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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">VEXAS syndrome&#8212;a new autoinflammatory disease involving Vacuoles&#44; the E-1 ubiquitin activating enzyme&#44; X-linkage&#44; Autoinflammation&#44; and Somatic mutations&#8212;was first described in 2020&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> This syndrome is caused by an acquired somatic mutation with an amino acid change &#40;a missense mutation&#41; in the <span class="elsevierStyleItalic">UBA1</span> gene&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> The <span class="elsevierStyleItalic">UBA1</span> gene codes for the E-1 ubiquitin-activating enzyme needed to initiate ubiquitination&#44; a posttranslational modification that regulates intracellular signaling and protein degradation and plays a key role in autophagy&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> This rare entity is caused by acquired mosaic mutations of the <span class="elsevierStyleItalic">UBA1</span> gene in myeloid progenitor cells&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">2</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Identifying new diseases with heterogeneous phenotypes and diverse clinical manifestations&#44; such as autoinflammatory diseases&#44; is a challenge&#46; The aforementioned study&#44; rather than grouping together patients with similar phenotypes and identifying mutations responsible for clinical pictures&#44; took the inverse diagnostic approach and focused on genotypes&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> The genome of patients suffering from undiagnosed systemic inflammatory processes and&#47;or recurrent fever was sequenced&#44; and in 25 men a common mutation was detected in codon 41 of the <span class="elsevierStyleItalic">UBA1</span> gene on the X chromosome&#46; To date&#44; 3 variants of the mutation have been identified&#8212;pMet41Thr&#44; pMet41Val&#44; and pMet41Leu&#8212;and although they had initially only been described in men&#44; they have also been detected in women as a consequence of the inactivation of one X chromosome&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">3</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Most of the patients in the first series described presented with recurrent fever&#44; cutaneous manifestations&#44; lung involvement&#44; ear or nose polychondritis&#44; and hematological disorders such as macrocytic anemia or myelodysplastic syndromes&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> Another characteristic of those patients was the presence of vacuoles in erythroid and myeloid precursors in bone marrow biopsies&#46; It is likely that in the future new clinical characteristics&#44; such as eye or gastrointestinal involvement&#44; joint pain&#44; or adenopathy will be added to the initial description of phenotypes&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">3</span></a> The patients in whom the mutation was detected had been diagnosed with&#44; or had met the criteria for&#44; relapsing polychondritis&#44; Sweet syndrome&#44; polyarteritis nodosa &#40;PAN&#41;&#44; or giant cell arteritis&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Dermatologic manifestations&#44; which were present in more than 80&#37; of patients&#44; are among the most frequent clinical features and precede systemic symptoms in more than half of the cases&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">1&#44;4</span></a> Cutaneous manifestations can be similar to those of other known dermatoses&#44; such as Sweet syndrome&#44; and may include pink or violaceous edematous papules on the neck and trunk&#44; erythematous-violaceous plaques and nodules&#44; livedo racemose&#44; or vasculitic lesions similar to those found in PAN&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> Histopathologically&#44; the skin lesions are characterized by the presence of a dense dermal neutrophilic infiltrate&#44; with variable leukocytoclastic degradation and vessel infiltration&#44; and in some cases&#44; venous thrombosis&#46; The infiltrate consists of neutrophils mixed with precursor myeloid cells positive for CD163 &#40;immature neutrophils and metamyelocytes&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> In some cases signs of PAN were found in addition to neutrophilic dermatosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">3&#44;4</span></a> Sanger sequencing for <span class="elsevierStyleItalic">UBA1</span> in biopsies suggests that the infiltrate is clonal and that the cutaneous manifestations are therefore probably more a consequence of the infiltrate than of an autoinflammatory state&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">An algorithm was recently proposed to detect the mutation in patients previously diagnosed with relapsing polychondritis&#46; Given that frequent and diverse cutaneous manifestations are involved in VEXAS syndrome&#44; it would be useful to reach a similar consensus for male patients diagnosed with Sweet syndrome in dermatology departments&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">2</span></a></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Funding</span><p id="par0040" class="elsevierStylePara elsevierViewall">This work has not received any type of funding&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Conflicts of Interest</span><p id="par0045" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest&#46;</p></span></span>"
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Resident's Forum
RF-VEXAS Syndrome: A New Autoinflammatory Disease
FR-Síndrome VEXAS: Una nueva enfermedad autoinflamatoria
M. Fernández-Parradoa,
Autor para correspondencia
, H. Perandones-Gonzálezb
a Servicio de Dermatología, Hospital Universitario de Navarra, Navarra, Spain
