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Ketoacidosis as a debut to type 1B diabetes mellitus in a patient with Turner's syndrome
Cetoacidosis como inicio de diabetes mellitus tipo 1B en una paciente con síndrome de Turner
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This is partly explained by the increasing incidence of diabetes mellitus (DM) and cardiovascular diseases.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> There is an increased risk of developing both type 2 DM (relative risk, 4.4) and type 1 DM (DM1) (relative risk, 11.6) as compared to the general population.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Development of frank DM during childhood is however exceptional, and is usually more commonly associated to treatment with GH or sex hormones.<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2,3</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The unusual case of a two-year-old patient with DM1 of a non-autoimmune origin in whom TS was diagnosed is reported. Few patients with TS in whom DM1 has developed in childhood have been reported,<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3–6</span></a> and this is the youngest known.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Our patient was a Roumanian girl aged 2 years and 4 months with polyuria, polydipsia, and weight stagnation for the past two weeks. She weighed 8.100<span class="elsevierStyleHsp" style=""></span>kg (−3.6 SDS) and measured 77.5<span class="elsevierStyleHsp" style=""></span>cm in height (−3.8 SDS). The patient had a unique phenotype, with anteverted, low-set pinnae, slight hypertelorism, and mandibular hypoplasia. Hyperglycemia (682<span class="elsevierStyleHsp" style=""></span>mg/dL) and metabolic acidosis (pH 7.13, pCO<span class="elsevierStyleInf">2</span> 20<span class="elsevierStyleHsp" style=""></span>mmHg, HCO<span class="elsevierStyleInf">3</span> 6.7<span class="elsevierStyleHsp" style=""></span>mmol/L, BE −20.6<span class="elsevierStyleHsp" style=""></span>mmol/L) were detected, which allowed for diagnosing diabetic ketoacidosis. Diabetes work-up was completed by measurement of HbA1c (11.1%) and C peptide (0.25<span class="elsevierStyleHsp" style=""></span>ng/mL; normal: 0.90–4<span class="elsevierStyleHsp" style=""></span>ng/mL), the latter by immunoluminescence. Tests for diabetes antibodies were requested (indirect immunofluorescence method: islet cell antibodies; radioisotopic method: insulin, glutamic acid decarboxylase, and tyrosine phosphatase antibodies) and they were all negative. There was no family history of autoimmune diseases. Type B DM1 was diagnosed based on the lack of evidence of autoimmunity.</p><p id="par0020" class="elsevierStylePara elsevierViewall">Because of the unique features and low height, karyotype was requested and was found to be consistent with TS. A cytogenetic study of 15 metaphases was performed from a culture stimulated with phytohemagglutinin, with a resolution of 400 bands, and an isodicentric X chromosome with long arms was seen, which was confirmed by the band technique C: 46,X,psu idic(X)(p11.2)[15].</p><p id="par0025" class="elsevierStylePara elsevierViewall">TS is associated to autoimmune conditions. Thus, when DM1 is diagnosed it appears logical to think that it is of the 1A type; however, some authors state that autoantibodies are more frequently negative in TS. This statement may however be conditioned by classification of DM based on the presence or absence of insulin dependence, which may lead to a wrong diagnosis of DM1 in patients with type 2 DM.<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3,7</span></a> On the other hand, some authors postulate the existence of mechanisms of destruction of pancreatic beta cells (PBCs) other than autoimmunity.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Insulin deficiency secondary to PBC dysfunction and worsening with age has been reported in TS. At the earliest ages, this insulin deficiency is compensated by increased insulin sensitivity, but this would gradually decrease over time, which would lead to carbohydrate intolerance or even DM. Pathogenesis of this condition is independent from increases in body mass index and hypogonadism associated to TS, and is similar to pathogenesis of the mature-onset diabetes of the young (MODY), secondary to haploinsufficiency of some transcription factors affecting PBC function.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">A potential relationship has been seen between metabolic diseases and presence of an isochromosome of the long arm of the X chromosome (iXq).