Neurophysiological evaluation of short-term outcome of pharmacological treatment of diabetic neuropathy

  • Milan Cvijanović Center of Vojvodina, *Neurology Clinic, Novi Sad, Serbia; University of Novi Sad, Faculty of Medicine, Novi Sad, Serbia
  • Svetlana Simić Center of Vojvodina, *Neurology Clinic, Novi Sad, Serbia; University of Novi Sad, Faculty of Medicine, Novi Sad, Serbia
  • Aleksandar Kopitović Center of Vojvodina, *Neurology Clinic, Novi Sad, Serbia; University of Novi Sad, Faculty of Medicine, Novi Sad, Serbia
  • Ranko Raičević Military Medical Academy, Neurology Clinic, Belgrade, Serbia; University of Defence, Faculty of Medicine of the Military Medical Academy, Belgrade, Serbia
Keywords: diabetic neuropathies, electromyography, drug therapy, thioctic acid, thiamine monophosphate, gabapentin, treatment outcome,

Abstract


Background/Aim. Diabetic polyneuropathy (DPN) is a very frequent and progressive disease that severely impairs the overall quality of life, accompanied by a high rate of disability. For these reasons, the testing of therapeutic agents for this disease is increasing. Methods. We tested the most frequently used drugs for diabetic neuropathy in our area, along with electrophysiological monitoring in order to avoid subjectivity and the "placebo effect". A total of 120 patients were divided into four groups: three groups who received alpha-lipoic acid, benfotiamine or gabapentin respectively, and the control group who did not receive any treatment. In all the patients we analyzed motor conduction velocity, distal latency, sensory conduction velocity, F wave and F wave chronodispersion before and after treatment with each drug. Results. It is evident that some drugs had a favorable impact on the condition of the peripheral nerves. Alpha-lipoic acid and benfotiamine had an impact on the recovery of the nerve, i.e. pathophysiological processes, whereas gabapentin had no impact on the recovery, similarly to the control group without any treatment. Electrophysiological indicators had different sensitivity to detect conditions of the peripheral neurons. The best effect, in terms of increased sensory conduction velocity, had the patients treated with alpha-lipoic acid. Conclusion. The effect of alpha-lipoic acid and benfotiamine on the condition of peripheral nerve was evident. The failure of recovery, i.e. deterioration of electrophysiological parameters in patients who did not receive neuroprotective therapy suggests the need of permanent medication and periodic electrophysiological monitoring of patients with diabetic polyneuropathy.

References

Vinik AI. Management of neuropathy and foot problems in diabetic patients. Clin Cornerstone 2003; 5(2): 38−55.

Vinik AI, Mitchell BD, Leichter SB, Wagner AL, O'Brian JT, Georges LP. Epidemiology of the complications of diabetes. In: Leslie RD, Robbins DC, editors. Diabetes Clinical Science in Practice. Cambridge, United Kingdom: Cambridge University Press; 1995. p. 221−87.

Hotta N, Tojota T, Matsuoka K, Shigeta Y, Kikkawa R, Kaneko T, et al. Clinical efficacy of fidarestat, a novel aldose reductase in-hibitor, for diabetic peripheral neuropathy: a 52-week multi-center placebo-controlled double-blind parallel group study. Diabetes Care 2001; 24(10): 1776−82.

Pluijms W, Huygen F, Cheng J, Mekhail N, van Kleef M, Van Zundert J, et al. Evidence-based interventional pain medicine according to clinical diagnoses. 18. Painful diabetic polyneuropathy. Pain Pract 2011; 11(2): 191−8.

American Diabetes Association. Standards of medical care in di-abetes-2012. Diabetes Care 2012; 35 Suppl 1: S11−63.

Greene DA, Stevens MJ, Feldman EL. Glycemic control. In: Dyck PJ, Thomas PK, editors. Diabetic Neuropathy. 2nd ed. Philadel-phia: W.B. Saunders Company; 1999. p. 297−315.

