scholarly journals Diabetic Dead-in-Bed Syndrome: A Possible Link to a Cardiac Ion Channelopathy

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Jonathan R. Skinner ◽  
Renate Marquis-Nicholson ◽  
Alix Luangpraseuth ◽  
Rick Cutfield ◽  
Jackie Crawford ◽  
...  

Sudden unexpected nocturnal death among patients with diabetes occurs approximately ten times more commonly than in the general population. Malignant ventricular arrhythmia due to Brugada syndrome has been postulated as a cause, since a glucose-insulin bolus can unmask the Brugada electrocardiographic signature in genetically predisposed individuals. In this report we present a 16-year-old male with insulin-dependent diabetes who died suddenly at night. His diabetes had been well controlled, without significant hypoglycaemia. At autopsy, he had a full stomach and a glucose level of 7 mmol/L in vitreous humor, excluding hypoglycaemia. Genetic analysis of autopsy DNA revealed a missense mutation, c.370A>G (p.Ile124Val), in theGPD1Lgene. A parent carried the same mutation and has QT prolongation. Mutations in this gene have been linked to Brugada syndrome and sudden infant death. The patient may have died from a ventricular arrhythmia, secondary to occult Brugada syndrome, triggered by a full stomach and insulin. The data suggest that molecular autopsies are warranted to investigate other cases of the diabetic dead-in-bed syndrome.

2001 ◽  
Vol 280 (1) ◽  
pp. H354-H360 ◽  
Author(s):  
Xiaoping Wan ◽  
Shenghan Chen ◽  
Azita Sadeghpour ◽  
Qing Wang ◽  
Glenn E. Kirsch

Idiopathic ventricular fibrillation (IVF) can cause sudden death in both adults and children. One form of IVF (Brugada syndrome), characterized by S-T segment elevation (STE) in the electrocardiogram, has been linked to mutations of SCN5A, the gene encoding the voltage-gated cardiac Na+ channel. A missense mutation of SCN5A that substitutes glutamine for leucine at codon 567 (L567Q, in the cytoplasmic linker between domains I and II) is identified with sudden infant death and Brugada syndrome in one family. However, neither the functional effect of the L567Q mutation nor the molecular mechanism underlying the pathogenicity of the mutation is known. Patch-clamp analysis of L567Q channels expressed in human embryonic kidney cells revealed a marked acceleration and a negative shift in the voltage dependence of inactivation. Unlike other Brugada mutations, this phenotype was expressed independently of temperature or auxiliary β1-subunits. These results support a proposed linkage between Brugada syndrome and some instances of sudden infant death and the hypothesis that reduced Na+ conductance is the primary cause of IVF with STE.


2016 ◽  
Vol 67 (13) ◽  
pp. 1653-1654 ◽  
Author(s):  
Ignasi Anguera ◽  
Arcadio García-Alberola ◽  
Paolo Dallaglio ◽  
Jorge Toquero ◽  
Luisa Pérez ◽  
...  

2021 ◽  
Vol 9 (5) ◽  
pp. 1083-1087
Author(s):  
Kavita Kavita ◽  
Chaudhary J P ◽  
Om Prakash Sharma

Human breast milk serves as a source of nutrition which is uncontaminated by environmental pathogen. Multiple immunological factors produced by the mother’s immune system are transported to infant through breast milk and are associated with a protective role against infection in children. It reduces the incidence of infantile diarrhoea, sudden Infant Death Syndrome (SIDS), allergic/hypersensitivity diseases, and development of Type 1 (insulin de- pendent) and Type 2 (non-insulin dependent) diabetes mellitus relative to the use of infant formula. In Ayurveda, ‘Kasyapa’ defines pure breast milk as that which the baby thrives well and both the mother and baby remain happy, healthy, and free from any ailment. Breast milk promotes growth and development and acts as a tonic for all the tissues. In Ayurveda text, many herbs are described for improving breast milk under the name “Stanyajanana”. Keywords: Sthanyajana, Kasyapa, SIDS


PEDIATRICS ◽  
2001 ◽  
Vol 107 (4) ◽  
pp. 809.1-809 ◽  
Author(s):  
Simone Albers ◽  
Harvey L. Levy

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