<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> Schoemaker et al.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> investigated causes of death in TS and found that in iXq karyotypes increased mortality was related to DM. It is hypothesized that there are genes in X chromosome involved in PBC function, and that haploinsufficiency of such genes could account for DM occurrence. This is also supported by the close similarity between type MODY diabetes and changes in carbohydrate metabolism in patients with TS.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> There are also studies reporting a greater prevalence of DM1 related to findings made in the short arm of the X chromosome (Xp). Bakalov et al.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> suggested that the greater incidence of DM in TS may be due to haploinsufficiency of genes located in chromosome Xp, so that DM incidence will be higher in patients with Xp monosomy (45X; delXp; iXq), with a normal incidence in long arm deletions (delXq), where both Xp arms are preserved. However, the greater incidence of DM in iXq patients may also be explained by overexpression of genes located in chromosome Xq which would escape inactivation, and which would be related to PBC function, and to another series of systemic processes which would promote a pro-inflammatory state. These statements are supported by a study conducted in 2008 showing a higher mortality rate in iXq patients,<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> and by the fact that there is also a greater incidence of DM in patients with Klinefelter syndrome (47XXY) and in 48 XXYY patients, in whom there are supernumerary copies of Xq.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Association of TS and DM1 may actually be due to mechanisms inherent to chromosomal findings. Association of TS to autoimmunity is however widely known, and a potential, currently undetectable autoimmune basis cannot therefore be ruled out with full certainty. Regular autoantibody monitoring is therefore recommended.</p><p id="par0045" class="elsevierStylePara elsevierViewall">Association of DM to genetic syndromes provides unique information for studying the genetic cases of carbohydrate metabolism. There is still a long road ahead before knowing the pathophysiological and genetic bases justifying DM1 occurrence in TS. New advances in genetic testing, as well as creation of multicenter databases, will allow for more complete understanding of this syndrome and PBC pathophysiology.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflict of interest</span><p id="par0050" class="elsevierStylePara elsevierViewall">The authors state that they have no conflicts of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Conflict of interest" ] 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: Navarro Moreno C, Cañabate Reche F, Vicente Pintor A, Vela Enríquez F, Benavides Román MR. Cetoacidosis como inicio de diabetes mellitus tipo 1<span class="elsevierStyleHsp" style=""></span>B en una paciente con síndrome de Turner. Endocrinol Nutr. 2014;61:439–441.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:10 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Mortality in women with Turner syndrome in great Britain: a national cohort study" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:5 [ 0 => "M.J. Schoemaker" 1 => "A.J. Swerdlow" 2 => "C.D. Higgins" 3 => "A.F. Wright" 4 => "P.A. 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Bennett" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.2337/dc06-0145" "Revista" => array:6 [ "tituloSerie" => "Diabetes Care" "fecha" => "2006" "volumen" => "29" "paginaInicial" => "1591" "paginaFinal" => "1598" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/16801584" "web" => "Medline" ] ] ] ] ] ] ] ] 8 => array:3 [ "identificador" => "bib0045" "etiqueta" => "9" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "X-chromosome gene dosage and the risk of diabetes in Turner syndrome" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:4 [ 0 => "V.K. Bakalov" 1 => "C. Chenh" 2 => "J. Zhou" 3 => "A. Bondy" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1210/jc.2009-0384" "Revista" => array:6 [ "tituloSerie" => "J Clin Endocrinol Metab" "fecha" => "2009" "volumen" => "94" "paginaInicial" => "3289" "paginaFinal" => "3296" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/19567529" "web" => "Medline" ] ] ] ] ] ] ] ] 9 => array:3 [ "identificador" => "bib0050" "etiqueta" => "10" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Metabolic control and insulin administration in a girl with turner syndrome and type 1 diabetes during long-term growth hormone therapy" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "E. Pankowska" 1 => "M. Szalecki" 2 => "T.E. Romer" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:6 [ "tituloSerie" => "Pediatr Endocrinol Diabetes Metab" "fecha" => "2007" "volumen" => "13" "paginaInicial" => "213" "paginaFinal" => "215" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/18042318" "web" => "Medline" ] ] ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/21735093/0000006100000008/v1_201410080024/S2173509314001512/v1_201410080024/en/main.assets" "Apartado" => array:4 [ "identificador" => "5823" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Scientific letters" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/21735093/0000006100000008/v1_201410080024/S2173509314001512/v1_201410080024/en/main.pdf?idApp=UINPBA00004N&text.app=https://www.elsevier.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2173509314001512?idApp=UINPBA00004N" ]
| Year/Month | Html | Total | |
|---|---|---|---|
| 2024 November | 5 | 0 | 5 |
| 2024 October | 14 | 5 | 19 |
| 2024 September | 21 | 5 | 26 |
| 2024 August | 22 | 7 | 29 |
| 2024 July | 10 | 9 | 19 |
| 2024 June | 23 | 9 | 32 |
| 2024 May | 12 | 2 | 14 |
| 2024 April | 22 | 3 | 25 |
| 2024 March | 23 | 8 | 31 |
| 2024 February | 12 | 10 | 22 |
| 2024 January | 25 | 12 | 37 |
| 2023 December | 25 | 12 | 37 |
| 2023 November | 22 | 5 | 27 |
| 2023 October | 38 | 23 | 61 |
| 2023 September | 23 | 3 | 26 |
| 2023 August | 20 | 9 | 29 |
| 2023 July | 30 | 8 | 38 |
| 2023 June | 25 | 8 | 33 |
| 2023 May | 25 | 10 | 35 |
| 2023 April | 21 | 4 | 25 |
| 2023 March | 21 | 0 | 21 |
| 2023 February | 10 | 9 | 19 |
| 2023 January | 18 | 4 | 22 |
| 2022 December | 15 | 15 | 30 |
| 2022 November | 26 | 20 | 46 |
| 2022 October | 18 | 35 | 53 |
| 2022 September | 25 | 13 | 38 |
| 2022 August | 12 | 13 | 25 |
| 2022 July | 22 | 8 | 30 |
| 2022 June | 21 | 12 | 33 |
| 2022 May | 16 | 21 | 37 |
| 2022 April | 22 | 14 | 36 |
| 2022 March | 23 | 9 | 32 |
| 2022 February | 9 | 9 | 18 |
| 2022 January | 23 | 12 | 35 |
| 2021 December | 18 | 11 | 29 |
| 2021 November | 18 | 9 | 27 |
| 2021 October | 7 | 14 | 21 |
| 2021 September | 18 | 15 | 33 |
| 2021 August | 19 | 8 | 27 |
| 2021 July | 15 | 11 | 26 |
| 2021 June | 21 | 8 | 29 |
| 2021 May | 17 | 14 | 31 |
| 2021 April | 24 | 9 | 33 |
| 2021 March | 32 | 10 | 42 |
| 2021 February | 18 | 9 | 27 |
| 2021 January | 13 | 15 | 28 |
| 2020 December | 14 | 5 | 19 |
| 2020 November | 15 | 9 | 24 |
| 2020 October | 7 | 7 | 14 |
| 2020 September | 20 | 9 | 29 |
| 2020 August | 8 | 8 | 16 |
| 2020 July | 12 | 11 | 23 |
| 2020 June | 15 | 9 | 24 |
| 2020 May | 18 | 8 | 26 |
| 2020 April | 14 | 5 | 19 |
| 2020 March | 10 | 6 | 16 |
| 2020 February | 10 | 6 | 16 |
| 2020 January | 7 | 8 | 15 |
| 2019 December | 27 | 12 | 39 |
| 2019 November | 10 | 10 | 20 |
| 2019 October | 13 | 2 | 15 |
| 2019 September | 11 | 9 | 20 |
| 2019 August | 24 | 5 | 29 |
| 2019 July | 23 | 25 | 48 |
| 2019 June | 25 | 22 | 47 |
| 2019 May | 101 | 42 | 143 |
| 2019 April | 40 | 34 | 74 |
| 2019 March | 7 | 5 | 12 |
| 2019 February | 14 | 6 | 20 |
| 2019 January | 7 | 6 | 13 |
| 2018 December | 11 | 3 | 14 |
| 2018 November | 6 | 1 | 7 |
| 2018 October | 14 | 3 | 17 |
| 2018 September | 10 | 2 | 12 |
| 2018 August | 8 | 1 | 9 |
| 2018 July | 19 | 4 | 23 |
| 2018 June | 8 | 2 | 10 |
| 2018 May | 10 | 3 | 13 |
| 2018 April | 26 | 2 | 28 |
| 2018 March | 4 | 1 | 5 |
| 2018 February | 3 | 1 | 4 |
| 2018 January | 8 | 6 | 14 |
| 2017 December | 3 | 0 | 3 |
| 2017 November | 8 | 2 | 10 |
| 2017 October | 11 | 1 | 12 |
| 2017 September | 7 | 9 | 16 |
| 2017 August | 16 | 4 | 20 |
| 2017 July | 23 | 2 | 25 |
| 2017 June | 19 | 4 | 23 |
| 2017 May | 22 | 2 | 24 |
| 2017 April | 19 | 2 | 21 |
| 2017 March | 33 | 1 | 34 |
| 2017 February | 39 | 4 | 43 |
| 2017 January | 12 | 2 | 14 |
| 2016 December | 13 | 5 | 18 |
| 2016 November | 14 | 4 | 18 |
| 2016 October | 27 | 4 | 31 |
| 2016 September | 18 | 2 | 20 |
| 2016 August | 8 | 4 | 12 |
| 2016 July | 14 | 1 | 15 |
| 2016 June | 18 | 4 | 22 |
| 2016 May | 15 | 1 | 16 |
| 2016 April | 7 | 5 | 12 |
| 2016 March | 13 | 2 | 15 |
| 2016 February | 18 | 6 | 24 |
| 2016 January | 20 | 4 | 24 |
| 2015 December | 14 | 4 | 18 |
| 2015 November | 18 | 5 | 23 |
| 2014 October | 0 | 1 | 1 |
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