Callaghan BC, Little AA, Feldman EL, Hughes RA. Enhanced glucose control for preventing and treating diabetic neuropa-thy. Cochrane Database Syst Rev 2012; 6: CD007543.

Attal N, Cruccu G, Baron R, Haanpää M, Hansson P, Jensen TS, et al. European ederation of Neurological Societies. EFNS guide-lines on the pharmacological treatment of neuropathic pain: 2010 revision. Eur J Neurol 2010; 17(9): 1113−e88.

Dworkin RH, Connor AO, Backonja M, Farrar JT, Finnerup NB, Jensen TS, et al. Pharmacologic management of neuropathic pain: Evidence-based recommendations. Pain 2007; 132(3): 237−51.

Schreeb KH, Freudenthaler S, Vormfelde SV, Gundert-Remy U, Glei-ter CH. Comparative bioavailability of two vitamin B1 prepara-tions: benfotiamine and thiamine mononitrate. Eur J Clin Pharmacol 1997; 52(4): 319−20.

Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, et al. Benfotiamine blocks three major pathways of hyperglycem-ic damage and prevents experimental diabetic retinopathy. Nat Med 2003; 9(3): 294−9.

Stracke H, Gaus W, Achenbach U, Federlin K, Bretzel RG. Benfo-tiamine in diabetic polyneuropathy (BENDIP): results of a randomised, double blind, placebo-controlled clinical study. Exp Clin Endocrinol Diabetes 2008; 116(10): 600−5.

Mijnhout GS, Alkhalaf A, Kleefstra N, Bilo HJ. Alpha lipoic acid: a new treatment for neuropathic pain in patients with diabetes? Neth J Med 2010; 68(4): 158−62.

Vallianou N, Evangelopoulos A, Koutalas P. Alpha-lipoic Acid and diabetic neuropathy. Rev Diabet Stud 2009; 6(4): 230−6.

Shaikh AS, Somani RS. Animal models and biomarkers of neu-ropathy in diabetic rodents. Indian J Pharmacol 2010; 42(3): 129−34.

Dordević G, Durić S, Apostolskit S, Dordević V, Zivković M. Total antioxidant blood capacity in patients with type 2 diabetes mel-litus and distal symmetrical polyneuropathy. Vojnosanit Pregl 2008; 65(9): 663−9. (Serbian)

Ewing DJ, Clarke BF. Diabetic autonomic neuropathy, present insights and future prospects. Diabetes Care 1986; 9(6): 648−65.

Cryer FE. Atherogenic hypoglycemia in IDDM. Consequences, risk factors and prevention.In: Home PD, Marshall S, Alberti KG, Krall L, editors. Diabetes Annual. Amsterdam: Elsevier; 1993. p. 317−31.

Ziegler D, Sohr CG, Nourooz-Zadeh J. Oxidative stress and anti-oxidant defense in relation to the severity of diabetic polyneu-ropathy and cardiovascular autonomic neuropathy. Diabetes Care 2004; 27(9): 2178−83.

Ziegler D, Ametov A, Barinov A, Dyck PJ, Gurieva I, Low PA, et al. Oral treatment with alpha-lipoic acid improves symptomatic diabetic polyneuropathy: The SYDNEY 2 trial. Diabetes Care 2006; 29(11): 2365−70.

Ziegler D. Thioctic acid for patients with symptomatic diabetic polyneuropathy: A critical review. Treat Endocrinol 2004; 3(3): 173−89.

Várkonyi T, Putz Z, Keresztes K, Martos T, Lengyel C, Stirban A, et al. Current options and perspectives in the treatment of diabetic neuropathy. Curr Pharm Des 2013; 19(27): 4981−5007.

Fraser DA, Diep LM, Hovden IA, Nilsen KB, Sveen KA, Seljeflot I, et al. The effects of long-term oral benfotiamine supplementa-tion on peripheral nerve function and inflammatory markers in patients with type 1 diabetes: A 24-month, double-blind, randomized, placebo-controlled trial. Diabetes Care 2012; 35(5): 1095−7.

Published
2017/09/19
Section
Original Paper