Editorial article
Hyperuricemia and gout: The impact of ultrasonography
Hiperuricemia y gota: impacto de la ecografía
a Unidad Metabólico-Vascular, Servicio de Medicina Interna, Hospital Universitario La Paz, Instituto de Investigación Hospital Universitario La Paz (IdiPAZ), Madrid, Spain
b Servicio de Reumatología, Hospital Universitario La Paz, Instituto de Investigación Hospital Universitario La Paz (IdiPAZ), Madrid, Spain
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"documento" => "article" "crossmark" => 1 "subdocumento" => "sco" "cita" => "Med Clin. 2016;146:65-6" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "en" => array:10 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Editorial article</span>" "titulo" => "Post-thrombotic syndrome: A pending issue" "tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "65" "paginaFinal" => "66" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Síndrome postrombótico: una asignatura pendiente" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Francisco Gabriel Botella" "autores" => array:1 [ 0 => array:2 [ "nombre" => "Francisco" "apellidos" => "Gabriel Botella" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0025775315004522" "doi" => "10.1016/j.medcli.2015.07.006" "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/S0025775315004522?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020616301425?idApp=UINPBA00004N" "url" => "/23870206/0000014600000002/v1_201605240650/S2387020616301425/v1_201605240650/en/main.assets" ] "en" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Editorial article</span>" "titulo" => "Hyperuricemia and gout: The impact of ultrasonography" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "67" "paginaFinal" => "68" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Juan García Puig, Eugenio de Miguel" "autores" => array:2 [ 0 => array:4 [ "nombre" => "Juan" "apellidos" => "García Puig" "email" => array:1 [ 0 => "juangarciapuig@gmail.com" ] "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" => "Eugenio" "apellidos" => "de Miguel" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Unidad Metabólico-Vascular, Servicio de Medicina Interna, Hospital Universitario La Paz, Instituto de Investigación Hospital Universitario La Paz (IdiPAZ), Madrid, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Servicio de Reumatología, Hospital Universitario La Paz, Instituto de Investigación Hospital Universitario La Paz (IdiPAZ), Madrid, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Hiperuricemia y gota: impacto de la ecografía" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Hyperuricemia is the increased levels of serum monosodium urate (uric acid). Gout is secondary to the inflammatory response that the deposit of monosodium urate causes in the tissues. Gout is the most frequent inflammatory joint disease in the general population. The prevalence of hyperuricemia and gout increases with age and depends on the population studied. In the area of Madrid and in the general population, we have found a hyperuricemia prevalence (>7.0<span class="elsevierStyleHsp" style=""></span>mg/dl) 11.3% (95% CI 8.3–13.9).<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">1</span></a> The prevalence of gout is up to 7% of men aged over 65 and 3% of women over 85.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">2</span></a> In 2010 it was estimated that the gout disability-adjusted life years had increased from 76,000 (95% CI 48–112) in 1990 to 114,000 (95% CI 72–167) in 2010.<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">3</span></a> This increased prevalence of hyperuricemia and gout can be related to the epidemic of overweight and obesity in developed countries, and trend toward dietary modifications to increased consumption of foods high in purines, alcoholic beverages (beer) and soft drinks sweetened with fructose.<a class="elsevierStyleCrossRefs" href="#bib0170"><span class="elsevierStyleSup">4,5</span></a> In most patients, increased serum urate concentration (hyperuricemia) is due to a diminished kidney excretion of uric acid,<a class="elsevierStyleCrossRefs" href="#bib0180"><span class="elsevierStyleSup">6,7</span></a> which, in many cases, is determined by an increased or decreased function of certain kidney<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">7,8</span></a> and intestinal transporters.<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">9</span></a> Hyperuricemia not only leads to an increased risk of gout. It has also been associated with heart and kidney disease, and can be expression of a widespread atherosclerosis.<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">10</span></a> It seems appropriate to know the phase or stage of a particular patient with hyperuricemia and/or gout.</p><p id="par0010" class="elsevierStylePara elsevierViewall">Every disease runs through different developmental stages; hence the diversity of clinical manifestations. The most common clinical manifestation of gout is acute inflammation (<24<span class="elsevierStyleHsp" style=""></span>h) that involves the first metatarsophalangeal joint of the big toe (podagra).<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">11</span></a> The initial presentation may affect other joints such as forefoot, ankles, knees, elbows, wrists, and metacarpophalangeal and interphalangeal joints.<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">12</span></a> The pathogenesis of the inflammatory process lies in the phagocytosis of monosodium urate crystals deposited in the joints (“microtophi”), which may remain asymptomatic for many years. Various imaging techniques have shown that many patients with gout (Rx, simple or dual power CT, MRI, ultrasound) and asymptomatic hyperuricemia (ultrasound, dual power CT), apparently non-tophaceous, have deposits of monosodium urate (“microtophi”).<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">13</span></a> This has led to a new classification of hyperuricemia and gout in 4 stages (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>),<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">14</span></a> which is a certain conceptual revolution for the diagnosis and treatment of hyperuricemia and gout.</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">Asymptomatic hyperuricemia is frequently associated with situations that increase vascular risk (obesity, hypertension, diabetes, dyslipidemia, metabolic syndrome),<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">15</span></a> and it has also been postulated as an independent vascular risk factor.