title: What characteristics at baseline are associated with the glucose-lowering effect of colestimide in patients with type 2 diabetes and hypercholesterolemia according to response to treatment?
abstract: Colestimide, an anion exchange resin, reportedly improves glycemic control in patients with type 2 diabetes. However, no studies of the glucose-lowering effect of colestimide have identified responders and nonresponders. In the present study, we compared glycemic control, lipids, and body-mass index (BMI) among patients with type 2 diabetes receiving colestimide (n=59) until 24 weeks after the start of treatment. Subjects were classified as responders to treatment (n=40), who showed a 15% or greater decrease in glycated hemoglobin (HbA1c) or a 20% or greater decrease in plasma glucose level or both after 24 weeks of colestimide treatment as compared with baseline; nonresponders showed HbA1c>11.5% or fasting plasma glucose (FPG)>250 mg/dL during the course of the study and <15% decrease in HbA1c levels or <20% decrease in FPG levels or both after 24 weeks of colestimide treatment as compared with baseline. In responders, FPG decreased significantly from 196 ± 91 mg/dL to 125 ± 47 mg/dL after 24 weeks (P<0.001), and HbA1c decreased from 9.1% ± 2.0% to 7.0% ± 0.9% (P<0.001). In nonresponders, HbA1c decreased significantly from 7.7% ± 2.9% to 7.6% ± 1.2% (P<0.05). Multiple logistic regression analysis revealed that baseline HbA1c and the presence of cholelithiasis were significant determinants of the response to colestimide treatment when corrected for sex, age, triglyceride levels, and BMI at baseline and the presence of fatty liver. In conclusion, baseline HbA1c and the presence of cholelithiasis have strong and independent influences on the glucose-lowering effect of colestimide.
authors.affiliation: Department of Cardiovascular Medicine, Nippon Medical School, Tokyo, Japan. t-suzuki@nms.ac.jp
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Suzuki
authors.forename: Misako
authors.initials: M
authors.lastname: Tsunoda-Kubota
authors.forename: Junya
authors.initials: J
authors.lastname: Aoyama
authors.forename: Shoko
authors.initials: S
authors.lastname: Futami-Suda
authors.forename: Masao
authors.initials: M
authors.lastname: Hashimoto
authors.forename: Yoshimasa
authors.initials: Y
authors.lastname: Igari
authors.forename: Kentaro
authors.initials: K
authors.lastname: Watanabe
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Kigawa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nakano
authors.forename: Kenzo
authors.initials: K
authors.lastname: Oba
mesh_terms: D000368:Aged; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D002769:Cholelithiasis / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy; D004811:Epichlorohydrin / Q000627:therapeutic use*; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D006937:Hypercholesterolemia / Q000188:drug therapy*; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007093:Imidazoles / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D012044:Regression Analysis; D012117:Resins, Synthetic / Q000627:therapeutic use*; D013997:Time Factors; D016896:Treatment Outcome; D014280:Triglycerides / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D004811:Epichlorohydrin; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007093:Imidazoles; D012117:Resins, Synthetic; D014280:Triglycerides; C417427:colestimide