b Servicio de Dermatología, Complejo Asistencial Universitario de León, León, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">VEXAS syndrome&#8212;a new autoinflammatory disease involving Vacuoles&#44; the E-1 ubiquitin activating enzyme&#44; X-linkage&#44; Autoinflammation&#44; and Somatic mutations&#8212;was first described in 2020&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> This syndrome is caused by an acquired somatic mutation with an amino acid change &#40;a missense mutation&#41; in the <span class="elsevierStyleItalic">UBA1</span> gene&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> The <span class="elsevierStyleItalic">UBA1</span> gene codes for the E-1 ubiquitin-activating enzyme needed to initiate ubiquitination&#44; a posttranslational modification that regulates intracellular signaling and protein degradation and plays a key role in autophagy&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> This rare entity is caused by acquired mosaic mutations of the <span class="elsevierStyleItalic">UBA1</span> gene in myeloid progenitor cells&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">2</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Identifying new diseases with heterogeneous phenotypes and diverse clinical manifestations&#44; such as autoinflammatory diseases&#44; is a challenge&#46; The aforementioned study&#44; rather than grouping together patients with similar phenotypes and identifying mutations responsible for clinical pictures&#44; took the inverse diagnostic approach and focused on genotypes&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> The genome of patients suffering from undiagnosed systemic inflammatory processes and&#47;or recurrent fever was sequenced&#44; and in 25 men a common mutation was detected in codon 41 of the <span class="elsevierStyleItalic">UBA1</span> gene on the X chromosome&#46; To date&#44; 3 variants of the mutation have been identified&#8212;pMet41Thr&#44; pMet41Val&#44; and pMet41Leu&#8212;and although they had initially only been described in men&#44; they have also been detected in women as a consequence of the inactivation of one X chromosome&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">3</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Most of the patients in the first series described presented with recurrent fever&#44; cutaneous manifestations&#44; lung involvement&#44; ear or nose polychondritis&#44; and hematological disorders such as macrocytic anemia or myelodysplastic syndromes&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">1</span></a> Another characteristic of those patients was the presence of vacuoles in erythroid and myeloid precursors in bone marrow biopsies&#46; It is likely that in the future new clinical characteristics&#44; such as eye or gastrointestinal involvement&#44; joint pain&#44; or adenopathy will be added to the initial description of phenotypes&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">3</span></a> The patients in whom the mutation was detected had been diagnosed with&#44; or had met the criteria for&#44; relapsing polychondritis&#44; Sweet syndrome&#44; polyarteritis nodosa &#40;PAN&#41;&#44; or giant cell arteritis&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Dermatologic manifestations&#44; which were present in more than 80&#37; of patients&#44; are among the most frequent clinical features and precede systemic symptoms in more than half of the cases&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">1&#44;4</span></a> Cutaneous manifestations can be similar to those of other known dermatoses&#44; such as Sweet syndrome&#44; and may include pink or violaceous edematous papules on the neck and trunk&#44; erythematous-violaceous plaques and nodules&#44; livedo racemose&#44; or vasculitic lesions similar to those found in PAN&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> Histopathologically&#44; the skin lesions are characterized by the presence of a dense dermal neutrophilic infiltrate&#44; with variable leukocytoclastic degradation and vessel infiltration&#44; and in some cases&#44; venous thrombosis&#46; The infiltrate consists of neutrophils mixed with precursor myeloid cells positive for CD163 &#40;immature neutrophils and metamyelocytes&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a> In some cases signs of PAN were found in addition to neutrophilic dermatosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">3&#44;4</span></a> Sanger sequencing for <span class="elsevierStyleItalic">UBA1</span> in biopsies suggests that the infiltrate is clonal and that the cutaneous manifestations are therefore probably more a consequence of the infiltrate than of an autoinflammatory state&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">An algorithm was recently proposed to detect the mutation in patients previously diagnosed with relapsing polychondritis&#46; Given that frequent and diverse cutaneous manifestations are involved in VEXAS syndrome&#44; it would be useful to reach a similar consensus for male patients diagnosed with Sweet syndrome in dermatology departments&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">2</span></a></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Funding</span><p id="par0040" class="elsevierStylePara elsevierViewall">This work has not received any type of funding&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Conflicts of Interest</span><p id="par0045" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest&#46;</p></span></span>"
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ISSN: 00017310
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Actas Dermo-Sifiliográficas
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¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?