<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>2182-7230</journal-id>
<journal-title><![CDATA[Revista Nutrícias]]></journal-title>
<abbrev-journal-title><![CDATA[Nutrícias]]></abbrev-journal-title>
<issn>2182-7230</issn>
<publisher>
<publisher-name><![CDATA[Associação Portuguesa dos Nutricionistas]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S2182-72302013000400006</article-id>
<title-group>
<article-title xml:lang="pt"><![CDATA[Estratégias para Intervenção Nutricional na Hiperuricémia e Gota]]></article-title>
<article-title xml:lang="en"><![CDATA[Strategies for Nutritional Intervention in Hyperuricemia and Gout]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Martins]]></surname>
<given-names><![CDATA[João]]></given-names>
</name>
<xref ref-type="aff" rid="A01"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Jorge]]></surname>
<given-names><![CDATA[Eunice]]></given-names>
</name>
<xref ref-type="aff" rid="A02"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Camolas]]></surname>
<given-names><![CDATA[José]]></given-names>
</name>
<xref ref-type="aff" rid="A03"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Carmo]]></surname>
<given-names><![CDATA[Isabel do]]></given-names>
</name>
<xref ref-type="aff" rid="A04"/>
</contrib>
</contrib-group>
<aff id="A01">
<institution><![CDATA[,Instituto Superior de Ciências da Saúde Egas Moniz  ]]></institution>
<addr-line><![CDATA[Caparica ]]></addr-line>
<country>Portugal</country>
</aff>
<aff id="A02">
<institution><![CDATA[,Universidade do Porto Faculdade de Ciências da Nutrição e Alimentação ]]></institution>
<addr-line><![CDATA[Porto ]]></addr-line>
<country>Portugal</country>
</aff>
<aff id="A03">
<institution><![CDATA[,Hospital de Santa Maria  ]]></institution>
<addr-line><![CDATA[Lisboa ]]></addr-line>
<country>Portugal</country>
</aff>
<aff id="A04">
<institution><![CDATA[,Universidade de Lisboa Faculdade de Medicina ]]></institution>
<addr-line><![CDATA[Lisboa ]]></addr-line>
<country>Portugal</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2013</year>
</pub-date>
<numero>19</numero>
<fpage>28</fpage>
<lpage>31</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_arttext&amp;pid=S2182-72302013000400006&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_abstract&amp;pid=S2182-72302013000400006&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_pdf&amp;pid=S2182-72302013000400006&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="pt"><p><![CDATA[A prevalência de hiperuricémia e gota tem vindo a aumentar na população portuguesa, nos últimos anos, à semelhança do que acontece com outros países desenvolvidos. O objectivo deste artigo é fazer uma revisão de evidência disponível, relativamente à intervenção nutricional nestas patologias, tendo em vista identificar estratégias para a intervenção nutricional em doentes com hiperuricémia e gota, com maior potencial de efectividade. Considerando que a hiperuricémia e a gota se associam frequentemente à obesidade, hipertensão arterial, dislipidémia, aterosclerose e síndrome metabólica, estes doentes representam uma oportunidade singular para uma avaliação e uma orientação nutricional mais abrangente.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[The prevalence of hyperuricemia and gout have been increasing in the Portuguese population, in recent years, similar to what happens with other developed countries. The purpose of this article is to review the available evidence in relation to nutritional intervention in these pathologies, in order to identify strategies for nutritional intervention in patients with hyperuricemia and gout, with greater potential for effectiveness. Whereas hyperuricemia and gout is often associated with obesity, hypertension, dyslipidemia, atherosclerosis and metabolic syndrome, these patients represent a unique opportunity for an evaluation and a more comprehensive nutritional guidance.]]></p></abstract>
<kwd-group>
<kwd lng="pt"><![CDATA[Gota]]></kwd>
<kwd lng="pt"><![CDATA[Hiperuricémia]]></kwd>
