyleItalic">gold standard for the diagnosis</span> of gout is the observation of MSU crystals in biological samples by microscopy. The possibility of obtaining and analysing samples is not widely available in clinical practice, except in specialised care. Therefore, classification criteria are used. However, considering that uricemia correction treatment can be not only long, but lifelong, the accuracy of diagnosis is of great clinical relevance.</p><p id="par0085" class="elsevierStylePara elsevierViewall">The classification criteria used in the last quarter of the <span class="elsevierStyleSmallCaps">XX</span> century, published in one of the most cited articles on gout,<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a> were never validated and suffered from important methodological errors. In 2015, the <span class="elsevierStyleItalic">new classification criteria</span> endorsed by the American and European Societies of Rheumatology<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a> were published, which included clinical, laboratory and imaging variables, weighted both positively and negatively.</p><p id="par0090" class="elsevierStylePara elsevierViewall">New imaging techniques, namely ultrasound<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a> and dual-energy computed tomography or DECT,<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a> have been shown to be highly specific for diagnosis, although their sensitivity may vary depending on the amount of deposit.<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">18,19</span></a> Imaging by ultrasound or DECT may not only contribute to the diagnosis, but may also allow monitoring of the response of urate deposition to urate-lowering therapy.<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">21</span></a></p><p id="par0095" class="elsevierStylePara elsevierViewall">A validated self-reported <span class="elsevierStyleItalic">definition of gout attack</span> has been established, allowing us to account for the reduction of clinical manifestations during treatment, both in clinical practice and in clinical trials.<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">22</span></a></p><p id="par0100" class="elsevierStylePara elsevierViewall">Finally, contrary to the academically accepted assertion that gout was never associated with other inflammatory joint diseases, it has been shown that the <span class="elsevierStyleItalic">prevalence of other associated diseases</span> is that which corresponds to the general population. Therefore, a previous diagnosis of gout does not exclude the subsequent occurrence of another inflammatory joint disease and vice versa.<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a></p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Treatment</span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Treatment hierarchy</span><p id="par0105" class="elsevierStylePara elsevierViewall">In the textbooks in use, an order is established that implicitly ranks treatment options in a way that prioritizes what is obvious (symptoms) over what is underlying (deposit): attacks first, then prevention, and finally the reduction of blood uric acid levels. In recent years we have proposed a <span class="elsevierStyleItalic">reverse</span> hierarchy, whereby treating the cause leads to the resolution of symptoms: firstly the reduction of blood uric acid levels which will lead to remission or cure of gout; secondly, the prevention of attacks during the initial period of blood uric acid reduction and control; finally, the treatment of gout attacks, should they occur, with self-management by the patients (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>).</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Reduction of uric acid levels</span><p id="par0110" class="elsevierStylePara elsevierViewall">The <span class="elsevierStyleItalic">treatment of gout is suboptimal</span> even in developed countries where the achievement of therapeutic targets is encouraged. High rates are only achieved when specific programmes are implemented, as demonstrated in a recent trial.<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a> Lack of adherence to treatment is one of the major causes of therapeutic failure in the treatment of chronic diseases, such as gout, which is considered one of the entities with the worst treatment compliance.<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">25</span></a> However, patient <span class="elsevierStyleItalic">information and empowerment</span> has been shown to achieve adherence rates similar to those achieved in clinical trials, challenging whether patients are ultimately responsible for low adherence.<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a></p><p id="par0115" class="elsevierStylePara elsevierViewall">As for general lifestyle measures, as mentioned above, diet has little influence, unlike obesity,<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> so a moderate intake of alcohol and sweetened beverages, an optimal weight and a Mediterranean diet are recommended.</p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Therapeutic targets</span><p id="par0120" class="elsevierStylePara elsevierViewall">At the end of the <span class="elsevierStyleSmallCaps">XX</span> century, uric acid-lowering treatment came to be regarded as having no measurable effect on the course of gout.