Statin therapy and neuropathy in type 1 diabetes: A cross-sectional study.
Dyslipidaemia contributes to the pathogenesis of diabetic peripheral neuropathy (DPN). While statins improve cardiovascular outcomes in diabetes, their potential neurotoxic effects remain debated. This study examined the impact of statin use on neuropathy in type 1 diabetes mellitus (T1DM).
Participants with T1DM (n = 160) and healthy controls (n = 64) underwent symptom and clinical evaluation of DPN, cardiac autonomic neuropathy (CAN) and corneal confocal microscopy (CCM). T1DM participants were stratified by statin use (non-statin: n = 68; statin treated: n = 92).
There were significant differences between the non-statin and statin patients with T1DM and healthy controls for the diabetic neuropathy symptom score (DNS) (0.49 ± 0.14 vs. 0.90 ± 0.13 vs. 0.15 ± 0.13, p < 0.001), neuropathy disability score (NDS) (2.55 ± 0.29 vs. 3.67 ± 0.26 vs. 0.44 ± 0.28, p < 0.001), vibration perception threshold (13.68 ± 1.16 vs. 16.03 ± 1.03 vs. 6.05 ± 1.08, p < 0.001), corneal nerve fibre density (19.61 ± 1.04 vs. 19.02 ± 0.92 vs. 28.48 ± 0.97, p < 0.001), branch density (20.40 ± 2.21 vs. 21.39 ± 1.94 vs. 37.31 ± 2.05, p < 0.001), fibre length (11.97 ± 0.51 vs. 11.51 ± 0.45 vs. 16.55 ± 0.47, p < 0.001), DB-HRV (26.27 ± 1.76 vs. 24.21 ± 1.51 vs. 30.18 ± 1.67, p = 0.033) and 30:15 ratio (1.32 ± 0.04 vs. 1.21 ± 0.03 vs. 1.15 ± 0.07, p = 0.033). Despite the statin group being significantly older (p < 0.001) with a higher BMI (p = 0.001) and longer duration of diabetes (p < 0.001), statin-treated patients showed no significant differences in most neuropathy measures, except DNS (p = 0.04), NDS (p = 0.009) and 30:15 ratio (p = 0.04).
This study demonstrates that individuals with T1DM exhibit neuropathic symptoms and disability, increased vibration perception thresholds, corneal nerve fibre loss and evidence of CAN. However, statin therapy was associated with comparable measures of DPN and CAN, despite statin-treated patients having a longer duration of diabetes and a higher BMI.
Participants with T1DM (n = 160) and healthy controls (n = 64) underwent symptom and clinical evaluation of DPN, cardiac autonomic neuropathy (CAN) and corneal confocal microscopy (CCM). T1DM participants were stratified by statin use (non-statin: n = 68; statin treated: n = 92).
There were significant differences between the non-statin and statin patients with T1DM and healthy controls for the diabetic neuropathy symptom score (DNS) (0.49 ± 0.14 vs. 0.90 ± 0.13 vs. 0.15 ± 0.13, p < 0.001), neuropathy disability score (NDS) (2.55 ± 0.29 vs. 3.67 ± 0.26 vs. 0.44 ± 0.28, p < 0.001), vibration perception threshold (13.68 ± 1.16 vs. 16.03 ± 1.03 vs. 6.05 ± 1.08, p < 0.001), corneal nerve fibre density (19.61 ± 1.04 vs. 19.02 ± 0.92 vs. 28.48 ± 0.97, p < 0.001), branch density (20.40 ± 2.21 vs. 21.39 ± 1.94 vs. 37.31 ± 2.05, p < 0.001), fibre length (11.97 ± 0.51 vs. 11.51 ± 0.45 vs. 16.55 ± 0.47, p < 0.001), DB-HRV (26.27 ± 1.76 vs. 24.21 ± 1.51 vs. 30.18 ± 1.67, p = 0.033) and 30:15 ratio (1.32 ± 0.04 vs. 1.21 ± 0.03 vs. 1.15 ± 0.07, p = 0.033). Despite the statin group being significantly older (p < 0.001) with a higher BMI (p = 0.001) and longer duration of diabetes (p < 0.001), statin-treated patients showed no significant differences in most neuropathy measures, except DNS (p = 0.04), NDS (p = 0.009) and 30:15 ratio (p = 0.04).
This study demonstrates that individuals with T1DM exhibit neuropathic symptoms and disability, increased vibration perception thresholds, corneal nerve fibre loss and evidence of CAN. However, statin therapy was associated with comparable measures of DPN and CAN, despite statin-treated patients having a longer duration of diabetes and a higher BMI.
Authors
Pasha Pasha, Kamath Kamath, Linn Linn, Kalteniece Kalteniece, Bashir Bashir, Schofield Schofield, Malik Malik, Azmi Azmi, Ferdousi Ferdousi, Soran Soran
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