title: Association of KCNJ11 E23K gene polymorphism with hypoglycemia in sulfonylurea-treated type 2 diabetic patients.
abstract: OBJECTIVE
  In addition to sulfonylurea-induced severe hypoglycemia, which however is not common in T2DM patients treated solely with oral hypoglycemic drugs, mild hypoglycemia is a frequent adverse event affecting many patients treated with oral hypoglycemic drugs and has a serious impact in patient adherence to therapy and everyday clinical practice. The aim of the present study was to investigate the possible association of KCNJ11 E23K polymorphism with incidence of sulfonylurea-induced mild hypoglycemic events.
  
  
  METHODS
  176 T2DM patients receiving sulfonylurea were included in the study, including 92 that had experienced drug-associated hypoglycemia and 84 that had never experienced hypoglycemia while on sulfonylurea treatment. KCNJ11 E23K polymorphism was detected by use of PCR-RFLP method.
  
  
  RESULTS
  Frequencies of KCNJ11 E23K genotypes and alleles were not different between hypoglycemic and non-hypoglycemic T2DM patients (p=0.35 and p=0.47, respectively). In logistic regression analysis before and after adjustment for other factors known to affect this condition (age, body mass index, sulfonylurea mean daily dose, duration of T2DM, renal function and CYP2C9 genotype) KCNJ11 E23K polymorphism did not affect hypoglycemia risk.
  
  
  CONCLUSIONS
  KCNJ11 E23K polymorphism is not associated with increased risk of mild hypoglycemia in sulfonylurea-treated T2DM patients.
authors.affiliation: Laboratory of Pharmacology, Medical School, Democritus University of Thrace, Greece. gragia@med.duth.gr
authors.forename: Georgia
authors.initials: G
authors.lastname: Ragia
authors.forename: Anna
authors.initials: A
authors.lastname: Tavridou
authors.forename: Ioannis
authors.initials: I
authors.lastname: Petridis
authors.forename: Vangelis G
authors.initials: VG
authors.lastname: Manolopoulos
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D001189:Aryl Hydrocarbon Hydroxylases / Q000235:genetics; D065729:Cytochrome P-450 CYP2C9; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000188:drug therapy / Q000235:genetics; D005260:Female; D005838:Genotype; D005907:Gliclazide / Q000009:adverse effects / Q000494:pharmacology*; D018698:Glutamic Acid; D006442:Glycated Hemoglobin / Q000378:metabolism*; D006115:Greece; D006801:Humans; D007003:Hypoglycemia / Q000097:blood* / Q000139:chemically induced / Q000235:genetics; D008239:Lysine; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D024661:Potassium Channels, Inwardly Rectifying / Q000187:drug effects / Q000235:genetics*; D013453:Sulfonylurea Compounds / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D000099161:Kcnj11 Channel
chemical_list: D001189:Aryl Hydrocarbon Hydroxylases; D065729:Cytochrome P-450 CYP2C9; D005907:Gliclazide; D018698:Glutamic Acid; D006442:Glycated Hemoglobin; D008239:Lysine; D024661:Potassium Channels, Inwardly Rectifying; D013453:Sulfonylurea Compounds; D000099161:Kcnj11 Channel; C517652:hemoglobin A1c protein, human; C057619:glimepiride; C450260:CYP2C9 protein, human