<kwd lng="pt"><![CDATA[Purinas]]></kwd>
<kwd lng="pt"><![CDATA[Obesidade]]></kwd>
<kwd lng="pt"><![CDATA[Etanol]]></kwd>
<kwd lng="pt"><![CDATA[Frutose]]></kwd>
<kwd lng="en"><![CDATA[Gout]]></kwd>
<kwd lng="en"><![CDATA[Hyperuricemia]]></kwd>
<kwd lng="en"><![CDATA[Purines]]></kwd>
<kwd lng="en"><![CDATA[Obesity]]></kwd>
<kwd lng="en"><![CDATA[Ethanol]]></kwd>
<kwd lng="en"><![CDATA[Fructose]]></kwd>
</kwd-group>
</article-meta>
</front><body><![CDATA[ <p align="right"><b>ARTIGO DE REVIS&#195;O</p></b> <br/> <br/><b >Estrat&#233;gias para Interven&#231;&#227;o Nutricional na Hiperuric&#233;mia e Gota</b> <br/> <br/><b >Strategies for Nutritional Intervention in Hyperuricemia and Gout</b>     <p>&nbsp;</p>     <p> <b>Jo&#227;o Martins<sup>1</sup>; Eunice Jorge<sup>2</sup>; Jos&#233; Camolas<sup>3</sup>; Isabel do Carmo<sup>4</sup></b> <br/>      <p ><sup>1</sup>Estagi&#225;rio de Ci&#234;ncias da Nutri&#231;&#227;o, Instituto Superior de Ci&#234;ncias da Sa&#250;de Egas Moniz, Via Alternativa ao Monte da Caparica, 2829 - 511 Caparica, Portugal      <br><sup>2</sup>Estagi&#225;ria de Ci&#234;ncias da Nutri&#231;&#227;o, Faculdade de Ci&#234;ncias da Nutri&#231;&#227;o e Alimenta&#231;&#227;o da Universidade do Porto, Rua Dr. Roberto Frias, s/n, 4200-465 Porto, Portugal     <br><sup>3</sup>Nutricionista, Servi&#231;o de Endocrinologia, Diabetes e Metabolismo, Hospital de Santa Maria, Avenida Professor Egas Moniz, 1649-035 Lisboa, Portugal      <br><sup>4</sup>M&#233;dica Endocrinologista, Faculdade de Medicina da Universidade de Lisboa, Avenida Professor Egas Moniz, 1649-028 Lisboa, Portugal     <p><a href="#c0">Endere&#231;o para correspond&#234;ncia</a><a name="topc0"></a></p>     <p>&nbsp;</p>     <p><b >RESUMO</b></p>     ]]></body>
<body><![CDATA[<p>  <br/>A preval&#234;ncia de hiperuric&#233;mia e gota tem vindo a aumentar na popula&#231;&#227;o portuguesa, nos &#250;ltimos anos, &#224; semelhan&#231;a do que acontece com outros pa&#237;ses desenvolvidos. O objectivo deste artigo &#233; fazer uma revis&#227;o de evid&#234;ncia dispon&#237;vel, relativamente &#224; interven&#231;&#227;o nutricional nestas patologias, tendo em vista identificar estrat&#233;gias para a interven&#231;&#227;o nutricional em doentes com hiperuric&#233;mia e gota, com maior potencial de efectividade. Considerando que a hiperuric&#233;mia e a gota se associam frequentemente &#224; obesidade, hipertens&#227;o arterial, dislipid&#233;mia, aterosclerose e s&#237;ndrome metab&#243;lica, estes doentes representam uma oportunidade singular para uma avalia&#231;&#227;o e uma orienta&#231;&#227;o nutricional mais abrangente.  </p>     <p><b >Palavras-Chave</b>: Gota, Hiperuric&#233;mia, Purinas, Obesidade, Etanol, Frutose  </p>     <p>&nbsp;</p>  <hr>     <p>&nbsp;</p>     <p><b >ABSTRACT</b> </p>      <p>The prevalence of hyperuricemia and gout have been increasing in the Portuguese population, in recent years, similar to what happens with other developed countries. The purpose of this article is to review the available evidence in relation to nutritional intervention in these pathologies, in order to identify strategies for nutritional intervention in patients with hyperuricemia and gout, with greater potential for effectiveness. Whereas hyperuricemia and gout is often associated with obesity, hypertension, dyslipidemia, atherosclerosis and metabolic syndrome, these patients represent a unique opportunity for an evaluation and a more comprehensive nutritional guidance. </p>     <p><b >keywords</b>: Gout, Hyperuricemia, Purines, Obesity, Ethanol, Fructose </p>      <p>&nbsp;</p> <hr>     <p>&nbsp;</p>     <p><b >INTRODU&#199;&#195;O</b>     ]]></body>
