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"documento" => "simple-article" "crossmark" => 1 "subdocumento" => "cor" "cita" => "Med Clin. 2016;146:374-5" "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">Letter to the Editor</span>" "titulo" => "Herpes simplex virus encephalitis during pregnancy: Maternal and neonatal outcomes" "tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "374" "paginaFinal" => "375" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Encefalitis por virus herpes simple durante la gestación: evolución materna y neonatal" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Alejandro Avila-Alvarez, Luis Ignacio Devesa, Fernando Mosteiro Pereira, Elvira Clavero Fernández" "autores" => array:4 [ 0 => array:2 [ "nombre" => "Alejandro" "apellidos" => "Avila-Alvarez" ] 1 => array:2 [ "nombre" => "Luis Ignacio" "apellidos" => "Devesa" ] 2 => array:2 [ "nombre" => "Fernando" "apellidos" => "Mosteiro Pereira" ] 3 => array:2 [ "nombre" => "Elvira" "apellidos" => "Clavero Fernández" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0025775315006168" "doi" => "10.1016/j.medcli.2015.10.023" "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/S0025775315006168?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020616302868?idApp=UINPBA00004N" "url" => "/23870206/0000014600000008/v1_201607210236/S2387020616302868/v1_201607210236/en/main.assets" ] "en" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Letter to the Editor</span>" "titulo" => "Familial hypokalemic periodic paralysis associated with autoimmune thyroiditis" "tieneTextoCompleto" => true "saludo" => "<span class="elsevierStyleItalic">Dear Editor</span>," "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "375" "paginaFinal" => "376" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Marta Cano Megías, Loreto Fernández Rodríguez, Javier Mancha Ramos, José Luis Espinosa Figueroa" "autores" => array:4 [ 0 => array:4 [ "nombre" => "Marta" "apellidos" => "Cano Megías" "email" => array:1 [ 0 => "mcanomegias@gmail.com" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:2 [ "nombre" => "Loreto" "apellidos" => "Fernández Rodríguez" ] 2 => array:2 [ "nombre" => "Javier" "apellidos" => "Mancha Ramos" ] 3 => array:2 [ "nombre" => "José Luis" "apellidos" => "Espinosa Figueroa" ] ] "afiliaciones" => array:1 [ 0 => array:2 [ "entidad" => "Servicio de Nefrología, Hospital Universitario Príncipe de Asturias, Alcalá de Henares, Madrid, Spain" "identificador" => "aff0005" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Parálisis periódica hipopotasémica familiar asociada a tiroiditis autoinmune" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Hypokalemic paralysis (HP) is an emergency that can be fatal without the proper treatment and diagnosis. The periodic form (HPP) is caused by mutations in voltage-gated ion channels of the skeletal muscle.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,2</span></a> It is characterized by recurrent episodes of flaccid muscle paralysis associated with a decreased concentration of potassium due to a sudden shift of potassium into the inner cell, with a normal total body content. Usually, patients are asymptomatic between crises, with normal potassium levels in plasma. Genetic diagnosis is important if there is clinical suspicion, as there is a genotype–phenotype correlation.<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">3,4</span></a> We describe one of the first cases of familial HPP by mutation in the gene <span class="elsevierStyleItalic">CACNA1S</span> associated with autoimmune thyroiditis.</p><p id="par0010" class="elsevierStylePara elsevierViewall">A 17-year-old male with subclinical autoimmune hypothyroidism detected at the time of diagnosis of an HP episode. The patient came back to the emergency room with flaccid tetraparesis and severe hypokalaemia. A decrease in urinary excretion of potassium was observed, but no other laboratory abnormalities. The electrocardiogram showed bradycardia with first-degree AV block. Intense exercise and high intake of carbohydrates the day before stood out as possible triggers in the case history. Treatment was started with intravenous and oral potassium chloride administration. In the early hours of the start of treatment, the patient experienced a worsening of hypokalaemia. Potassium levels remained normal between crises. During the second crisis, the patient received levothyroxine replacement therapy without evidence or clinical suspicion of hyperthyroidism. Family history included episodes of HPP in 3 maternal uncles, so a genetic study was performed, demonstrating the presence of the R528H (p.Arg528His) heterozygous mutation in the <span class="elsevierStyleItalic">CACNA1S gene.</span> This mutation was also observed in the mother, aunt and in 3 maternal uncles. Both mother and aunt reported no episodes of muscle weakness.