<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a> Subsequent studies have shown, both in cohorts and in clinical trials, that achieving <span class="elsevierStyleItalic">targeted uric acid levels reduces urate deposition in tissues</span> and is associated with a reduction in clinical manifestations, in some cases in a permanent manner.<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">28</span></a></p><p id="par0125" class="elsevierStylePara elsevierViewall">It has been shown that the <span class="elsevierStyleItalic">reduction of deposits is a function directly proportional to the reduction of blood uric acid levels</span>, by measuring both subcutaneous<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a> and joint<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">30</span></a> tophi: the lower the uric acid level, the faster the reduction. All this led to the proposal of a targeted treatment strategy,<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">31</span></a> currently accepted as a T2T strategy or «Treat to Target».<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">32</span></a> This approach has been adopted by most of the recommendations in use.</p><p id="par0130" class="elsevierStylePara elsevierViewall">After the concept of target treatment strategy, the <span class="elsevierStyleItalic">concept of therapeutic target and preventive target emerges.</span> If the therapeutic target treatment succeeds in dissolving all the MSU crystals in the long term, from that moment on, the treatment would not be aimed at treating the deposit, but at preventing its subsequent formation by adjusting the treatment to a preventive uric acid level target. The fact that patients who discontinue treatment after a long period of therapeutic target only relapse when their blood uric acid levels again exceed plasma urate concentration limits seems to confirm this hypothesis.<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">33</span></a> The current <span class="elsevierStyleItalic">recommendations</span> in Europe and the USA suggest a therapeutic uric acid target of between 5−6 mg/dl, but even below 5 mg/dl in patients with severe gout (with polyarticular, erosive or tophaceous involvement) and a subsequent preventive uric acid target of 6−7 mg/dl.</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Direct clinical outcomes associated with target treatment</span><p id="par0135" class="elsevierStylePara elsevierViewall">The <span class="elsevierStyleItalic">definition for remission of gout</span> is based on the absence of attacks and tophi and a maintained control of target uric acid levels, together with low patient global and pain scores.<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">34</span></a> However, the achievement of this status according to this definition may be limited by the presence of sequelae due to structural joint damage caused by gout or the presence of associated disease, such as osteoarthritis.</p><p id="par0140" class="elsevierStylePara elsevierViewall">The first effect of uric acid target therapy is the <span class="elsevierStyleItalic">progressive reduction in the frequency of gout attacks</span>, usually within one year and associated with the perception of disease remission.<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">35</span></a> In order to ensure adherence to treatment, it is essential that patients know that gout attacks may still occur, even in spite of optimal therapeutic targeting, for a period of 1–2 years. Both the prescription of adequate colchicine prevention during this period and education on the self-management of attacks as soon as they are recognised by the patient<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">22</span></a> through the prescription of anti-inflammatory treatment, always adapted to the co-morbidity that may exist, are of paramount importance.</p><p id="par0145" class="elsevierStylePara elsevierViewall">The reduction of tophi is a function of the level of blood uric acid, as we have already mentioned. Trials with <span class="elsevierStyleItalic">uric acid-lowering drugs</span>, such as pegloticase, have shown very rapid clearance, with 50% clearance of tophi in less than 6 months.<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">36</span></a></p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Indirect outcomes associated with treatment</span><p id="par0150" class="elsevierStylePara elsevierViewall">Long-term treatment of gout using <span class="elsevierStyleItalic">therapeutic targeting has been associated with lower overall mortality and cardiovascular mortality rates in cohort studies</span>.<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">37</span></a><span class="elsevierStyleItalic">More recently, the FAST trial, comparing allopurinol to febuxostat, showed that, in a prespecified analysis, patients treated with febuxostat who achieved uric acid levels lower than 5 mg/dl showed a lower primary cardiovascular outcome rate (mortality or cardiovascular event)</span>.<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">38</span></a></p><p id="par0155" class="elsevierStylePara elsevierViewall">Other possible, but not clearly demonstrated, beneficial effects of uric acid-lowering treatment on renal and cardiovascular events in patients with gout have been claimed.