Association of glycaemia with lipids in adults with type 1 diabetes: modification by dyslipidaemia medication.
OBJECTIVE
Hyperglycaemia and dyslipidaemia are common metabolic abnormalities in adults with type 1 diabetes and both increase cardiovascular disease (CVD) risk. The hypothesis of this study was that change in HbA(1c) over 6 years would be associated with change in fasting lipids in adults with type 1 diabetes.


METHODS
The Coronary Artery Calcification in Type 1 Diabetes (CACTI) study examined 652 patients with type 1 diabetes (54% female); 559 and 543 had follow-up visits at 3 and 6 years. Baseline age (mean ± SD) was 37 ± 9 years, diabetes duration 23 ± 9 years, and HbA(1c) 8.0 ± 1.3%. Use of dyslipidaemia medication was 17%, 32%, and 46% at the three visits. Separate longitudinal mixed models were fitted to examine the relationship between change in HbA(1c) and change in fasting total cholesterol (TC), HDL-cholesterol (HDL-c), LDL-cholesterol (LDL-c), log triacylglycerols (TG), and non-HDL-cholesterol (non-HDL-c). Because of an interaction between dyslipidaemia medication use and association of HbA(1c) with lipids, results were stratified by dyslipidaemia medication use.


RESULTS
Among patients not using dyslipidaemia medication, a higher HbA(1c) was associated with significantly worse levels of the lipids TC, LDL-c, TG and non-HDL-c (per 1% change in HbA1c, TC 0.101 mmol/l, 95% CI 0.050, 0.152; LDL-c 0.103 mmol/l, 95% CI 0.058, 0.148; TG 0.052 mmol/l, 95% CI 0.024, 0.081; and non-HDL-c 0.129 mmol/l, 95% CI 0.078, 0.180) but not HDL-c (-0.20 mmol/l, 95% CI -0.047, 0.007). The associations between HbA(1c) and any lipid outcome among those on dyslipidaemia medication were in the same direction, but attenuated compared with persons not on medication.


CONCLUSIONS
Change in HbA(1c) is significantly associated with change in fasting lipids, but dyslipidaemia medications may be required to optimise lipid and cardiovascular health.
Maahs
D M
DM
Barbara Davis Center for Childhood Diabetes, University of Colorado Denver, Mail Stop A140, PO Box 6511, Aurora, CO 80045, USA. David.Maahs@ucdenver.edu
Ogden
L G
LG
Dabelea
D
D
Snell-Bergeon
J K
JK
Daniels
S R
SR
Hamman
R F
RF
Rewers
M
M
D000328:Adult; D001786:Blood Glucose / Q000032:analysis* / Q000187:drug effects* / Q000378:metabolism; D002114:Calcinosis / Q000188:drug therapy / Q000453:epidemiology / Q000209:etiology; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000453:epidemiology / Q000209:etiology; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D003925:Diabetic Angiopathies / Q000188:drug therapy / Q000453:epidemiology / Q000209:etiology; D050171:Dyslipidemias / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D000960:Hypolipidemic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D050356:Lipid Metabolism / Q000187:drug effects; D008055:Lipids / Q000032:analysis*; D008297:Male; D008875:Middle Aged; D055815:Young Adult
D001786:Blood Glucose; D000960:Hypolipidemic Agents; D008055:Lipids
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