<?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>2182-2395</journal-id>
<journal-title><![CDATA[Revista da Sociedade Portuguesa de Dermatologia e Venereologia]]></journal-title>
<abbrev-journal-title><![CDATA[Rev Soc Port Dermatol Venereol]]></abbrev-journal-title>
<issn>2182-2395</issn>
<publisher>
<publisher-name><![CDATA[Sociedade Portuguesa de Dermatologia e Venereologia]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S2182-23952021000200043</article-id>
<article-id pub-id-type="doi">10.29021/spdv.79.2.1394</article-id>
<title-group>
<article-title xml:lang="pt"><![CDATA[Biomarcadores na Urticária Crónica Espontânea]]></article-title>
<article-title xml:lang="en"><![CDATA[Biomarkers in Chronic Spontaneous Urticaria]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Nunes]]></surname>
<given-names><![CDATA[Inês Pratas]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Gonçalo]]></surname>
<given-names><![CDATA[Margarida]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidade de Coimbra Faculdade de Medicina ]]></institution>
<addr-line><![CDATA[Coimbra ]]></addr-line>
<country>Portugal</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidade de Coimbra Faculdade de Medicina Dermatologia, Centro Hospitalar e Universitário de Coimbra]]></institution>
<addr-line><![CDATA[Coimbra ]]></addr-line>
<country>Portugal</country>
</aff>
<pub-date pub-type="pub">
<day>30</day>
<month>06</month>
<year>2021</year>
</pub-date>
<pub-date pub-type="epub">
<day>30</day>
<month>06</month>
<year>2021</year>
</pub-date>
<volume>79</volume>
<numero>2</numero>
<fpage>43</fpage>
<lpage>50</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_arttext&amp;pid=S2182-23952021000200043&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_abstract&amp;pid=S2182-23952021000200043&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_pdf&amp;pid=S2182-23952021000200043&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="pt"><p><![CDATA[RESUMO   Introdução:  Atualmente, a compreensão sobre a etiopatogenia da urticária crónica espontânea é escassa. Devido à carência de dados sobre a sua etiologia, o tratamento disponível tem apenas como objetivo o controlo sintomático, com a maioria dos doentes a serem resistentes à primeira e segunda linha terapêutica (anti-H1 de segunda geração). Tendo em conta o seu impacto no doente e o difícil controlo sintomatológico, surgiu a necessidade de investigar marcadores de resposta ao tratamento da urticária crónica espontânea.  Métodos:  Realizou-se uma revisão sobre biomarcadores que permitem guiar na prática clínica a escalada terapêutica destes doentes, permitindo um controlo mais eficaz e precoce da urticária.  Resultados:  Na urticária crónica espontânea (UCE) têm sido investigados muitos biomarcadores, mas são ainda escassos e por vezes contraditórios os resultados sobre a sua capacidade de prever a resposta à terapêutica. A maioria dos estudos é concordante na menor reatividade aos anti-H1 perante níveis de PCR ou D-dímeros elevados e nas formas de UCE autoimunes. Neste último caso, se predominarem anticorpos IgG anti-Fc&#949;RI ou anti-IgE (autoimunidade tipo IIb), os doentes habitualmente têm o teste do soro autólogo e o teste de ativação dos basófilos positivos, basopenia, eosinopenia e IgE sérica total baixa ou muito baixa, e a resposta ao omalizumab costuma ser pobre e/ou lenta, mas tendencialmente favorável à ciclosporina. Se predominar a IgE anti-self (autoimundade tipo I ou autoalergia) a IgE sérica total é normal ou elevada, na ausência dos marcadores característicos da autoimunidade IIb, e a resposta à ciclosporina é pobre, mas bastante favorável e rápida ao omalizumb. A elevação dos D-dímeros prediz uma reposta desfavorável aos três fármacos.  Conclusão:  Na UCE resistente aos anti-histamínicos de segunda geração, habitualmente com PCR e D-dímeros elevados, os doentes que respondem favoravelmente à ciclosporina e lentamente ao omalizumab têm normalmente uma autoimunidade tipo IIb subjacente e os doentes refratários à terapêutica com ciclosporina e que respondem rapidamente ao omalizumab têm subjacente uma autoimunidade tipo I ou autoalérgica. Estes subtipos podem ser indiretamente avaliados pelos níveis séricos de IgE total, pelos valores de basófilos e eosinófilos circulantes e pelos testes do soro autólogo e de ativação dos basófilos. Contudo, são ainda necessários mais estudos para estabelecer biomarcadores mais precisos que auxiliem na seleção da escalada terapêutica.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[ABSTRACT   Introduction:  At present, the understanding about chronic spontaneous urticarial (CSU) is relatively scarce, particularly with regard to its etiopathogenesis. Due to the lack of data on etiology, the available treatment is only aimed at symptomatic control, with the majority of patients being resistant both to the first and second lines of therapy. Taking into account the impact that CSU may have on the patient and the current difficulties in its control, investigation of biomarkers that predict response to treatment if highly needed.  Methods:  A review was conducted on biomarkers that allow guiding the therapeutic escalation of these patients in clinical practice, allowing a more effective and early control of urticaria.  Results: Many biomarkers are being studied to predict response to therapy, but definitive results are still missing. Nevertheless, most studies point out that a high C-reactive protein or D-dimer, as well as autoimmune-based urticaria, are usually linked to a poor response to anti-H1. In which concerns the two subtypes of auto-immunity involved in CSU, if IgG anti-Fc&#949;RI or anti-IgE predominates (autoimmunity type IIb), patients usually have a positive autologous serum skin test (ASST), a positive basophil activation test (BAT), basopenia, eosinopenia and low or very-low total serum IgE, and response to omalizumab will be slow and/or poor, but there is tendency to a favourable outcome on cyclosporine. If IgE anti-self predominates (autoimmunity type I or autoallergy), response to cyclosporine will be poor, but positive and rapid to omalizumb, and these patients usually have a normal or high IgE that will increase after omalizumab therapy, whereas the other parameters typical of type IIb are absent. High D-dimer predicts an unfavourable response to the three therapies.  Conclusion: In CSU resistant to second-generation antihistamines, patients who respond favourably to cyclosporine and slowly to omalizumab have mostly underlying type IIb autoimmunity, whereas patients refractory to cyclosporine therapy, but who respond rapidly to omalizumab, have underlying type I or auto-allergic autoimmunity. These subtypes can be indirectly evaluated by total serum IgE, blood cell count, ASST and BAT, but more studies with large cohorts are needed to have more correct predictive data on patients&#8217; response to therapy in CSU.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[Biomarkers]]></kwd>
<kwd lng="en"><![CDATA[Urticaria/diagnosis]]></kwd>
<kwd lng="en"><![CDATA[Urticaria/drug therapy]]></kwd>
<kwd lng="pt"><![CDATA[Biomarcadores]]></kwd>
<kwd lng="pt"><![CDATA[Urticaria/diagnóstico]]></kwd>
<kwd lng="pt"><![CDATA[Urticaria /tratamento farmacológico.]]></kwd>
</kwd-group>
</article-meta>
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