<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">39</span></a> It is not clear if the effects of treatment are related to the reduction of uric acid levels,<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">40</span></a> urate deposits<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> are due to a pharmacodynamic effect (inhibition of xanthine oxido-reductase)<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">41</span></a> or the cessation of attacks and thus of the use of non-steroidal anti-inflammatory drugs (NSAIDs).<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">42</span></a> We must emphasize, however, that the <span class="elsevierStyleItalic">Spanish Agency of Medicines and Medical Devices (AEMPS) does not include asymptomatic hyperuricemia as an indication for uric acid-lowering treatment</span> in patients with cardiovascular or renal disease.</p></span></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Uric acid-lowering drugs</span><p id="par0160" class="elsevierStylePara elsevierViewall">Three drugs are registered and available in Spain with an indication for reducing uric acid levels in patients with gout: allopurinol and benzbromarone, from the second half of the <span class="elsevierStyleSmallCaps">XX</span> century, and febuxostat, from the <span class="elsevierStyleSmallCaps">XXI</span> century. Pegloticase and lesinurad were positively assessed by the EMA in the second decade of this century and subsequently withdrawn for commercial reasons. Treatment combinations typically include a xanthine oxidase inhibitor and a uricosuric drug.</p><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Xanthine oxidoreductase (XOR) inhibitors: allopurinol and febuxostat</span><p id="par0165" class="elsevierStylePara elsevierViewall">Allopurinol and febuxostat are globally approved for the treatment of gout, uric acid nephrolithiasis, and the prevention of tumour lysis syndrome. Another XOR inhibitor, topiroxostat, is approved in Japan.</p><p id="par0170" class="elsevierStylePara elsevierViewall">Allopurinol <span class="elsevierStyleItalic">is metabolised to oxypurinol</span>, a metabolite that exerts most of the pharmacodynamic effect by inhibiting the reduced isoform of XOR and is almost entirely eliminated by the kidneys. Therefore, allopurinol toxicity is linked to the presence of chronic kidney disease (reduction of glomerular filtration rate), the use of diuretics (interaction with URAT1 transporter), as well as the presence of genetic predisposition in subjects carrying the HLA-B*5801 allele.<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">43</span></a> Allopurinol toxicity is rare, but can be very serious, especially when it results in serious cutaneous adverse reactions or drug rash with eosinophilia and systemic symptoms (DRESS).</p><p id="par0175" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Allopurinol toxicity can be prevented</span><a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">44</span></a> by a slowly progressive escalation from initially low doses<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">45</span></a> (1 or 2 mg/day per ml/min of estimated glomerular filtration rate) to the dose required to achieve therapeutic target levels. However, we must highlight that, in this study, 9/132 patients died in the 12-month study period, all with adjusted high doses and none included in the safety analysis.</p><p id="par0180" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Febuxostat</span> was introduced in the first decade of this century and is an inhibitor of both XOR isoforms, making it a potent uric acid-lowering agent. Its clearance is partly hepatic and as inactive metabolites, so its pharmacokinetics is not as dependent on renal function. The results of the <span class="elsevierStyleItalic">Cardiovascular Safety of Febuxostat and Allopurinol in Patients with Gout and Cardiovascular Morbidities</span> (CARES) trial, widely criticised for the loss of half of the patients to follow-up, showed a higher overall and cardiovascular mortality rate with febuxostat compared to allopurinol.<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">46</span></a></p><p id="par0185" class="elsevierStylePara elsevierViewall">On the contrary, the <span class="elsevierStyleItalic">Febuxostat versus Allopurinol Streaming Trial</span> (FAST) conducted in Europe,<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">38</span></a> with higher doses of both drugs and losing less than 10% of patients, showed no such effect on overall or cardiovascular mortality or cardiovascular events. For this reason, EMA changed its SmPC in January 2022, eliminating the previous prescription limitation for patients with previous major cardiovascular events (MCE) and recommending that treatment in patients with MCE be carried out with caution and with frequent monitoring.</p><p id="par0190" class="elsevierStylePara elsevierViewall">Adverse reactions of hypersensitivity to febuxostat, mostly cutaneous, have been reported, although they occur less often than with allopurinol.</p></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Uricosurics: benzbromarone</span><p id="par0195" class="elsevierStylePara elsevierViewall">After withdrawing <span class="elsevierStyleItalic">lesinurad</span> from the market, the only drug with uricosuric effect available for prescription in Spain was <span class="elsevierStyleItalic">benzbromarone</span>, even so, its indications were limited (intolerance or inefficacy with XOR inhibitors, severe gout or nephropathy/kidney transplant) and to initial prescription only by specialists in Nephrology or Rheumatology.