Artículo
Comprando el artículo el PDF del mismo podrá ser descargado
Precio 19,34 €
Comprar ahora
array:23 [ "pii" => "S2530016420302512" "issn" => "25300164" "doi" => "10.1016/j.endinu.2020.10.006" "estado" => "S300" "fechaPublicacion" => "2022-02-01" "aid" => "1108" "copyright" => "SEEN y SED" "copyrightAnyo" => "2020" "documento" => "simple-article" "crossmark" => 1 "subdocumento" => "crp" "cita" => "Endocrinol Diabetes Nutr. 2022;69:149-50" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "itemSiguiente" => array:19 [ "pii" => "S2530016421000768" "issn" => "25300164" "doi" => "10.1016/j.endinu.2020.11.007" "estado" => "S300" "fechaPublicacion" => "2022-02-01" "aid" => "1141" "copyright" => "SEEN y SED" "documento" => "simple-article" "crossmark" => 1 "subdocumento" => "crp" "cita" => "Endocrinol Diabetes Nutr. 2022;69:151-2" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "es" => array:11 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Carta científica</span>" "titulo" => "Diabetes mellitus secundaria a enfermedad relacionada con la IgG4" "tienePdf" => "es" "tieneTextoCompleto" => "es" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "151" "paginaFinal" => "152" ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "Diabetes mellitus secondary to IgG4-related disease" ] ] "contieneTextoCompleto" => array:1 [ "es" => true ] "contienePdf" => array:1 [ "es" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0010" "etiqueta" => "Figura 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 935 "Ancho" => 1874 "Tamanyo" => 229228 ] ] "descripcion" => array:1 [ "es" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">(A) Imágenes axiales y coronales de PET-TC que muestran afectación de múltiples órganos: glándula submaxilar izquierda, adenopatías axilares y mediastínicas, páncreas y próstata. (B) Las imágenes de la PET-TC de control después de 2 ciclos de tratamiento con rituximab y prednisona demostraron una respuesta metabólica completa en todas las ubicaciones previamente afectadas.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "David Males-Maldonado, Laura Mola Reyes, Alba Martín González, Adolfo Gómez Grande, Sonsoles Guadalix Iglesias" "autores" => array:5 [ 0 => array:2 [ "nombre" => "David" "apellidos" => "Males-Maldonado" ] 1 => array:2 [ "nombre" => "Laura" "apellidos" => "Mola Reyes" ] 2 => array:2 [ "nombre" => "Alba" "apellidos" => "Martín González" ] 3 => array:2 [ "nombre" => "Adolfo" "apellidos" => "Gómez Grande" ] 4 => array:2 [ "nombre" => "Sonsoles" "apellidos" => "Guadalix Iglesias" ] ] ] ] ] "idiomaDefecto" => "es" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S2530018022000166" "doi" => "10.1016/j.endien.2022.02.003" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2530018022000166?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2530016421000768?idApp=UINPBA00004N" "url" => "/25300164/0000006900000002/v2_202202021023/S2530016421000768/v2_202202021023/es/main.assets" ] "itemAnterior" => array:18 [ "pii" => "S2530016421001518" "issn" => "25300164" "doi" => "10.1016/j.endinu.2021.03.004" "estado" => "S300" "fechaPublicacion" => "2022-02-01" "aid" => "1183" "copyright" => "SEEN y SED" "documento" => "article" "crossmark" => 1 "subdocumento" => "fla" "cita" => "Endocrinol Diabetes Nutr. 2022;69:144-8" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "en" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Special article</span>" "titulo" => "Immunonutrition for the acute treatment of MELAS syndrome" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "es" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "144" "paginaFinal" => "148" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Inmunonutrición para el tratamiento agudo del síndrome MELAS" ] ] "contieneResumen" => array:2 [ "en" => true "es" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1386 "Ancho" => 2508 "Tamanyo" => 212005 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Cellular mechanisms of the interventions.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Elizabeth Pérez-Cruz, Carolina González-Rivera, Luz del Carmen Gabriela Valencia-Olvera" "autores" => array:3 [ 0 => array:2 [ "nombre" => "Elizabeth" "apellidos" => "Pérez-Cruz" ] 1 => array:2 [ "nombre" => "Carolina" "apellidos" => "González-Rivera" ] 2 => array:2 [ "nombre" => "Luz del Carmen Gabriela" "apellidos" => "Valencia-Olvera" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2530016421001518?idApp=UINPBA00004N" "url" => "/25300164/0000006900000002/v2_202202021023/S2530016421001518/v2_202202021023/en/main.assets" ] "en" => array:12 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Scientific letter</span>" "titulo" => "Neonatal diabetes onset mimicking an organic acidemia" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "149" "paginaFinal" => "150" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Ana Prado-Carro, Rebeca Sáez-Soto, Raquel Díaz-Soto, Ana