<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">16</span></a> Regardless of its etiology, asymptomatic hyperuricemia is considered a benign entity that evolves only occasionally to gout. The probability of this happening is proportional to serum urate concentrations and time of evolution. When uric acid levels are ≥10.0<span class="elsevierStyleHsp" style=""></span>mg/dl, after 5 years, gout occurs in about 50% of patients.<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">17</span></a> European and American guidelines do not recommend hypouricemic treatment in subjects with asymptomatic hyperuricemia.<a class="elsevierStyleCrossRefs" href="#bib0160"><span class="elsevierStyleSup">2,18–21</span></a> For years we have hypothesized that prolonged high levels of uric acid (≥7.0<span class="elsevierStyleHsp" style=""></span>mg/dl), might lead to monosodium urate crystals with subsequent inflammation. We first report that one third of patients with asymptomatic hyperuricemia have silent monosodium urate crystal deposits (“microtophi”) and that 25% of these patients show signs of inflammation.<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">22</span></a> Subsequently, 3 other studies in patients with prolonged asymptomatic hyperuricemia (≥2 years) have confirmed deposits of monosodium urate in 34–42%, and 24% of these patients have obvious inflammation (doppler signal).<a class="elsevierStyleCrossRefs" href="#bib0265"><span class="elsevierStyleSup">23–25</span></a> These reports lead to two important questions: (a) if a patient with “asymptomatic hyperuricemia” (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>, A) has tophi, should the patient be considered a patient with asymptomatic gout or tophaceous gout (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>, B or D)?, and (b) if a patient has asymptomatic tophi with evidence of inflammation (doppler signal), should they be treated with hypouricemic drugs? If the answer to both questions is yes, this would be a major paradigm shift; every patient with long-standing asymptomatic hyperuricemia should undergo a joint ultrasound (knee and metatarsophalangeal joints). The management of resources should consider that this examination can be performed in less than 10<span class="elsevierStyleHsp" style=""></span>min.<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">26</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Clinicians know well that the manifestations of the disease depend largely on the sagacity of the observer and the availability of additional tests. In a review of 14 studies, about half of the patients with gout had tophi when they were examined under ultrasound.<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">27</span></a> Therefore, the clinical diagnosis of “nontophaceous gout” (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>, C), nowadays, is questionable if an ultrasound is not performed. What would it mean to implement ultrasound examination of knees and metatarsophalangeal joints in all patients with gout? Let's mention two apparent benefits: (a) it would modify the classification (a patient with non tophaceous gout would be reclassified in the tophaceous gout group [<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>C would become D]), and (b) in patients with urate deposits, the hypouricemic treatment would be modulated in two aspects. On the one hand, we would try to keep the uric acid below 5.0<span class="elsevierStyleHsp" style=""></span>mg/dl for complete resorption of tophi as soon as possible. Even 2 years after onset with hypouricemic treatment, many patients with gout showed tophi and signs of inflammation.<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">28</span></a> On the other hand, the finding of tophi and signs of inflammation, forces the hypouricemic treatment to be accompanied by appropriate prophylaxis to prevent attacks of acute inflammation, allegedly triggered by reabsorption of urate crystals.<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">29</span></a> The ultrasound follow-up, when detecting tophi, would let know its evolution and establish: (a) the intensity of hypouricemic treatment, and (b) whether or not it is advisable to maintain a preventive treatment of acute gout.<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">30</span></a> The current availability of ultrasound makes it likely that before long we have the necessary studies to verify these possible “apparent benefits.”</p><p id="par0025" class="elsevierStylePara elsevierViewall">One final thought: imaging techniques can help to better clinical classification of asymptomatic hyperuricemia and gout, and perhaps carry out a more rational treatment, but never replace the clinician's judgment and individualized treatment. This is the art of medicine.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: García Puig J, de Miguel E. Hiperuricemia y gota: impacto de la ecografía. Med Clin (Barc). 2016;146:67–68.</p>" ] ] "multimedia" => array:1 [ 0 => array:8 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at1" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleItalic">Hyperuricemia</span> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>A. Patients with increased serum urate and no evidence of deposits of monosodium urate. Examples: heart failure, metabolic syndrome \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>B. Patients with increased serum urate and evidence of deposits of monosodium urate. Examples: same patients as in A, with “microtophi” \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleVsp" style="height:0.5px"></span> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleItalic">Gout</span> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>C. Patients who report some characteristic gout attack, with no evidence of deposits of monosodium urate \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>D. Patients who report some characteristic gout attack, with evidence of deposits of monosodium urate (“tophi or microtophi”) \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab1062186.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Clinical stages in which patients with hyperuricemia or gout can be classified, when using imaging techniques (such as ultrasound).</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:30 [ 0 => array:3 [ "identificador" => "bib0155" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Serum urate, metabolic syndrome and cardiovascular risk factors. A population-based study" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "J.G. 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