</p><p id="par0200" class="elsevierStylePara elsevierViewall">Benzbromarone is an amiodarone analogue with no vascular or antiarrhythmic effect, but a potent inhibitor of the renal transporter URAT1, inducing renal urate leak. Contrary to claims made at the end of the last century, benzbromarone has been shown to be effective<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">47</span></a> in patients with moderate renal disease (filtration rates up to 20−30 ml/min), the risk of nephrolithiasis is low and associated with urinary pH < 5.5, being able to monitor the estimation of the concentration of undissociated uric acid in urine.<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">48</span></a> Its limitation for prescription stems from the uncommon risk of developing severe liver toxicity by inducing mitochondrial toxicity and worsening of fatty liver.<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">49</span></a></p><p id="par0205" class="elsevierStylePara elsevierViewall">A potent uricosuric URAT1<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">50</span></a> inhibitor, <span class="elsevierStyleItalic">dotinurad,</span> also effective in patients with moderate nephropathy and no apparent hepatic toxicity, has recently been marketed in Japan and could be prescribed as a foreign medicine.</p></span><span id="sec0075" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Uricase agents</span><p id="par0210" class="elsevierStylePara elsevierViewall">The European Commission approved the marketing of <span class="elsevierStyleItalic">pegloticase</span> in 2012 but it was withdrawn shortly afterwards for commercial reasons. Pegloticase is a recombinant pegylated baboon uricase for parenteral use (associated with polyethylene glycol [PEG] chains) so as to reduce its immunogenicity and increase its half-life. Long-term uricemia response rates are close to 50%,<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">51</span></a> both due to loss of effectiveness and infusion reactions associated with the presence or development of anti-PEG antibodies.<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">52</span></a> It may be prescribed as a foreign medication in cases of severe gout where there are no therapeutic alternatives.</p><p id="par0215" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Rasburicase</span> is approved in Spain for the prevention of tumour lysis syndrome. Its half-life is very short, and its immunogenicity is very high in the medium-long term, so it is not useful in clinical practice.</p></span></span><span id="sec0080" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">Prevention of gout attacks</span><p id="par0220" class="elsevierStylePara elsevierViewall">Most recommendations already support the <span class="elsevierStyleItalic">prevention of gout attacks at the start of treatment</span><span class="elsevierStyleBold">.</span> This should be prolonged, at least 6 months, as short regimens of less than 3 months have not been shown to be effective.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a> In the <span class="elsevierStyleItalic">Febuxostat Open-label Clinical trial of Urate-lowering efficacy and Safety</span> (FOCUS) comparing febuxostat with allopurinol, and without prevention at one-year follow-up, patients with tophi reported more than 30% of attacks, compared to less than 10% of patients without tophi.<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">54</span></a> Although based on indirect evidence, we must consider longer-term prevention in patients with tophaceous gout.</p><p id="par0225" class="elsevierStylePara elsevierViewall">Only colchicine has an approved indication in Spain for the prevention of gout attacks. The first published SmPC, after more than 3 centuries of prescription, dates back to the second decade of this century in Spain. It is a drug with a narrow therapeutic margin and subject to surveillance monitoring and should be used at low doses (1 mg/day, lower dose in patients with moderate kidney or liver disease, contraindicated in severe kidney or liver disease, a combination of these or cardiomyopathy). The use of NSAIDs and glucocorticoids for the prevention of gout is entirely empirical, not based on published evidence.</p></span><span id="sec0085" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">Treatment of inflammation</span><p id="par0230" class="elsevierStylePara elsevierViewall">NSAIDs and glucocorticoids are effective and widely prescribed for the treatment of gout attacks. However, the comorbidity that patients may present may limit their use.</p><p id="par0235" class="elsevierStylePara elsevierViewall">Colchicine is a lipophilic alkaloid with a long half-life and is indicated for the prevention and treatment of gout attacks, among other uses. It is a safe drug when the prescription is in accordance with current recommendations. Low doses of colchicine (the regimen in the AEMPS SmPC indicates a maximum of 2 mg/day, a maximum of 6 mg cumulative, a maximum of 4 days of treatment and not to be repeated within another 7 days) have been shown to be effective in gout attacks. This recommendation is based on an efficacy and safety study of these low doses compared to high doses,<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">55</span></a> which found that the earlier hourly dose schedule, compared to low doses, showed a much higher rate of toxicity with the same efficacy. However, the limitation of this study is that less than half of the patients reduced at least half of their pre-treatment pain within 3 days.