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Familial HPP is an autosomal dominant channelopathy of the sarcolemma, with incomplete penetrance in women.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a> The <span class="elsevierStyleItalic">CACNA1S</span> gene mutation is responsible for 70–80% of cases. The defect is found in the alpha subunit of the calcium channel sensitive to Cav1<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a> dihydropyridines. In 10% of cases, the HPP is due to mutations in the <span class="elsevierStyleItalic">SCN4A</span> gene, encoding the alpha subunit of the Nav1.4 sodium channel. Both channels have similar structures, and when altered, they cannot regulate the ion flow in muscle cells, reducing the muscle contraction ability.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">1,2</span></a> However, the relationship of these muscle channels with the massive influx of intracellular potassium is not clearly established, mainly at muscular level. This ion influx is favoured by an increase in the activity of the sodium-potassium adenosine triphosphatase-(Na.K-ATPase) pump. Intense exercise, high intake of carbohydrates and salt, energy drinks, alcohol, cold and stress, as well as the use of certain drugs<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">4,5</span></a> have been described as triggers for the crises.</p><p id="par0020" class="elsevierStylePara elsevierViewall">This disorder is not associated with cardiac function abnormalities, except for the proarrhythmogenic effect of severe hypokalaemia during the episodes. In this regard, some extramuscular expression of voltage-gated Nav1.4 sodium channel was found in the heart muscle, which could have an additional proarrhythmic effect to that of hypokalaemia <span class="elsevierStyleItalic">per se</span>.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">2,6</span></a> The mechanism by which hypokalaemia and paralysis are resolved is unknown, although treatment with potassium during the episode decreases the time of recovery.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> Potassium, <span class="elsevierStyleItalic">per se</span>, stimulates the activity of the Na-K-ATPase pump, increasing the flow of potassium into the cells; therefore, there must be other factors influencing hypokalaemia recovery.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a> Because the total body potassium content is normal, potassium administration must be done carefully. The intensive potassium intravenous administration during the final phase of the episode, when paralysis disappears, can lead to a rebound hyperkalaemia, which can be fatal, so cardiac monitoring is needed. In contrast, rebound hypokalaemia may occur in some cases, as the one described. These patients often have greater hypovolemia and increased plasma renin activity, which makes them susceptible to a decrease in potassium during volume repletion.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Thyrotoxicosis is the most common endocrine disease associated with HPP in the Asian population. Mutations in the <span class="elsevierStyleItalic">KCNJ18</span> gene have been identified in up to 33% of cases with thyrotoxic HPP. This gene encodes a potassium channel, Kir2.6, which expresses in the muscle and whose transcription is regulated by the thyroid hormone.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> Despite the clinical resemblance to the familial form, genetic assays of Thyrotoxic HPP cases have not identified their association with known familial HPP mutations.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a> There are few cases in the medical literature of non-periodic HP associated with hypothyroidism and autoimmune thyroiditis, but as far as we know, this would be the first reported case of HPP caused by the mutation of the <span class="elsevierStyleItalic">CACNA1S</span> gene associated with Hashimoto's thyroiditis.</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: Cano Megías M, Fernández Rodríguez L, Mancha Ramos J, Espinosa Figueroa JL. Parálisis periódica hipopotasémica familiar asociada a tiroiditis autoinmune. Med Clin (Barc). 2016;146:375–376.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:10 [ 0 => array:3 [ "identificador" => "bib0055" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Muscle channelopathies: does the predicted channel gating pore offer new treatment insights for hypokalaemic periodic paralysis?" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "E. Matthews" 1 => "M.G. 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Letter to the Editor
Familial hypokalemic periodic paralysis associated with autoimmune thyroiditis
Parálisis periódica hipopotasémica familiar asociada a tiroiditis autoinmune
Marta Cano Megías
, Loreto Fernández Rodríguez, Javier Mancha Ramos, José Luis Espinosa Figueroa
Corresponding author
Servicio de Nefrología, Hospital Universitario Príncipe de Asturias, Alcalá de Henares, Madrid, Spain