Moreno-Álvarez, Ana E. Laso-Alonso" "autores" => array:5 [ 0 => array:3 [ "nombre" => "Ana" "apellidos" => "Prado-Carro" "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 1 => array:3 [ "nombre" => "Rebeca" "apellidos" => "Sáez-Soto" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 2 => array:3 [ "nombre" => "Raquel" "apellidos" => "Díaz-Soto" "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] 3 => array:3 [ "nombre" => "Ana" "apellidos" => "Moreno-Álvarez" "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] 4 => array:4 [ "nombre" => "Ana E." "apellidos" => "Laso-Alonso" "email" => array:1 [ 0 => "anaelisalasoalonso@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" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Pediatric Service, Complejo Hospitalario Universitario de A Coruña, As Xubias 84, 15006 A Coruña. Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Department of Endocrinology, Pediatric Service, Complejo Hospitalario Universitario de A Coruña, As Xubias 84, 15006 A Coruña, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Pediatric Intensive Care Unit, Complejo Hospitalario Universitario de A Coruña, As Xubias 84, 15006 A Coruña. Spain" "etiqueta" => "c" "identificador" => "aff0015" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Debut de diabetes neonatal simulando una acidemia orgánica" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Neonatal diabetes mellitus (NDM) is a rare disorder (1/215,000–500,000 births). Its onset usually occurs during the first 6 months of life, even though some cases may appear in children aged up to 18 months of age.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">1</span></a> It can be transient, with spontaneous resolution within the first weeks of life (median duration 12 weeks), or permanent. Permanent DM is associated with mutations in <span class="elsevierStyleItalic">KCNJ11</span>, <span class="elsevierStyleItalic">ABCC8</span> and <span class="elsevierStyleItalic">INS</span> genes in up to 53% of the cases.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">2</span></a><span class="elsevierStyleItalic">KCNJ11</span> and <span class="elsevierStyleItalic">ABCC8</span> genes code for the Kir6.2 and SUR1 subunits of the ATP-sensitive potassium (K-ATP) channel, which plays a central role in glucose-stimulated insulin secretion from the pancreatic β-cell.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">3</span></a> This channel is involved in an essential step in insulin secretion. The channel consists of two types of essential subunits: the pore forming subunit Kir6.2 and the regulatory subunit sulfonylurea receptor 1 (SUR1) which is the target for sulfonylureas.</p><p id="par0010" class="elsevierStylePara elsevierViewall">As NDM is a rare disorder, the diagnosis may be delayed. The prevalence of diabetes due to a mutation in <span class="elsevierStyleItalic">KCNJ11</span> is uncertain, between 34 and 64% patients with permanent diabetes.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">3</span></a> Presentation with metabolic acidosis and hyperammonemia may be mistaken for an organic acidemia.</p><p id="par0015" class="elsevierStylePara elsevierViewall">We present the case of a 3-month old female, born at term (37 weeks and 4 days) by emergent c-section delivery due to fetal bradichardia. Antenatal diagnosis of intrauterine growth restriction had been made in the 34th week of pregnancy, with a normal doppler birth weight was 2030<span class="elsevierStyleHsp" style=""></span>g (p2, −2.2 SD). Neonatal blood glucose was 72<span class="elsevierStyleHsp" style=""></span>mg/dl. Family history was unremarkable.</p><p id="par0020" class="elsevierStylePara elsevierViewall">The baby presented with lethargy, tachypnea and feeding refusal. She had had cough and nasal congestion in the past few days without fever. On admission she had clinical features of ketoacidosis with Kussmaul breathing, mucous dehydration and compromised distal perfussion. On physical examination her heart rate was 199<span class="elsevierStyleHsp" style=""></span>bpm and her respiratory rate was 63<span class="elsevierStyleHsp" style=""></span>bpm. Her weight was 4.04<span class="elsevierStyleHsp" style=""></span>kg (<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>1, −2.4 SD), length 62<span class="elsevierStyleHsp" style=""></span>cm (<span class="elsevierStyleItalic">p</span>70) and head circumference 30.5<span class="elsevierStyleHsp" style=""></span>cm (<span class="elsevierStyleItalic">p</span>2). No dysmorphisms were observed.