</p><p id="par0240" class="elsevierStylePara elsevierViewall">IL-1 inhibitors (IL-1i) have been tried for the treatment of gout. <span class="elsevierStyleItalic">Canakinumab</span> is a potent IL-1® inhibiting long half-life IgG monoclonal antibody that was positively evaluated by EMA as a treatment for attacks of gout in situations where there are no therapeutic alternatives.<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">56</span></a> However, the Therapeutic Positioning Report of the AEMPS states that it is not an indication funded by the National Health System. <span class="elsevierStyleItalic">Anakinra</span> is a short half-life IL-1 antagonist that binds to the IL-1 receptor and its accessory protein (IL-1r-IL-1-rap), blocking its interaction with IL-1. The indication of gout is not approved in Spain, although there are clinical trials that show its efficacy,<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">57</span></a> so it can be prescribed off-label.</p><p id="par0245" class="elsevierStylePara elsevierViewall">Tetracosactide is the initial active 24-amino acid fragment of adrenocorticotropic hormone (ACTH), which has been marketed in Spain since the last century and whose SmPC dates from 2018. Like ACTH, it has been effective in the treatment of gout<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">58</span></a> for more than 5 decades, but its mechanism of action is not mediated by the induction of endogenous cortisol as currently academically believed, because the induced cortisol levels are not therapeutic, and it is also effective in patients chronically treated with glucocorticoids and showing suppression of adrenocortical function. The mechanism of action of ACTH in gout seems to be related to the activation of the melatonin receptor 3 in neutrophils.<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">59</span></a> In Spain, a stock preparation of 1 mg is available for intramuscular administration and another of 0.25 mg for intravenous administration.</p></span><span id="sec0090" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0110">Education</span><p id="par0250" class="elsevierStylePara elsevierViewall">As in all chronic diseases, the education of patients with gout has a considerable impact.<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a> It should be noted here that because of misinformation, namely that patients perceive gout as an unresolvable and usually self-inflicted disease, patients feel they must tolerate the persistence of symptoms.<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">60</span></a> Nothing could be further from our expectations as physicians in this 21st century (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>).</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia></span><span id="sec0095" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0115">Funding</span><p id="par0255" class="elsevierStylePara elsevierViewall">FRP has been partially funded by the <span class="elsevierStyleGrantSponsor" id="gs0005">Cruces Rheumatologists Association 02/21</span>.</p></span><span id="sec0100" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0120">Conflict of interests</span><p id="par0260" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflict of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:17 [ 0 => array:3 [ "identificador" => "xres1738151" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1533263" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres1738152" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1533262" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Concepts" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Epidemiology" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Pathophysiology" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Clinical signs and symptoms" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "Diagnosis" ] 9 => array:3 [ "identificador" => "sec0030" "titulo" => "Treatment" "secciones" => array:5 [ 0 => array:2 [ "identificador" => "sec0035" "titulo" => "Treatment hierarchy" ] 1 => array:2 [ "identificador" => "sec0040" "titulo" => "Reduction of uric acid levels" ] 2 => array:2 [ "identificador" => "sec0045" "titulo" => "Therapeutic targets" ] 3 => array:2 [ "identificador" => "sec0050" "titulo" => "Direct clinical outcomes associated with target treatment" ] 4 => array:2 [ "identificador" => "sec0055" "titulo" => "Indirect outcomes associated with treatment" ] ] ] 10 => array:3 [ "identificador" => "sec0060" "titulo" => "Uric acid-lowering drugs" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0065" "titulo" => "Xanthine oxidoreductase (XOR) inhibitors: allopurinol and febuxostat" ] 1 => array:2 [ "identificador" => "sec0070" "titulo" => "Uricosurics: benzbromarone" ] 2 => array:2 [ "identificador" => "sec0075" "titulo" => "Uricase agents" ] ] ] 11 => array:2 [ "identificador" => "sec0080" "titulo" => "Prevention of gout attacks" ] 12 => array:2 [ "identificador" => "sec0085" "titulo" => "Treatment