Letter to the Editor
S1455X CFTR Mutation and Upper Airway Colonization With Pseudomonas aeruginosa
Mutación S1455X del CFTR y colonización de vías aéreas altas por Pseudomonas aeruginosa
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Kaditis, Stavros-Eleftherios Doudounakis" "autores" => array:4 [ 0 => array:3 [ "nombre" => "Efthimia" "apellidos" => "Kalampouka" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 1 => array:4 [ "nombre" => "Argyri" "apellidos" => "Petrocheilou" "email" => array:1 [ 0 => "apetroch@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" ] ] ] 2 => array:3 [ "nombre" => "Athanasios G." "apellidos" => "Kaditis" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 3 => array:3 [ "nombre" => "Stavros-Eleftherios" "apellidos" => "Doudounakis" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Cystic fibrosis Center, Agia Sophia Children's Hospital, Atenas, Greece" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "First Department of Pediatrics, University of Athens Medical School, Agia Sophia Children's Hospital, Atenas, Greece" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Mutación S1455X del CFTR y colonización de vías aéreas altas por <span class="elsevierStyleItalic">Pseudomonas aeruginosa</span>" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Cystic fibrosis (CF) is a classic example of an autosomal recessive genetic disorder, and multiple variant forms of this disease have been identified. It is caused by CF transmembrane conductance regulator (CFTR) dysfunction resulting from CFTR gene mutations. Not all CFTR mutations are associated with disease expression. The S1455X mutation is very uncommon (0.22% prevalence in our patient population). Individuals with this mutation have only very mild symptoms, if any. We present the first report of twin brothers, both S1455X mutation-carriers, with <span class="elsevierStyleItalic">Pseudomonas aeruginosa</span> colonization of the upper airways.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1–4</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Patients A and B are 2-year-old monozygotic twin brothers. After birth, patient A was admitted to the neonatal intensive care unit for 7 days due to mild breathing difficulties. Routine neonatal immunoreactive trypsinogen screening results were close to the upper limit of normal (65<span class="elsevierStyleHsp" style=""></span>mcg/l; normal value<77<span class="elsevierStyleHsp" style=""></span>mcg/l). When patient A was 7 months old he suffered bronchitis, for which he received inhaled albuterol and fluticasone. At the age of 13 months, he was admitted to a pediatric intensive care unit with lethargy due to severe hyponatremic dehydration and hypochloremic and hypokalemic metabolic alkalosis. At that time a definitive diagnosis of CF was given (chloride sweat levels of 101.6<span class="elsevierStyleHsp" style=""></span>mEq/l and 105.8<span class="elsevierStyleHsp" style=""></span>mEq/l; mutations: F508del and S1455X). The patient has pancreatic sufficiency and normal growth (weight: 75th–90th percentile; height: 90th percentile). Serial pharyngeal swab cultures grew <span class="elsevierStyleItalic">Pseudomonas aeruginosa</span>.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Following his brother's diagnosis, at the age of 13 months patient B was also diagnosed with CF (chloride sweat levels: 80.7<span class="elsevierStyleHsp" style=""></span>mEq/l and 81.7<span class="elsevierStyleHsp" style=""></span>mEq/l, mutations: F508del and S1455X). Similarly, he has pancreatic sufficiency and good growth (weight, 50th percentile; height: 75th percentile). Repeated pharyngeal swab cultures grew <span class="elsevierStyleItalic">Pseudomonas aeruginosa.</span></p><p id="par0020" class="elsevierStylePara elsevierViewall">The case of these two brothers suggests that the S1455X mutation of the CFTR gene in combination with the F508del mutation may be associated with early <span class="elsevierStyleItalic">Pseudomonas aeruginosa</span> colonization of the upper airways. This observation has not been previously reported in the literature. In other reported cases of S1455X CFTR mutation, the sweat test was abnormal, but no respiratory disorders were detected.<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1,2</span></a> Only one case of a child with mild pulmonary disease due to <span class="elsevierStyleItalic">Haemophilus influenza</span> infection and persistent hyponatremia during a heat wave has been described.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">S1455X is a nonsense mutation causing premature transcriptional termination of CFTR. More specifically, the codon for serine at residue 1455 is replaced by a stop codon, hence the designation S1455X.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> In the initial description from Mickle et al.,<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> the S1455X mutation was associated with isolated elevated chloride levels in sweat. <span class="elsevierStyleItalic">In vitro</span> testing predicted preserved CFTR function in lung and pancreatic cells.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Subsequently, Moyer et al.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> suggested that the CFTR-S1455 chloride channel defect was caused by mispolarization to the lateral membrane instead of to the apical membrane.</p><p id="par0030" class="elsevierStylePara elsevierViewall">The two cases previously described in the literature as compound heterozygotes for the F508del and S1455X mutations presented a mild phenotype in the sense that S1455X was associated with minor symptoms and a favorable prognosis, even when accompanied by such a severe mutation as F508del.<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2,3</span></a> Although our pediatric patients are carriers of this same genotype, they appear to have a more severe clinical presentation than that predicted by other authors, leading us to speculate on the possibility of a predominant F508del mutation. Our cases underline the concept of a variable correlation between the CF genotype and phenotype.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Authorship</span><p id="par0035" class="elsevierStylePara elsevierViewall">Efthimia Kalampouka and Argyri Petrocheilou participated equally in the authorship of this letter.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Authorship" ] 1 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Kalampouka E, Petrocheilou A, Kaditis AG, Doudounakis SE. Mutación S1455X del CFTR y colonización de vías aéreas altas por <span class="elsevierStyleItalic">Pseudomonas aeruginosa</span>. Arch Bronconeumol. 2014;50:499–500.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:4 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "A mutation in the cystic fibrosis transmembrane conductance regulator gene associated with elevated sweat chloride concentrations in the absence of cystic fibrosis" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "J.E. Mickle" 1 => "M. Macek Jr." 2 => "S.B. Fulmer-Smentek" 3 => "M.M. Egan" 4 => "E. Schwiebert" 5 => "W. Guggino" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:6 [ "tituloSerie" => "Hum Mol Genet" "fecha" => "1998" "volumen" => "7" "paginaInicial" => "729" "paginaFinal" => "735" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/9499426" "web" => "Medline" ] ] ] ] ] ] ] ] 1 => array:3 [ "identificador" => "bib0010" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Isolated elevated sweat chloride concentrations in the presence of the rare mutation S1455X: an extremely mild form of CFTR dysfunction" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "D. Salvatore" 1 => "R. Tomaiuolo" 2 => "B. Vanacore" 3 => "A. Elce" 4 => "G. Castaldo" 5 => "F. Salvatore" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1002/ajmg.a.30518" "Revista" => array:6 [ "tituloSerie" => "Am J Med Genet A" "fecha" => "2005" "volumen" => "133A" "paginaInicial" => "207" "paginaFinal" => "208" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/15666307" "web" => "Medline" ] ] ] ] ] ] ] ] 2 => array:3 [ "identificador" => "bib0015" "etiqueta" => "3" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Mild cystic fibrosis revealed by persistent hyponatremia during the French 2003 heat wave, associated with the S1455X C-terminus CFTR mutation" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "R. Epaud" 1 => "E. Girodon" 2 => "H. Corvol" 3 => "F. Niel" 4 => "V. Guigonis" 5 => "A. Clement" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1111/j.1399-0004.2005.00525.x" "Revista" => array:6 [ "tituloSerie" => "Clin Genet" "fecha" => "2005" "volumen" => "68" "paginaInicial" => "552" "paginaFinal" => "553" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/16283887" "web" => "Medline" ] ] ] ] ] ] ] ] 3 => array:3 [ "identificador" => "bib0020" "etiqueta" => "4" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "A PDZ-interacting domain in CFTR is an apical membrane polarization signal" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "B.D. Moyer" 1 => "J. Denton" 2 => "K.H. Karlson" 3 => "D. Reynolds" 4 => "S. Wang" 5 => "J.E. Mickle" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1172/JCI7453" "Revista" => array:6 [ "tituloSerie" => "J Clin Investig" "fecha" => "1999" "volumen" => "104" "paginaInicial" => "1353" "paginaFinal" => "1361" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/10562297" "web" => "Medline" ] ] ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/15792129/0000005000000011/v1_201410310135/S1579212914002560/v1_201410310135/en/main.assets" "Apartado" => array:4 [ "identificador" => "14576" "tipo" => "SECCION" "es" => array:2 [ "titulo" => "Letters to the editor" "idiomaDefecto" => true ] "idiomaDefecto" => "es" ] "PDF" => "https://static.elsevier.es/multimedia/15792129/0000005000000011/v1_201410310135/S1579212914002560/v1_201410310135/en/main.pdf?idApp=UINPBA00003Z&text.app=https://archbronconeumol.org/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S1579212914002560?idApp=UINPBA00003Z" ]
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| 2020 May | 24 | 15 | 39 |
| 2020 April | 32 | 25 | 57 |
| 2020 March | 19 | 10 | 29 |
| 2020 February | 35 | 19 | 54 |
| 2020 January | 56 | 15 | 71 |
| 2019 December | 28 | 18 | 46 |
| 2019 November | 18 | 26 | 44 |
| 2019 October | 21 | 12 | 33 |
| 2019 September | 18 | 23 | 41 |
| 2019 August | 21 | 18 | 39 |
| 2019 July | 20 | 23 | 43 |
| 2019 June | 24 | 6 | 30 |
| 2019 May | 22 | 14 | 36 |
| 2019 April | 20 | 18 | 38 |
| 2019 March | 42 | 20 | 62 |
| 2019 February | 29 | 15 | 44 |
| 2019 January | 26 | 27 | 53 |
| 2018 December | 40 | 17 | 57 |
| 2018 November | 55 | 17 | 72 |
| 2018 October | 55 | 29 | 84 |
| 2018 September | 38 | 11 | 49 |
| 2018 May | 13 | 0 | 13 |
| 2018 April | 30 | 7 | 37 |
| 2018 March | 31 | 1 | 32 |
| 2018 February | 39 | 6 | 45 |
| 2018 January | 31 | 6 | 37 |
| 2017 December | 56 | 7 | 63 |
| 2017 November | 34 | 5 | 39 |
| 2017 October | 18 | 6 | 24 |
| 2017 September | 31 | 6 | 37 |
| 2017 August | 42 | 15 | 57 |
| 2017 July | 39 | 8 | 47 |
| 2017 June | 38 | 15 | 53 |
| 2017 May | 42 | 4 | 46 |
| 2017 April | 31 | 6 | 37 |
| 2017 March | 33 | 3 | 36 |
| 2017 February | 31 | 5 | 36 |
| 2017 January | 18 | 3 | 21 |
| 2016 December | 19 | 6 | 25 |
| 2016 November | 31 | 8 | 39 |
| 2016 October | 24 | 15 | 39 |
| 2016 September | 32 | 12 | 44 |
| 2016 August | 41 | 7 | 48 |
| 2016 July | 14 | 6 | 20 |
| 2016 March | 2 | 0 | 2 |
| 2016 February | 2 | 0 | 2 |
| 2015 December | 2 | 0 | 2 |
| 2015 October | 59 | 3 | 62 |
| 2015 September | 37 | 3 | 40 |
| 2015 August | 52 | 16 | 68 |
| 2015 July | 35 | 7 | 42 |
| 2015 June | 34 | 3 | 37 |
| 2015 May | 43 | 14 | 57 |
| 2015 April | 26 | 7 | 33 |
| 2015 March | 36 | 9 | 45 |
| 2015 February | 32 | 16 | 48 |
| 2015 January | 2 | 1 | 3 |
| 2014 November | 0 | 2 | 2 |
Show all