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Lab test revealed metabolic acidosis with high gap anion, hyperglycemia and ketosis. Venous blood pH was 7.04 and basses excess −23.3<span class="elsevierStyleHsp" style=""></span>mmol/L. Blood glucose was 844<span class="elsevierStyleHsp" style=""></span>mg/dl, ketonemia was 4<span class="elsevierStyleHsp" style=""></span>mmol/L and ketonuria was found. Serum ammonia was 288.9<span class="elsevierStyleHsp" style=""></span>μmol/L, and lactic acid was 10.9<span class="elsevierStyleHsp" style=""></span>mg/dL. Hyperglycemia was treated with intravenous fluids and continuous intravenous insulin perfusion. Ketoacidosis with hyperammonemia led to suspect an inherited metabolic disorder with organic acidemia so further diagnosis tests were performed and treatment for hyperammonemia was initiated (phenylbutyrate, <span class="elsevierStyleSmallCaps">l</span>-arginine, n-carbamyl-glutamate).</p><p id="par0030" class="elsevierStylePara elsevierViewall">Euglycemia was achieved within the first 12<span class="elsevierStyleHsp" style=""></span>h. Intravenous insulin perfusion was adjusted with capilar glucose values. C-peptide levels were 0.11<span class="elsevierStyleHsp" style=""></span>ng/ml.</p><p id="par0035" class="elsevierStylePara elsevierViewall">Hyperammonemia was decreasing within the first 24<span class="elsevierStyleHsp" style=""></span>h. Treatment for hyperammonemia was interrupted within 60<span class="elsevierStyleHsp" style=""></span>h with normal values of ammonia (11.0–32.0<span class="elsevierStyleHsp" style=""></span>μmol/L). Diagnostic tests for organic acydemias and inherited metabolic disorders were negative (aminoacid and organic acid levels in blood and urine).</p><p id="par0040" class="elsevierStylePara elsevierViewall">With the suspected diagnosis of neonatal diabetes, intravenous insulin perfusion was switched to continuous subcutaneous insulin infusion (CSII) and continuous glucose monitoring were initiated (Medtroning 640G integrated system®). The patient was discharged home and follow-up showed good metabolic control.</p><p id="par0045" class="elsevierStylePara elsevierViewall">A sequence analysis of the coding and intronic and exonic flanking regions of 12 genes related to neonatal diabetes was performed (Ampliseq custom panel/Ion Torrent™ PGM), which revealed heterozygosity for a “de novo” mutation in exon 1 of the <span class="elsevierStyleItalic">KCNJ11</span> gene. The mutation led to a substitution of guanine for adenine in position 149 (c.149G>A), which led to a substitution in the protein structure of the arginine in position 50 by glutamine (p.Arg50Gln). This mutation was previously described in association with neonatal diabetes both transient and permanent, with favorable response to sulfonylureas.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">3</span></a> Genetic testing for both parents was negative.</p><p id="par0050" class="elsevierStylePara elsevierViewall">The patient was readmitted to discontinue subcutaneous insulin infusion and initiate oral therapy with glibenclamide, once the mutation was confirmed and a glucagon test was performed. Oral glibenclamide was initiated at 0.1<span class="elsevierStyleHsp" style=""></span>mg/kg/d while the insulin dose was gradually tapered. Gliblenclamide was continued at 0.8<span class="elsevierStyleHsp" style=""></span>mg/kg/d divided into 2 dosis on discharge. Home monitoring of blood glucose indicated successful transition to sulfonylurea therapy. Treatment with sulfonylurea was whitdrawn at 14 months with good subsequent glycemic control until today. During the follow up the patient showed appropriate neurological development.</p><p id="par0055" class="elsevierStylePara elsevierViewall">Both neonatal diabetes mellitus and organic acidemias can lead to ketoacidosis in the neonatal period.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">4</span></a> Similar onset and clinical features may delay or mistake initial diagnosis and approach. Also similar laboratory findings are confounding to the clinician. Hyperammonemia may mislead the diagnosis of diabetic ketoacidosis as shown in this case. According to the literature, ammonia levels may rise with hyperinsulinism resulting from mutations in the glutamate dehydrogenase linked mechanism for insulin secretion. Glutamate dehydrogenase is expressed in the pancreas and liver and catalyzes oxidative deamination of glutamate to a-ketoglutamate, resulting in ammonia production. High levels of leucine and glutamic acid were reported in patients during diabetic ketoacidosis, leucine being an allosteric activator of glutamate dehydrogenase.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">5</span></a> Akanshka et al. hypothesize dual mechanisms for hyperammonemia in a 6-month patient who presented with similar clinical features as our index patient and with a final diagnosis of neonatal diabetes. Aminoacid and organic acid levels in our patients were tested, showing no abnormalities. The authors also hypothesize that the utilization of glutamate by the glutamate dehydrogenase may compromise its availability for n-acetylglutamate synthesis (activator of carbamylphosphate synthase in the urea cycle) resulting in an impairment in the urea cycle. In our index patient urea levels were slightly elevated for her age at admission with normalization within the first 24<span class="elsevierStyleHsp" style=""></span>h.