of inflammation" ] 13 => array:2 [ "identificador" => "sec0090" "titulo" => "Education" ] 14 => array:2 [ "identificador" => "sec0095" "titulo" => "Funding" ] 15 => array:2 [ "identificador" => "sec0100" "titulo" => "Conflict of interests" ] 16 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2021-10-14" "fechaAceptado" => "2022-01-03" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1533263" "palabras" => array:5 [ 0 => "Gout" 1 => "Diagnosis" 2 => "Treatment" 3 => "Review" 4 => "Update" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1533262" "palabras" => array:5 [ 0 => "Gota" 1 => "Diagnóstico" 2 => "Tratamiento" 3 => "Revisión" 4 => "Puesta al día" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">A considerable improvement in the knowledge of gout has taken place in the two decades of the XXIth century. Definitions of disease, estate, and clinical situations, along with a new nomenclature, have been agreed. More importantly, the concept of gout as a “curable” or “controllable” disease has bee settled.</p><p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">We know for the first time its prevalence in Spain. Factors associated to disease, the genetics that condition the predisposition to develop hyperuricemia and the structure and functions of the transportome complex that control the renal and intestinal handling of urate have been examined.</p><p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Imaging techniques have come to support diagnosis. Different primary therapeutic targets have been defined depending on the burden of disease, and targets for secondary prevention considered. We know how to best prescribe available medications and prevent the risk of adverse events.</p><p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Finally, we have understood the importance of adherence, education, and empower patients during treatment instead of blaming them.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">En las dos décadas de este siglo, se ha desarrollado un amplio conocimiento sobre la gota. Hemos definido la enfermedad, los estados y las situaciones clínicas y cambiado su nomenclatura, así como asentado el concepto de enfermedad por depósito “curable” o “remisible”.</p><p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Conocemos ya su alta prevalencia en España y los factores asociados a la enfermedad, la genética que condiciona mayoritariamente la predisposición a la hiperuricemia y la estructura y las funciones del complejo transportoma implicado en el manejo renal e intestinal del ácido úrico.</p><p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">Las técnicas de imagen han aportado nuevos medios al diagnóstico. Hemos establecido las distintas dianas terapéuticas según la carga de enfermedad y las dianas de prevención secundaria, y aprendido a emplear mejor los medicamentos disponibles, a optimizar su prescripción y a prevenir los acontecimientos adversos.</p><p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Finalmente, hemos comprendido como mejorar la adherencia, educar e implicar a los pacientes en su tratamiento y a no culpabilizarlos.</p></span>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0010">Please cite this article as: Pérez Ruiz F, Pérez Herrero N, Gantes Pedraza MÁ. Gota. ¿Qué hay de nuevo, doctor? Med Clin (Barc). 2022;158:615–621.</p>" ] ] "multimedia" => array:4 [ 0 => array:8 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 803 "Ancho" => 1500 "Tamanyo" => 148578 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0070" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Pathophysiology of gout, from asymptomatic deposits in cartilage (arthroscopic images in the left column, from top to bottom in increasing size), through gout attack (central panel, neutrophilic arthritis in synovial fluid and synovial biopsy) to chronic granulomatous synovitis (right column, from top to bottom, chronic synovial hypertrophy, articular tophi and bone lesion). The onset of attacks is only the clinical expression of an underlying chronic disease. (With permission from PerezRuiz, 2021.)</p>" ] ] 1 => array:8 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 911 "Ancho" => 2917 "Tamanyo" => 156660 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0075" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Hierarchy of gout treatment: the basis is the correction of uricemia, which underpins the need for prevention during the initial phase of correction of urate levels, completed by the prescription of self-management treatment of gout attacks until they subside. (With permission from PerezRuiz, 2021.)</p>" ] ] 2 => array:8 [ "identificador" => "fig0015" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 765 "Ancho" => 1250 "Tamanyo" => 95052 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0080" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Patient previously diagnosed and treated between 2004 and 2009; referred in 2018 for gout refractory to high doses of uric acid-lowering drugs. Adherence to treatment was found to be 11% compared to the previously prescribed dose. A) Initial plain X-rays, with huge tophi (soft tissue enlargement), erosions and established joint damage. B) After treatment from 2018 to 2020 with a mean uricemia < 2 mg/dl, the patient remains attack-free and with resolution of tophi, but with persistence of destructive joint lesions.