Sulfonylurea-Responsive Diabetes in Childhood

Journal of Pediatrics

Volumn 150, Issue 5, 2007, Pages 553-555

  Landau, Zohar ^a   Wainstein, Julio ^a   Hanukoglu, Aaron ^a   Tuval, Myriam ^a   Lavie, Judith ^b   Glaser, Benjamin ^b  

^a TEL AVIV UNIVERSITY   (Israel)

^b HADASSAH HEBREW UNIVERSITY MEDICAL CENTER   (Israel)

Author keywords

[No Author keywords available]

Indexed keywords

GLIBENCLAMIDE; INSULIN; REPAGLINIDE;

ADOLESCENT; ADULT; ANAMNESIS; ARTICLE; BODY MASS; CHILD; CLINICAL ARTICLE; CLINICAL FEATURE; CONSANGUINEOUS MARRIAGE; CONTROLLED STUDY; DIABETES MELLITUS; DISEASE COURSE; DRUG RESPONSE; DRUG SUBSTITUTION; DRUG WITHDRAWAL; FEMALE; GENE; GENE MUTATION; GENETIC ANALYSIS; GESTATIONAL AGE; GLYCEMIC CONTROL; HUMAN; HYPERGLYCEMIA; KCNJ11 GENE; MALE; PARENT; PRIORITY JOURNAL; RESTRICTION FRAGMENT LENGTH POLYMORPHISM; SEQUENCE ANALYSIS;

ADULT; CHILD; DIABETES MELLITUS; FEMALE; GLYBURIDE; HUMANS; HYPOGLYCEMIC AGENTS; INFANT, NEWBORN; MALE; MUTATION; PEDIGREE; POTASSIUM CHANNELS, INWARDLY RECTIFYING; SULFONYLUREA COMPOUNDS;

EID: 34247166663     PISSN: 00223476     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.jpeds.2007.03.004     Document Type: Article

References (12)

1. Shield J.P., Gardner R.J., Wadsworth E.J., Whiteford M.L., James R.S., Robinson D.O., et al. Aetiopathology and genetic basis of neonatal diabetes. Arch Dis Child Fetal Neonatal Ed 76 (1997) F39-F42
2. Gloyn A.L., Reimann F., Girard C., Edghill E.L., Proks P., Pearson E.R., et al. Relapsing diabetes can result from moderately activating mutations in KCNJ11. Hum Mol Genet 14 (2005) 925-934
3. Babenko A.P., Polak M., Cave H., Busiah K., Czernichow P., Scharfmann R., et al. Activating mutations in the ABCC8 gene in neonatal diabetes mellitus. N Engl J Med 355 (2006) 456-466
4. von Muhlendahl K.E., and Herkenhoff H. Long-term course of neonatal diabetes. N Engl J Med 333 (1995) 704-708
5. Nestorowicz A., Inagaki N., Gonol T., Schoor K.P., Wilson B.A., Glaser B., et al. A nonsense mutation in the inward rectifier potassium channel gene, KIR6.2, is associated with familial hyperinsulinism. Diabetes 46 (1997) 1743-1748
6. Hani E.H., Boutin P., Durand E., Inoue H., Permutt M.A., Velho G., et al. Missense mutations in the pancreatic islet beta cell inwardly rectifying K+ channel gene (KIR6.2/BIR): a meta-analysis suggests a role in the polygenic basis of Type II diabetes mellitus in Caucasians. Diabetologia 41 (1998) 1511-1515
7. Flanagan S., Edghill E., Gloyn A., Mackay D., Temple I., Shield J., et al. Activating KCNJ11 gene mutations are a common cause of remitting diabetes that may be diagnosed as transient neonatal diabetes. Diabetic Medicine 23 (2006) 1
8. Yorifuji T., Nagashima K., Kurokawa K., Kawai M., Oishi M., Akazawa Y., et al. The C42R mutation in the Kir6.2 (KCNJ11) gene as a cause of transient neonatal diabetes, childhood diabetes, or later-onset, apparently type 2 diabetes mellitus. J Clin Endocrinol Metab 90 (2005) 3174-3178
9. Gloyn A.L., Pearson E.R., Antcliff J.F., Proks P., Bruining G.J., Slingerland A.S., et al. Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes. N Engl J Med 350 (2004) 1838-1849
10. Hattersley A.T., and Ashcroft F.M. Activating mutations in Kir6.2 and neonatal diabetes: new clinical syndromes, new scientific insights, and new therapy. Diabetes 54 (2005) 2503-2513
11. Sagen J.V., Raeder H., Hathout E., Shehadeh N., Gudmundsson K., Baevre H., et al. Permanent neonatal diabetes due to mutations in KCNJ11 encoding Kir6.2: patient characteristics and initial response to sulfonylurea therapy. Diabetes 53 (2004) 2713-2718
12. Flanagan S.E., Edghill E.L., Gloyn A.L., Ellard S., and Hattersley A.T. Mutations in KCNJ11, which encodes Kir6.2, are a common cause of diabetes diagnosed in the first 6 months of life, with the phenotype determined by genotype. Diabetologia 49 (2006) 1190-1197