</p><p id="par0060" class="elsevierStylePara elsevierViewall">Heterozygous activating mutations in <span class="elsevierStyleItalic">KCNJ11</span>, which encodes the kir6.2 subunit of the pancreatic K-ATP channel cause both permanent and transient neonatal diabetes.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">6</span></a> More than 90% of these patient respond to sulfonylureas.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">7</span></a> Approximately 50% of neonatal diabetes have K-channel mutations and therefore can be switched to sulfonylurea therapy, with improvement in glycemic control and quality of life. All patients with diabetes diagnosed before 6 months of age should be screened for these mutations.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">8</span></a></p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Authors’ contribution</span><p id="par0065" class="elsevierStylePara elsevierViewall">A.E. Laso and R. Saez performed the research and wrote the paper. A.M. Prado, R. Diaz and A. Moreno reviewed the paper. All authors have read and approved the final manuscript. All authors are accountable for all aspects of the work.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Funding sources</span><p id="par0070" class="elsevierStylePara elsevierViewall">This research has not received funding from public agencies, commercial agencies or non-profit entities.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Conflict of interest</span><p id="par0075" class="elsevierStylePara elsevierViewall">The authors declare no conflict of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:4 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Authors’ contribution" ] 1 => array:2 [ "identificador" => "sec0010" "titulo" => "Funding sources" ] 2 => array:2 [ "identificador" => "sec0015" "titulo" => "Conflict of interest" ] 3 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:8 [ 0 => array:3 [ "identificador" => "bib0045" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Neonatal diabetes mellitus due to a novel ABCC8 gene mutation mimicking an organic acidemia" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:4 [ 0 => "N. Akanksha" 1 => "N. Mamta" 2 => "K. Sunil" 3 => "S. Nalini" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1007/s12098-013-1102-z" "Revista" => array:6 [ "tituloSerie" => "Indian J Pediatr" "fecha" => "2014" "volumen" => "81" "paginaInicial" => "702" "paginaFinal" => "704" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/23783767" "web" => "Medline" ] ] ] ] ] ] ] ] 1 => array:3 [ "identificador" => "bib0050" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Insulin mutation screening in 1044 patients with diabetes: Mutations in the INS gene are a common cause of neonatal diabetes but rare cause of diabetes diagnosed in childhood or adulthood" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "E.L. Edghill" 1 => "S.E. Flanagan" 2 => "A.M. Patch" 3 => "C. Boustred" 4 => "A. Parish" 5 => "B. Shields" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.2337/db07-1405" "Revista" => array:6 [ "tituloSerie" => "Diabetes" "fecha" => "2008" "volumen" => "57" "paginaInicial" => "1034" "paginaFinal" => "1042" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/18162506" "web" => "Medline" ] ] ] ] ] ] ] ] 2 => array:3 [ "identificador" => "bib0055" "etiqueta" => "3" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Mutations in KCNJ11, which encodes Kir6.2, are common cause of diabetes diagnosed in the first 6 months of life, with the phenotype determined by genotype" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:5 [ 0 => "S.E. Flanagan" 1 => "E.L. Edghill" 2 => "A.L. Gloyn" 3 => "S. Ellard" 4 => "A.T. Hattersley" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1007/s00125-006-0246-z" "Revista" => array:6 [ "tituloSerie" => "Diabetologia" "fecha" => "2006" "volumen" => "49" "paginaInicial" => "1190" "paginaFinal" => "1197" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/16609879" "web" => "Medline" ] ] ] ] ] ] ] ] 3 => array:3 [ "identificador" => "bib0060" "etiqueta" => "4" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "The metabolic and molecular bases of inherited disease" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "J. Saudubray" 1 => "C. Charpentier" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Libro" => array:6 [ "edicion" => "8th ed." "fecha" => "2001" "paginaInicial" => "1327" "paginaFinal" => "1404" "editorial" => "McGRaw Hill" "editorialLocalizacion" => "New York" ] ] ] ] ] ] 4 => array:3 [ "identificador" => "bib0065" "etiqueta" => "5" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "What's new in metabolic and genetic hipoglycemias: diagnosis and management" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "V. Valayannopoulos" 