</p> <p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">With permission from ©PerezRuiz 2021.</p>" ] ] 3 => array:9 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "fuente" => "Adapted from Bursill et al.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a>" "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0085" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:2 [ "tablatextoimagen" => array:1 [ 0 => array:1 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Stage \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Nomenclature \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Definition \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Preclinical \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Asymptomatic hyperuricemia \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Hyperuricemia without gout \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Preclinical \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Asymptomatic deposition \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Proven deposition<a class="elsevierStyleCrossRef" href="#tblfn0005"><span class="elsevierStyleSup">a</span></a> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Preclinical \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Hyperuricemia with deposition \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Id. with hyperuricemia \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Clinical \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Gout \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Deposition with acute arthritis, chronic arthritis, or tophi \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Clinical \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Tophaceous gout \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Id. with subcutaneous tophi \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Clinical \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Erosive gout \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Id. with erosive lesion in image \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Developmental \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">First gout attack \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">First acute episode \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Developmental \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Recurring attacks \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">More than one episode \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Other stages \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Can be added \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">For example, chronic arthritis \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] ] ] "notaPie" => array:1 [ 0 => array:3 [ "identificador" => "tblfn0005" "etiqueta" => "a" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Deposits of monosodium urate monohydrate crystals shown by imaging or microscopy.</p>" ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Stages, nomenclature and definitions.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:60 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Persistent clinical inertia in gout in 2014: an observational French longitudinal patient database study" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:5 [ 0 => "M. 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Miyauchi" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1007/s12576-018-00658-1" "Revista" => array:6 [ "tituloSerie" => "J Physiol Sci" "fecha" => "2019" "volumen" => "69" "paginaInicial" => "399" "paginaFinal" => "408" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/30604288" "web" => "Medline" ] ] ] ] ] ] ] ] 5 => array:3 [ "identificador" => "bib0030" "etiqueta" => "6" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Computational lexical analysis of the language commonly used to describe gout" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "L.N. Edwards" 1 => "R. Malouf" 2 => "F. Perez-Ruiz" 3 => "P. Richette" 4 => "S. Southam" 5 => "M. 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Vargas-Santos" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1136/annrheumdis-2019-215933" "Revista" => array:6 [ "tituloSerie" => "Ann Rheum Dis" "fecha" => "2019" "volumen" => "78" "paginaInicial" => "1592" "paginaFinal" => "1600" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/31501138" "web" => "Medline" ] ] ] ] ] ] ] ] 7 => array:3 [ "identificador" => "bib0040" "etiqueta" => "8" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Prevalence of gout in the adult general population in Spain: Estimating the proportion of undiagnosed cases" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "N. Quilis" 1 => "F. Sivera" 2 => "D. Seoane-Mato" 3 => "F. Pérez-Ruiz" 4 => "C. Sánchez-Piedra" 5 => "F. 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Gout. What's up doc?
Gota. ¿Qué hay de nuevo, doctor?
a Servicio de Reumatología, Hospital Universitario Cruces, Osakidetza, OSI Enkarterri-Eskerraldea-Cruces, Grupo de Investigación en Artritis, Instituto de Investigación Biocruces-Bizkaia, Departamento de Medicina, Facultad de Medicina y Enfermería, Universidad del País Vasco, Baracaldo, Vizcaya, Spain
b Facultad de Medicina y Enfermería, Universidad del País Vasco
c Servicio Extremeño de Salud, Hospital Virgen del Camino, Sección de Reumatología, Plasencia, Cáceres, Spain