<body><![CDATA[<br/>Ao     longo da hist&#243;ria, a gota tem sido associada a alimentos ricos em purinas e ao     consumo excessivo de &#225;lcool (1). Tendo em conta que a sua incid&#234;ncia se     relacionava com um estilo de vida habitual nas pessoas com elevados recursos     econ&#243;micos, recebeu a designa&#231;&#227;o de &#8220;doen&#231;a dos reis&#8221; (1). A patologia foi     primeiramente identificada pelos eg&#237;pcios, em 2640 a. C., como podagra (gota     aguda, que ocorre na articula&#231;&#227;o metatarso-fal&#226;ngica prim&#225;ria) (1).     Posteriormente foi reconhecida por Hip&#243;crates, no s&#233;culo V a. C., como <i     >unwalkable disease</i>, tendo este sido     respons&#225;vel pela identifica&#231;&#227;o da liga&#231;&#227;o entre a doen&#231;a e o estilo de vida     ]]></body>
<body><![CDATA[luxuoso, distinguindo a podagra, como artrite dos ricos, do reumatismo, a     artrite dos pobres (1). O conceito de tofos gotosos foi descrito, pela primeira     vez, por Galen e Antoni van Leeuwenhoek (1632-1723), que descreveram o seu     aspecto macrosc&#243;pico, apesar de a sua composi&#231;&#227;o qu&#237;mica ser ainda desconhecida     (1). A primeira pessoa a mencionar a palavra &#8220;gota&#8221; foi Randolphus de Bocking (1197-1258)     (1). Mais tarde, Alfred Baring Garrod descreveu um m&#233;todo semi-quantitativo     para a medi&#231;&#227;o do &#225;cido &#250;rico no sangue ou na urina, sendo que este foi o     primeiro teste cl&#237;nico, alguma vez testado (2). Seegmiller foi respons&#225;vel pela     descri&#231;&#227;o do papel relevante da produ&#231;&#227;o excessiva e da excre&#231;&#227;o diminu&#237;da do     urato na patog&#233;nese da hiperuric&#233;mia (3). Relativamente ao tratamento da     ]]></body>
<body><![CDATA[hiperuric&#233;mia, Garrod foi um dos primeiros a sugerir que esta poderia ser     controlada baixando a ingest&#227;o de alimentos ricos em purinas, conceito esse que     se perpetuou at&#233; aos dias de hoje (1).      <br/>A     hiperuric&#233;mia consiste na presen&#231;a de n&#237;veis elevados de &#225;cido &#250;rico s&#233;rico,     devido &#224; sua produ&#231;&#227;o end&#243;gena elevada e &#224; excre&#231;&#227;o renal reduzida (4-6). O     valor normal da uricemia &#233; 5,0mg/dl, valor mantido &#224; custa da excre&#231;&#227;o do     excedente da produ&#231;&#227;o. Desta forma, valores s&#233;ricos de &#225;cido &#250;rico, superiores     ou iguais a 7mg/dL, nos homens, e a 6mg/dL, em mulheres, s&#227;o crit&#233;rios de     diagn&#243;stico para a hiperuric&#233;mia (4, 6). Esta diferen&#231;a entre sexos poder&#225;     ]]></body>
<body><![CDATA[estar relacionada com o aumento da excre&#231;&#227;o renal de &#225;cido &#250;rico induzida pelos     estrog&#233;nios nas mulheres e com o papel da obesidade abdominal, mais prevalente     nos homens, que se associa a uma diminui&#231;&#227;o da excre&#231;&#227;o de &#225;cido &#250;rico (4, 7).     Acima dos valores citados, h&#225; supersatura&#231;&#227;o de urato de s&#243;dio e consequente     propens&#227;o &#224; sua precipita&#231;&#227;o, originando os dep&#243;sitos de urato monoss&#243;dico     cristalizado (5). A hiperprodu&#231;&#227;o de &#225;cido &#250;rico pode ter causas gen&#233;ticas,     nomeadamente o aumento da afinidade da enzima fosforribosil-pirofosfato sintase     para &#945;-D-Ribose 5-fosfato, a resist&#234;ncia ao feedback negativo (do GMP,     GDP, AMP e ADP) aumentando a actividade das enzimas envolvidas no catabolismo     das purinas e d&#233;fices enzim&#225;ticos no metabolismo do &#225;cido &#250;rico (5-6, 8). As     ]]></body>
<body><![CDATA[situa&#231;&#245;es em que existe aumento da purinoss&#237;ntese de novo, nomeadamente, as     doen&#231;as em que h&#225; um aumento do turnover celular (por exemplo, doen&#231;a     neopl&#225;sica), os estados hipercatab&#243;licos e alguns f&#225;rmacos (por exemplo os     citot&#243;xicos) tamb&#233;m podem conduzir a hiperuric&#233;mia (5-6, 8). Apesar de o     consumo excessivo de purinas ser o mais reconhecido, de entre os factores     ambientais, os h&#225;bitos de ingest&#227;o de bebidas alco&#243;licas, a obesidade, as     dietas hiperproteicas ou hiperenerg&#233;ticas, a ingest&#227;o muito elevada de frutose     e o sedentarismo ser&#227;o igualmente importantes (4, 8, 10-15).      <br/>A     gota &#233; uma doen&#231;a reumatol&#243;gica, inflamat&#243;ria, metab&#243;lica, que resulta de uma     ]]></body>
<body><![CDATA[altera&#231;&#227;o do metabolismo das purinas e normalmente aparece associada &#224;     obesidade, piorando com a ingest&#227;o excessiva de &#225;lcool e gordura (4-6).     Caracteriza-se pela deposi&#231;&#227;o de cristais de urato nas articula&#231;&#245;es e progride     em 4 est&#225;dios: hiperuric&#233;mia assintom&#225;tica, artrite gotosa aguda (os cristais     de urato monoss&#243;dico presentes na articula&#231;&#227;o s&#227;o fagocitados por leuc&#243;citos,     levando &#224; mais frequente manifesta&#231;&#227;o inicial de gota), gota intercr&#237;tica     (per&#237;odo entre as crises agudas de gota com aus&#234;ncia total de sintomas) e gota     cr&#243;nica tof&#225;cea (acumula&#231;&#227;o de cristais em v&#225;rias localiza&#231;&#245;es, revelando um     estado prolongado e evolu&#237;do da doen&#231;a) (5, 8). Nem todos os indiv&#237;duos que     apresentam hiperuric&#233;mia desenvolvem gota, mas quase sempre doentes     ]]></body>
<body><![CDATA[diagnosticados com gota tiveram hiperuric&#233;mia assintom&#225;tica durante v&#225;rios anos     (4). Com o avan&#231;o da doen&#231;a, os sintomas ocorrem com maior frequ&#234;ncia, de forma     mais prolongada e com mais jun&#231;&#245;es articulares afectadas (17, 20-21). A     presen&#231;a de hiperuric&#233;mia n&#227;o &#233; apenas factor de risco para a artrite e gota     cr&#243;nica, tamb&#233;m o &#233; para a incid&#234;ncia de c&#225;lculos renais, eventos     cardiovasculares e mortalidade prematura (4, 6, 9). A hiperuric&#233;mia tamb&#233;m pode     surgir associada a outras patologias, das quais se destacam a s&#237;ndrome     metab&#243;lica, a hipertens&#227;o arterial, diabetes tipo 2 e a doen&#231;a renal cr&#243;nica     (4-6, 8-9, 16-19).     <br/><u>Epidemiologia     ]]></body>
<body><![CDATA[da Hiperuric&#233;mia e Gota</u><u></u>     <br/>A     evid&#234;ncia epidemiol&#243;gica, sugere que a preval&#234;ncia de gota aumentou nas &#250;ltimas     d&#233;cadas (20). Segundo dados do The National Health and Nutrition Examination     Survey, a preval&#234;ncia de gota nos adultos norte-americanos, em 2007-2008, era     de 3,9% (8,3 milh&#245;es de adultos), correspondendo a 5,9% no sexo masculino e a     2,0% nas mulheres (21). Foram observados n&#237;veis m&#233;dios de &#225;cido &#250;rico de 6,14     mg/dL nos homens e de 4,87 mg/dL nas mulheres, com preval&#234;ncias de     hiperuric&#233;mia de 21,2% e 21,6% respectivamente (21). Em termos comparativos, os     valores de hiperuric&#233;mia nos adultos portugueses s&#227;o inferiores, mas t&#234;m vindo     ]]></body>
<body><![CDATA[a aumentar (22). Num estudo epidemiol&#243;gico, realizado numa amostra de adultos,     representativa da cidade do Porto, foi verificada uma preval&#234;ncia de     hiperuric&#233;mia de 12,8%, sendo mais frequente nos homens (22).      <br/><u>Fisiopatologia     da Hiperuric&#233;mia e Gota</u><u></u>     <br/>a)     Catabolismo das purinas     <br/>O     &#225;cido &#250;rico prov&#233;m da degrada&#231;&#227;o das purinas (Adenina e Guanina; dois dos     nucle&#243;tidos que comp&#245;em o DNA e o RNA), aproximadamente 85% &#233; de produ&#231;&#227;o     ]]></body>
<body><![CDATA[end&#243;gena e cerca de 15% &#233; resultante da metaboliza&#231;&#227;o das nucleoprote&#237;nas     contidas nos alimentos (4, 6, 8, 23). Estes nucle&#243;tidos s&#227;o captados no f&#237;gado,     sendo degradados em nucleos&#237;deos, que posteriormente ser&#227;o convertidos em     hipoxantina e esta em xantina, pela enzima xantina oxidase, que tamb&#233;m converte     a xantina em &#225;cido &#250;rico, produto final da degrada&#231;&#227;o das purinas no organismo     humano (4, 8, 24).      <br/>b)     Fisiologia molecular do transporte e excre&#231;&#227;o do urato     <br/>Os     n&#237;veis s&#233;ricos de urato dependem do balan&#231;o entre a sua produ&#231;&#227;o e a excre&#231;&#227;o     ]]></body>
<body><![CDATA[(8, 17). Normalmente, o organismo elimina urato suficiente por via renal (70%),     e em menor propor&#231;&#227;o por via fecal (30%), mantendo uma concentra&#231;&#227;o plasm&#225;tica     entre 1,5 e 6,0 mg/dl nas mulheres e entre 2,5 e 7,0 mg/dl nos homens (6, 17).     O &#225;cido &#250;rico &#233; um &#225;cido fraco, que tem uma alta constante de dissocia&#231;&#227;o,     circulando no plasma (pH 7.4) principalmente na forma de urato, ligado &#224;     albumina (4, 6, 8, 24). Os c&#225;lculos de &#225;cido &#250;rico, formados em urinas com pH     &#225;cido, constituem entre 5 a 10% dos c&#225;lculos urin&#225;rios (8, 17, 24). A     hiperuricos&#250;ria, definida como sendo a excre&#231;&#227;o renal de urato superior a     800mg/dia nos homens e a 750mg/dia nas mulheres, pode ser uma causa de forma&#231;&#227;o     c&#225;lculos de urato. O tratamento dos c&#225;lculos de &#225;cido &#250;rico pode passar pela     ]]></body>
<body><![CDATA[alcaliza&#231;&#227;o da urina para pH de 6,0-6,5, por via da ingest&#227;o de fruta, legumes     e de &#225;gua mineral alcalina, por exemplo (17). Um estudo de interven&#231;&#227;o, numa     popula&#231;&#227;o de estudantes universit&#225;rias japonesas, concluiu que a alcaliza&#231;&#227;o da     urina, atrav&#233;s da modela&#231;&#227;o da ingest&#227;o nutricional, promove a excre&#231;&#227;o de     &#225;cido &#250;rico (18).     <br/>c)     Rela&#231;&#245;es entre Hiperuric&#233;mia, Obesidade e S&#237;ndroma Metab&#243;lica     <br/>A     hiperuric&#233;mia associa-se, frequentemente, a componentes da s&#237;ndrome metab&#243;lica,     como a obesidade e a dislipid&#233;mia, e com factores de risco para a doen&#231;a     ]]></body>
<body><![CDATA[cardiovascular (4-6, 8-10, 14, 16, 19-21, 25). Em indiv&#237;duos com diabetes tipo     2, a obesidade visceral associou-se positivamente &#224; uricemia (10). Este tipo de     adiposidade condiciona altera&#231;&#245;es metab&#243;licas, que contribuem para a     acidifica&#231;&#227;o da urina, promotora da forma&#231;&#227;o de c&#225;lculos de &#225;cido &#250;rico (26).      <br/>Tratamento     Farmacol&#243;gico da Hiperuric&#233;mia e Gota     <br/>O     tratamento farmacol&#243;gico da hiperuric&#233;mia faz-se, habitualmente, com recurso ao     Alopurinol, que actua como inibidor da enzima xantinaoxidase (converte a     hipoxantina em xantina e esta em &#225;cido &#250;rico), e uricos&#250;ricos (por exemplo,     ]]></body>
<body><![CDATA[probenicida ou sulfimpirazona), que bloqueiam a reabsor&#231;&#227;o tubular de urato,     aumentando a sua excre&#231;&#227;o (5). Em casos de artrite gotosa aguda pode ser     prescrita a colchicina, um f&#225;rmaco utilizado essencialmente nas primeiras 24     horas ap&#243;s a crise (5).     <br/><u>Interven&#231;&#227;o     Nutricional na Hiperuric&#233;mia e Gota</u><u></u>     <br/>Na     <a href ="/img/revistas/nut/n19/n19a06t1.jpg">Tabela 1</a> sintetiza-se alguma da evid&#234;ncia dispon&#237;vel, relativa &#224; influ&#234;ncia de     
alimentos e nutrientes seleccionados na incid&#234;ncia de gota.     <br/>a)     ]]></body>
<body><![CDATA[Papel do aporte proteico     <br/>Habitualmente     aos doentes com hiperuric&#233;mia e gota &#233; desaconselhado a ingest&#227;o de algumas     carnes e marisco, devido &#224; sua riqueza em purinas. De facto, alguns estudos     populacionais conclu&#237;ram que o consumo elevado de carne e de marisco est&#225;     associado a um risco aumentado de gota e de hiperuric&#233;mia (27, 31-32). No     entanto, nem todos os alimentos fornecedores de prote&#237;nas condicionar&#227;o estas     altera&#231;&#245;es, sendo que, por exemplo, o consumo de leite est&#225; associado a uma     redu&#231;&#227;o do risco, por via do papel uricos&#250;rico das prote&#237;nas do leite (27, 31).     Acresce que o consumo de prote&#237;na vegetal tamb&#233;m n&#227;o parece associar-se a um     ]]></body>
<body><![CDATA[acr&#233;scimo no risco de gota, mesmo quando se consideram vegetais fornecedores de     purinas (27). Note-se ainda que a ingest&#227;o total de prote&#237;na n&#227;o parece estar     directamente associada &#224; eleva&#231;&#227;o dos n&#237;veis s&#233;ricos de &#225;cido &#250;rico (31-33).     <br/>b)     Papel da restri&#231;&#227;o cal&#243;rica     <br/>A     insulinorresist&#234;ncia e a hiperleptin&#233;mia, associadas ao excesso de peso e &#224;     obesidade abdominal, parecem condicionar uma diminui&#231;&#227;o da excre&#231;&#227;o do &#225;cido     &#250;rico, aumentando assim os seus n&#237;veis s&#233;ricos (4, 10, 14). Em doentes com     hiperuric&#233;mia e excesso de peso, &#233; aconselhada uma restri&#231;&#227;o energ&#233;tica     ]]></body>
<body><![CDATA[moderada (33-34). A perda de peso pode representar uma estrat&#233;gia eficiente     para reduzir os n&#237;veis s&#233;ricos de &#225;cido &#250;rico, especialmente em mulheres na     p&#243;s-menopausa e em homens (35).     <br/>c)     Papel do aporte h&#237;drico     <br/>Os     c&#225;lculos de &#225;cido &#250;rico formam-se em urinas com pH &#225;cido (8, 36-37). Em     associa&#231;&#227;o a uma dieta que promova a alcaliniza&#231;&#227;o da urina (rica em citrato e     bicarbonato) &#233; recomend&#225;vel uma ingest&#227;o h&#237;drica que promova um volume de urina     a rondar os dois litros nas 24 horas (37). A ingest&#227;o de &#225;gua, por via do     ]]></body>
<body><![CDATA[aumento da excre&#231;&#227;o renal, conduz a uma diminui&#231;&#227;o dos n&#237;veis s&#233;ricos de &#225;cido     &#250;rico, bem como a uma menor probabilidade de forma&#231;&#227;o de c&#225;lculos renais. Em resumo,     recomenda-se a ingest&#227;o de cerca de 2-3 litros de l&#237;quidos por dia, dando-se     prefer&#234;ncia &#224; ingest&#227;o de &#225;gua (5).     <br/>d)     Papel do etanol     <br/>O     consumo de etanol pode induzir hiperuric&#233;mia, por diminui&#231;&#227;o da excre&#231;&#227;o e     aumento da produ&#231;&#227;o do &#225;cido &#250;rico (11-13). No seu metabolismo hep&#225;tico, o     etanol &#233; primeiro oxidado em acetalde&#237;do, que &#233; oxidado em acetato. O acetato &#233;     ]]></body>
<body><![CDATA[metabolizado em acetil-CoA e durante esta convers&#227;o o ATP &#233; desfosforilado em     AMP. Uma parte desse AMP pode entrar na via da degrada&#231;&#227;o do nucle&#243;tido de     adenina, conduzindo &#224; produ&#231;&#227;o de &#225;cido &#250;rico. Durante o metabolismo do etanol     ocorre o aumento dos n&#237;veis s&#233;ricos de lactato que, a n&#237;vel renal, condiciona     uma diminui&#231;&#227;o da uricos&#250;ria (4, 12-13, 33). Considerando os resultados obtidos     do Third National Health and Nutrition Examination Survey, efetuado numa     popula&#231;&#227;o de 14809 pessoas dos EUA, as diferentes bebidas alco&#243;licas (cerveja,     licor e vinho) t&#234;m diferente impacto nos valores s&#233;ricos de &#225;cido &#250;rico. O     consumo moderado de vinho (at&#233; um copo por dia) n&#227;o se associa ao aumento do     risco de hiperuric&#233;mia, em contraponto ao consumo de cerveja que confere um     ]]></body>
<body><![CDATA[risco maior (38). Al&#233;m do seu teor de &#225;lcool, a cerveja &#233; rica em purinas, em     especial guanosina, favorecendo assim a hiperuric&#233;mia e o risco de gota (39).     <br/>e)     Papel da Frutose     <br/>H&#225;     alguma evid&#234;ncia que associa a ingest&#227;o elevada de frutose com o aumento das     concentra&#231;&#245;es s&#233;ricas de &#225;cido &#250;rico (15, 40-41). Durante o seu metabolismo     hep&#225;tico, a frutose &#233; fosforilada a frutose 1-fosfato, por ac&#231;&#227;o da enzima     frutoquinase (4). Esta reac&#231;&#227;o estimula a hidr&#243;lise do ATP, com um subsequente     aumento de AMP (40). Posto isto, a enzima aldolase quebra a frutose 1-fosfato     ]]></body>