1 => "S. Romano" 2 => "K. Mention" 3 => "A. Vassault" 4 => "D. Rabier" 5 => "M. Polak" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1007/s00431-007-0600-2" "Revista" => array:6 [ "tituloSerie" => "Eur J Pediatr" "fecha" => "2008" "volumen" => "167" "paginaInicial" => "257" "paginaFinal" => "265" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/17912550" "web" => "Medline" ] ] ] ] ] ] ] ] 5 => array:3 [ "identificador" => "bib0070" "etiqueta" => "6" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Neonatal diabetes mellitus: chromosomal analysis in transient and permanent cases" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "C. Metz" 1 => "H. Cavé" 2 => "A.M. Bertrand" 3 => "C. Deffert" 4 => "B. Gueguem-Giroux" 5 => "P. Czernichow" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1067/mpd.2002.127089" "Revista" => array:6 [ "tituloSerie" => "J Pediatr" "fecha" => "2002" "volumen" => "141" "paginaInicial" => "483" "paginaFinal" => "489" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/12378186" "web" => "Medline" ] ] ] ] ] ] ] ] 6 => array:3 [ "identificador" => "bib0075" "etiqueta" => "7" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "E.R. Pearson" 1 => "I. Flechtner" 2 => "P.R. Njølstad" 3 => "M.T. Malecki" 4 => "S.E. Flanagan" 5 => "B. Larkin" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1056/NEJMoa061759" "Revista" => array:6 [ "tituloSerie" => "N Engl J Med" "fecha" => "2006" "volumen" => "355" "paginaInicial" => "467" "paginaFinal" => "477" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/16885550" "web" => "Medline" ] ] ] ] ] ] ] ] 7 => array:3 [ "identificador" => "bib0080" "etiqueta" => "8" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Permanent neonatal diabetes mellitus caused by a novel homozygous (T168A) glucokinase (GCK) mutation: initial response to oral sulphonylurea therapy" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "D. Turkkahraman" 1 => "I. Bircan" 2 => "N.D. Tribble" 3 => "S. Akçurin" 4 => "S. Ellard" 5 => "A.L. Gloyn" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1016/j.jpeds.2007.12.037" "Revista" => array:6 [ "tituloSerie" => "J Pediatr" "fecha" => "2008" "volumen" => "153" "paginaInicial" => "122" "paginaFinal" => "126" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/18571549" "web" => "Medline" ] ] ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/25300164/0000006900000002/v2_202202021023/S2530016420302512/v2_202202021023/en/main.assets" "Apartado" => array:4 [ "identificador" => "63843" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Cartas científicas" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/25300164/0000006900000002/v2_202202021023/S2530016420302512/v2_202202021023/en/main.pdf?idApp=UINPBA00004N&text.app=https://www.elsevier.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2530016420302512?idApp=UINPBA00004N" ]
Consulte los artículos y contenidos publicados en este medio, además de los e-sumarios de las revistas científicas en el mismo momento de publicación
Esté informado en todo momento gracias a las alertas y novedades
Acceda a promociones exclusivas en suscripciones, lanzamientos y cursos acreditados
Endocrinología, Diabetes y Nutrición es la revista órgano de expresión de la Sociedad Española de Endocrinología y Nutrición (SEEN) y de la Sociedad Española de Diabetes (SED). La publicación recoge el apasionante progreso registrado en el conocimiento de la fisiopatología endocrina tanto en el ámbito clínico como experimental, y es un fiel exponente de los avances de esta especialidad en nuestro país. Además de las secciones Originales y Notas clínicas, en las que se publican trabajos de gran calidad elaborados por diversos centros endocrinológicos clínicos y experimentales, la revista publica artículos de Revisión y Editoriales escritos por reconocidos especialistas de la endocrinología española con el fin de actualizar conocimientos y dar a conocer los avances más relevantes en la actualidad.
Index Medicus/MEDLINE, Excerpta Medica/EMBASE, SCOPUS, Science Citation Index Expanded, Journal Citation Reports/Science Edition, IBECS
Ver másEl factor de impacto mide la media del número de citaciones recibidas en un año por trabajos publicados en la publicación durante los dos años anteriores.
© Clarivate Analytics, Journal Citation Reports 2022
SJR es una prestigiosa métrica basada en la idea de que todas las citaciones no son iguales. SJR usa un algoritmo similar al page rank de Google; es una medida cuantitativa y cualitativa al impacto de una publicación.
Ver másSNIP permite comparar el impacto de revistas de diferentes campos temáticos, corrigiendo las diferencias en la probabilidad de ser citado que existe entre revistas de distintas materias.
Ver más¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?
Are you a health professional able to prescribe or dispense drugs?
Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos