Abstract
Background. Diabetes is a common cause of polyneuropathy. The development and progression of nephropathy, retinopathy, and neuropathy are closely related. Angiotensin-converting enzyme (ACE) inhibitors delay progression of both nephropathy and retinopathy. We investigated the effect of ACE inhibition on diabetic neuropathy. Methods. We recruited 41 normotensive patients with type I or type II diabetes and mild neuropathy into a randomised double-blind placebo-controlled trial. Changes in the neuropathy symptom and deficit scores, vibration-perception threshold, peripheral-nerve electrophysiology, and cardiovascular autonomic function, were assessed at 6 and 12 months. The primary endpoint was the change in peroneal nerve motor conduction velocity. Findings. We found no significant difference at baseline for age, HbA(1c), blood pressure, or severity of neuropathy between two groups. There was no change in HbA(1c) over the treatment period. Peroneal motor nerve conduction velocity (p = 0.03) and M-wave amplitude (p = 0.03) increased, and the F-wave latency (p = 0.03) decreased and sural nerve action potential amplitude increased (p = 0.04) significantly after 12 months of treatment with trandolapril compared with placebo. Vibration-perception threshold, autonomic function, and the neuropathy symptom and deficit score showed no improvement in either group. Interpretation. The ACE inhibitor trandolapril may improve peripheral neuropathy in normotensive patients with diabetes. Larger clinical trials are needed to confirm these data before changes to clinical practice can be advocated.
Original language | English |
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Pages (from-to) | 1978-1981 |
Number of pages | 4 |
Journal | Lancet |
Volume | 352 |
Issue number | 9145 |
DOIs | |
Publication status | Published - 26 Dec 1998 |
Externally published | Yes |
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ASJC Scopus subject areas
- Medicine(all)
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Effect of angiotensin-converting-enzyme (ACE) inhibitor trandolapril on human diabetic neuropathy : Randomised double-blind controlled trial. / Malik, Rayaz A.; Williamson, Sheila; Abbott, Caroline; Carrington, Anne L.; Iqbal, Jawaid; Schady, Wolfgang; Boulton, Andrew J M.
In: Lancet, Vol. 352, No. 9145, 26.12.1998, p. 1978-1981.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effect of angiotensin-converting-enzyme (ACE) inhibitor trandolapril on human diabetic neuropathy
T2 - Randomised double-blind controlled trial
AU - Malik, Rayaz A.
AU - Williamson, Sheila
AU - Abbott, Caroline
AU - Carrington, Anne L.
AU - Iqbal, Jawaid
AU - Schady, Wolfgang
AU - Boulton, Andrew J M
PY - 1998/12/26
Y1 - 1998/12/26
N2 - Background. Diabetes is a common cause of polyneuropathy. The development and progression of nephropathy, retinopathy, and neuropathy are closely related. Angiotensin-converting enzyme (ACE) inhibitors delay progression of both nephropathy and retinopathy. We investigated the effect of ACE inhibition on diabetic neuropathy. Methods. We recruited 41 normotensive patients with type I or type II diabetes and mild neuropathy into a randomised double-blind placebo-controlled trial. Changes in the neuropathy symptom and deficit scores, vibration-perception threshold, peripheral-nerve electrophysiology, and cardiovascular autonomic function, were assessed at 6 and 12 months. The primary endpoint was the change in peroneal nerve motor conduction velocity. Findings. We found no significant difference at baseline for age, HbA(1c), blood pressure, or severity of neuropathy between two groups. There was no change in HbA(1c) over the treatment period. Peroneal motor nerve conduction velocity (p = 0.03) and M-wave amplitude (p = 0.03) increased, and the F-wave latency (p = 0.03) decreased and sural nerve action potential amplitude increased (p = 0.04) significantly after 12 months of treatment with trandolapril compared with placebo. Vibration-perception threshold, autonomic function, and the neuropathy symptom and deficit score showed no improvement in either group. Interpretation. The ACE inhibitor trandolapril may improve peripheral neuropathy in normotensive patients with diabetes. Larger clinical trials are needed to confirm these data before changes to clinical practice can be advocated.
AB - Background. Diabetes is a common cause of polyneuropathy. The development and progression of nephropathy, retinopathy, and neuropathy are closely related. Angiotensin-converting enzyme (ACE) inhibitors delay progression of both nephropathy and retinopathy. We investigated the effect of ACE inhibition on diabetic neuropathy. Methods. We recruited 41 normotensive patients with type I or type II diabetes and mild neuropathy into a randomised double-blind placebo-controlled trial. Changes in the neuropathy symptom and deficit scores, vibration-perception threshold, peripheral-nerve electrophysiology, and cardiovascular autonomic function, were assessed at 6 and 12 months. The primary endpoint was the change in peroneal nerve motor conduction velocity. Findings. We found no significant difference at baseline for age, HbA(1c), blood pressure, or severity of neuropathy between two groups. There was no change in HbA(1c) over the treatment period. Peroneal motor nerve conduction velocity (p = 0.03) and M-wave amplitude (p = 0.03) increased, and the F-wave latency (p = 0.03) decreased and sural nerve action potential amplitude increased (p = 0.04) significantly after 12 months of treatment with trandolapril compared with placebo. Vibration-perception threshold, autonomic function, and the neuropathy symptom and deficit score showed no improvement in either group. Interpretation. The ACE inhibitor trandolapril may improve peripheral neuropathy in normotensive patients with diabetes. Larger clinical trials are needed to confirm these data before changes to clinical practice can be advocated.
UR - http://www.scopus.com/inward/record.url?scp=0032570130&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032570130&partnerID=8YFLogxK
U2 - 10.1016/S0140-6736(98)02478-7
DO - 10.1016/S0140-6736(98)02478-7
M3 - Article
C2 - 9872248
AN - SCOPUS:0032570130
VL - 352
SP - 1978
EP - 1981
JO - The Lancet
JF - The Lancet
SN - 0140-6736
IS - 9145
ER -