title: Glycemia (or, in women, estimated glucose disposal rate) predict lower extremity arterial disease events in type 1 diabetes.
abstract: The purpose of this study was to determine the predictors of lower extremity arterial disease (LEAD) events in a type 1 diabetes population. Data are from the Pittsburgh Epidemiology of Diabetes Complications Study of childhood onset type 1 diabetes. At baseline, the study population had a mean age 28 (range, 8 to 47) years and duration 19 (range, 7 to 37) years. LEAD events, assessed by questionnaire or clinical examination, were defined as claudication (Rose questionnaire), foot ulceration, or lower extremity amputation. Estimated glucose disposal rate (eGDR), a measure of insulin resistance, was calculated from glycosylated hemoglobin (HbA(1)), waist-to-hip ratio (WHR), and hypertension using an equation previously validated with hyperinsulinemic euglycemic clamp studies. There were incident LEAD events in 70 of 586 subjects during 10 years follow-up, giving an incidence density of 1.3 events/100 person-years. Incidence did not differ by gender. Major predictors of LEAD events were diabetes duration, low-density lipoprotein-cholesterol (LDL-C), heart rate, eGDR, log albumin excretion rate (AER), systolic blood pressure (SBP), hypertension, proliferative retinopathy, distal symmetric polyneuropathy, and overt nephropathy (each P <.001). HbA(1), low ankle brachial index (ABI) (<0.9), and a high ankle brachial difference (ABD) (SBP > or = 75 mm Hg) also predicted LEAD events. Cox modeling suggested that duration (P <.001), HbA(1) (P <.001), hypertension (P =.006), log albumin excretion rate (P =.011), and heart rate (P =.028) predicted events independently. The overall model with HbA(1) and hypertension was significantly better than with eGDR, while the alternate models in men were similar. In women, the model with eGDR showed a significantly better fit. Glycemia, insulin resistance, hypertension and renal disease are powerful predictors of symptomatic lower extremity arterial disease in type 1 diabetes.
authors.affiliation: Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, USA.
authors.forename: Jon C
authors.initials: JC
authors.lastname: Olson
authors.forename: John R
authors.initials: JR
authors.lastname: Erbey
authors.forename: Kimberly Y Z
authors.initials: KY
authors.lastname: Forrest
authors.forename: Katherine
authors.initials: K
authors.lastname: Williams
authors.forename: Dorothy J
authors.initials: DJ
authors.lastname: Becker
authors.forename: Trevor J
authors.initials: TJ
authors.lastname: Orchard
mesh_terms: D000293:Adolescent; D000328:Adult; D001158:Arteries / Q000473:pathology*; D001786:Blood Glucose / Q000378:metabolism*; D002648:Child; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000150:complications; D004562:Electrocardiography; D005260:Female; D006801:Humans; D007866:Leg / Q000098:blood supply*; D008297:Male; D008875:Middle Aged; D016491:Peripheral Vascular Diseases / Q000097:blood* / Q000150:complications; D012307:Risk Factors
chemical_list: D001786:Blood Glucose