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microvascular disease (MVD) is limited. We tested the association between HDL-C and MVD using prospective data from a large clinical trial of type 2 diabetics. Methods: 11,126 type 2 diabetics with ≥1 vascular risk factor were followed an average of 4.8 years. Cox proportional hazard models, adjusted for a wide range of covariates, were used to assess baseline HDL-C and development of new/worsening MVD; defined prospectively as a composite of total renal events (new/worsening albuminuria, doubling of creatinine ≥200 ␮mol/L, need for dialysis or death due to renal disease) and total eye events (new proliferative retinopathy, macular oedema, need for photocoagulation-therapy or diabetes-related blindness). Results: During follow-up, 32% of patients developed new or worsening MVD (28% renal and 6% retinal events). In patients who developed MVD compared to those who did not, mean baseline HDL-C was slightly lower (1.25 ± 0.35 mmol/L versus 1.26 ± 0.35 mmol/L, p = 0.05). For each 0.4 mmol/L (1 SD) higher baseline HDL-C there was a significant 5% decrease in MVD (adjusted HR = 0.95, 95%CI 0.91–0.99, p = 0.02), primarily driven by a 6% decrease in the risk of renal events (adjusted HR = 0.94, 95%CI 0.90–0.99, p = 0.01). There was no such association between baseline HDL-C and retinal events (adjusted HR = 1.02, 95%CI 0.92–1.12, p = 0.7). Conclusions: In patients with type 2 diabetes HDL-C level is an independent risk factor for the development of renal events, but not retinal events.

Abstracts CSANZ Abstracts 2011

S53

Method: 142 patients were selected as a sample of the overall patient cohort that attended the University of Melbourne Lipid Clinic at St Vincent’s Hospital from January 1995 to December 2010. Results: Forty patients (28%, 19 male, median age 61) referred with statin intolerance were reviewed. Main indications for intolerance were musculo-skeletal pain (n = 23, 58%) or elevated creatine kinase levels (n = 10, 25%). Median followup was five years. Following rechallenge, 32 patients (80%) were able to tolerate statins without significant adverse effects for a median period of 20 months. Management included steady dosage titration, combination with ezetimibe or fibrates (n = 20, 63%), and switching statins (median 2 switches, range 1–5). Six patients discontinued statins despite combination therapy (n = 4, 66%) and statin substitutions (median 2 switches, range 1–3). Two patients were lost to followup. Successfully rechallenged patients achieved improved fasting lipid profiles, with mean reduction in LDLcholesterol levels by 25.7% (−1.16 mmol/L, p < 0.001), total cholesterol levels by 21.1% (−1.49 mmol/L, p < 0.001), and triglyceride levels by 24.0% (−0.49 mmol/L, p < 0.05). 31% (n = 10) of these patients achieved target LDL-cholesterol levels (
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