<body><![CDATA[em dihidroxiacetonafosfato e D-gliceralde&#237;do (4). A ac&#231;&#227;o da frutoquinase &#233;     r&#225;pida, mas a reac&#231;&#227;o com a aldolase &#233; lenta, o que implica que, quando a     ingest&#227;o de frutose &#233; excessiva, exista uma acumula&#231;&#227;o da frutose     <br> 1-fosfato e uma diminui&#231;&#227;o da concentra&#231;&#227;o intracelular do fosfato inorg&#226;nico (4). A baixa disponibilidade de fosfato limita a forma&#231;&#227;o de ATP, assim o ADP ou o AMP resultantes deste metabolismo s&#227;o catabolizados, conduzindo &#224; hiperuric&#233;mia (4). Importa tamb&#233;m atentar &#224; import&#226;ncia da ingest&#227;o de sorbitol, que pode ser convertido em frutose com ac&#231;&#227;o da enzima sorbitol desidrogenase, podendo contribuir para o aumento da produ&#231;&#227;o de uratos (4).  <br/><u>Papel da Actividade F&#237;sica em Indiv&#237;duos com Hiperuric&#233;mia e Gota</u><u></u> <br/>A actividade f&#237;sica &#233; considerada um meio importante de preven&#231;&#227;o da hiperuric&#233;mia (15, 24). Em indiv&#237;duos do sexo masculino, concluiu-se que o risco de gota &#233; mais baixo naqueles que s&#227;o fisicamente mais ativos e que mant&#234;m o peso adequado (15). A pr&#225;tica de exerc&#237;cio f&#237;sico de intensidade moderada associa-se a concentra&#231;&#245;es mais baixas de &#225;cido &#250;rico, podendo ser &#250;til na preven&#231;&#227;o de gota (24). </p>     <p><b>AN&#193;LISE CR&#205;TICA</b> <br/>A alimenta&#231;&#227;o ser&#225; uma via segura e efectiva na preven&#231;&#227;o e abordagem terap&#234;utica da hiperuric&#233;mia e da gota. A evid&#234;ncia dispon&#237;vel sustenta a import&#226;ncia das estrat&#233;gias nutricionais, muito para al&#233;m da cl&#225;ssica restri&#231;&#227;o de purinas. Algumas refer&#234;ncias continuam a propor que o doente com gota opte pela evic&#231;&#227;o de alimentos ricos em purinas, tais como o porco, ca&#231;a, v&#237;sceras, charcutaria, conservas de peixe, mariscos, caf&#233;, ch&#225; e chocolate (5). No entanto, outros autores alargam a lista de alimentos a evitar ao etanol e ao consumo excessivo de frutose (5, 42). Na realidade, a associa&#231;&#227;o entre uma dieta hiperproteica, fonte de alimentos ricos em purinas, com a hiperuric&#233;mia e a gota, carece de documenta&#231;&#227;o cient&#237;fica adequada (28, 43). Embora as dietas hiperproteicas possam conter, concomitantemente, grandes quantidades de purinas, a sua ingest&#227;o n&#227;o est&#225; directamente associada com os n&#237;veis do &#225;cido &#250;rico s&#233;rico (31-33). Em boa verdade, Li-Ching e colaboradores j&#225; haviam chamado a aten&#231;&#227;o para o facto do consumo de alimentos ricos em purinas per se n&#227;o ser factor de risco importante para o aparecimento de gota (42). Numa abordagem hol&#237;stica do doente com hiperuric&#233;mia e/ou gota, recomenda-se que se rastreiem e tratem os fatores de risco cardiovascular, que fazem parte da s&#237;ndrome metab&#243;lica, nomeadamente a obesidade, hipertens&#227;o, hiperlipidemia, insulinorresist&#234;ncia e diabetes (44-45). De facto, existe investiga&#231;&#227;o que demonstrara um risco aumentado de gota em homens com IMC maior ou igual a 25, sendo que a magnitude dessa associa&#231;&#227;o varia positivamente com o aumento do IMC (46). Em doentes com aumento da adiposidade e naqueles com s&#237;ndrome de resist&#234;ncia &#224; insulina, a hiperuric&#233;mia tamb&#233;m estar&#225; associada a uma redu&#231;&#227;o na uricos&#250;ria (4, 47). Portanto, em doentes obesos, a orienta&#231;&#227;o diet&#233;tica deve ser no sentido de uma dieta hipocal&#243;rica, com vista ao controlo n&#227;o s&#243; da uricemia, mas tamb&#233;m do peso e das comorbilidades. Um aspecto de extrema import&#226;ncia na orienta&#231;&#227;o nutricional do doente com hiperuric&#233;mia ou gota &#233; o consumo de bebidas alco&#243;licas e de alimentos ricos em frutose. A ingest&#227;o de &#225;lcool aumenta a uricemia, por incrementar a degrada&#231;&#227;o do ATP em adenosina monofosfato (AMP), que &#233; rapidamente convertido em &#225;cido &#250;rico e tamb&#233;m por reduzir a excre&#231;&#227;o renal do &#225;cido &#250;rico (4, 11-13). Quanto &#224; ingest&#227;o de alimentos ricos em frutose, existe um grande conjunto de evid&#234;ncia cient&#237;fica que os associa ao aumento dos n&#237;veis s&#233;ricos de &#225;cido &#250;rico. Contudo, existe a necessidade de fazer um contraponto, relativamente ao tipo de alimentos ricos em frutose, uma vez que a fruta, por exemplo, &#233; respons&#225;vel pela alcaliniza&#231;&#227;o da urina, o que vai promover o aumento da excre&#231;&#227;o de &#225;cido &#250;rico. Por outro lado, este efeito uricos&#250;rico pode ser ainda incrementado pelo fornecimento concomitante de vitamina C (30).  </p>     <p><b>CONCLUS&#213;ES</b> <br/>A preval&#234;ncia da hiperuric&#233;mia tem vindo a aumentar na nossa popula&#231;&#227;o, sendo essencial definir linhas orientadoras para a interven&#231;&#227;o nutricional a este n&#237;vel. A hiperuric&#233;mia e a gota, geralmente, est&#227;o associadas com a obesidade, hipertens&#227;o, dislipid&#233;mia, aterosclerose e s&#237;ndrome metab&#243;lica. Neste contexto, um doente com gota representa uma oportunidade singular para uma avalia&#231;&#227;o mais abrangente e uma orienta&#231;&#227;o diet&#233;tica mais objetiva e esclarecida. Assim sendo, as linhas orientadoras em termos de interven&#231;&#227;o nutricional devem incidir nomeadamente: a) na adequa&#231;&#227;o do consumo de alimentos ricos em prote&#237;nas e purinas, por exemplo, assegurando o consumo adequado de leite e derivados; b) na prescri&#231;&#227;o de um plano alimentar estruturado e ligeiramente hipocal&#243;rico em casos de obesidade; c) na restri&#231;&#227;o de bebidas alco&#243;licas; d) na restri&#231;&#227;o de bebidas ou produtos alimentares com quantidades excessivas de frutose e/ou sorbitol; e) na ingest&#227;o di&#225;ria de cerca de dois litros de &#225;gua alcalina.  <br/>Neste contexto, a terap&#234;utica nutricional n&#227;o dever&#225; estar limitada &#224;s estrat&#233;gias de evic&#231;&#227;o de alimentos ricos em purinas, adoptando uma perspectiva hol&#237;stica, baseada na evid&#234;ncia dispon&#237;vel. Com este formato, constituir&#225; uma ferramenta potencialmente mais eficaz, ao dispor dos profissionais de sa&#250;de, nomeadamente os nutricionistas, na promo&#231;&#227;o de ganhos em sa&#250;de para os utentes. </p>     <p>&nbsp;</p>     <!-- ref --><p><b >REFER&#202;NCIAS BIBLIOGR&#193;FICAS</b> <br/>1. Nuki G, Simkin, PA. A concise history of gout and hyperuricemia and their treatment. Arthritis Research & Therapy 2006; 8: 1-5 <br/>2.    &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;[&#160;<a href="javascript:void(0);" onclick="javascript: window.open('/scielo.php?script=sci_nlinks&ref=1724478&pid=S2182-7230201300040000600001&lng=','','width=640,height=500,resizable=yes,scrollbars=1,menubar=yes,');">Links</a>&#160;]<!-- end-ref --><!-- ref --> Garrod AB. Observations on certain pathological conditions of the blood and urine in gout, rheumatism and Bright&#8217;s disease. 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Studies on the impaired metabolism of uric acid in obese subjects: marked reduction of renal urate excretion and its improvement by a low-calorie diet. Int J Obes 1986; 10: 255-64     &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;[&#160;<a href="javascript:void(0);" onclick="javascript: window.open('/scielo.php?script=sci_nlinks&ref=1724523&pid=S2182-7230201300040000600046&lng=','','width=640,height=500,resizable=yes,scrollbars=1,menubar=yes,');">Links</a>&#160;]<!-- end-ref --><p>&nbsp;</p>     <p>  <b ><a href="#topc0">Endere&#231;o para correspond&#234;ncia</a><a name="c0"></a></b> <br/>Jos&#233; Camolas <br/>Servi&#231;o de Endocrinologia, Diabetes e Metabolismo, Piso 6, Hospital de Santa Maria, Avenida Professor Egas Moniz 1649-028 Lisboa, Portugal     <br> <a href="mailto:jose.camolas@gmail.com ">jose.camolas@gmail.com </a></p> </p>  <br/>Recebido a 1 de Novembro de 2013 <br/>Aceite a 19 de Fevereiro de 2014 <br/>       ]]></body><back>
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