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Diabetic neuropathy

Diabetic neuropathies are neuropathic disorders that are associated with diabetes mellitus. These conditions usually result from diabetic microvascular injury involving small blood vessels that supply nerves (vasa nervorum). Relatively common conditions which may be associated with diabetic neuropathy include third nerve palsy; mononeuropathy; mononeuropathy multiplex; diabetic amyotrophy; a painful polyneuropathy; autonomic neuropathy; and thoracoabdominal neuropathy. more...

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Epidemiology

Diabetes is the leading cause of neuropathy in developed countries, and neuropathy is the most common complication and greatest source of morbidity and mortality in diabetes patients. It is estimated that the prevalence of neuropathy in diabetes patients is approximately 20%. Diabetic neuropathy is implicated in 50-75% of nontraumatic amputations.

The main risk factor for diabetic neuropathy is hyperglycemia. In the DCCT (Diabetes Control and Complications Trial, 1995) study, the annual incidence of neuropathy was 2% per year, but dropped to 0.56% with intensive treatment of Type 1 diabetics. The progression of neuropathy is dependent on the degree of glycemic control in both Type 1 and Type 2 diabetes. Duration of diabetes, age, cigarette smoking, hypertension, height and hyperlipidemia are also risk factors for diabetic neuropathy.

Pathology and pathogenesis

There are four factor involved in the development of diabetic neuropathy:

  1. Microvascular disease,
  2. Advanced glycated end products,
  3. Protein kinase C, and the
  4. Polyol pathway.

Microvascular disease

Vascular and neural diseases are closely related and intertwined. Blood vessels depend on normal nerve function, and nerves depend on adequate blood flow. The first pathological change in the microvasculature is vasoconstriction. As the disease progresses, neuronal dysfunction correlates closely with the development of vascular abnormalities, such as capillary basement membrane thickening and endothelial hyperplasia, which contribute to diminished oxygen tension and hypoxia. Neuronal ischemia is a well-established characteristic of diabetic neuropathy. Vasodilator agents (e.g., angiotensin-converting-enzyme inhibitors, α1-antagonists) can lead to substantial improvements in neuronal blood flow, with corresponding improvements in nerve conduction velocities. Thus, microvascular dysfunction occurs early in diabetes, parallels the progression of neural dysfunction, and may be sufficient to support the severity of structural, functional, and clinical changes observed in diabetic neuropathy.

Advanced glycated end products

Elevated intracellular levels of glucose cause a non-enzymatic covalent bonding with proteins, which alters their structure and destroys their function. Certain of these glycated proteins are implicated in the pathology of diabetic neuropathy and other long term complications of diabetes.

Protein kinase C (PKC)

PKC is implicated in the pathology of diabetic neuropathy. Increased levels of glucose cause an increase in intracellular diacylglycerol, which activates PKC. PKC inhibitors in animal models will increase nerve conduction velocity by increasing neuronal blood flow.

Read more at Wikipedia.org


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Effects of 3-month treatment with the antioxidant alpha-lipoic acid in diabetic peripheral neuropathy
From Alternative Medicine Review, 3/1/05 by Negrisanu G.

Negrisanu G, Rosu M, Bolte B, et al. Rom J Intern Med 1999;37(3):297-306.

Alpha lipoic acid is a natural antioxidant that has been suggested to improve symptoms of diabetic neuropathy. To assess these potential benefits, a cohort of 26 type 2 diabetic patients with symptomatic peripheral neuropathy (stage 2) received a daily dose of 600 mg alpha-lipoic acid, and were followed for a 3 month-period. No dropout was noted. At the end of the follow-up period, in 20 subjects (76.9%) there was a 1-stage regression of somatic neuropathy (from symptomatic to asymptomatic neuropathy, and in 5 patients (19.2%) no signs of neuropathy were found. The nerve conduction velocity of motor fibers improved from 36.8 (95% Confidence Interval CI = 30.9-42.7) meters/second to 41.3 (95% CI = 39.5-43.0) meters/second (p = 0.049, paired t test). Mean blood glucose measured was significantly lower at 3 months than at baseline [197.9 (95% CI = 170.1225.7) versus 162.2 (95% CI = 146.1-178.2 mg/dl, p = 0.02, paired t test)]. In a multiple linear regression model with age, sex, body mass index, diabetes duration and the difference between blood glucose values at 3 months and at baseline as explanatory variables, the increment in nerve conduction velocity was not accounted for by the improved glycemic control. Women, thinner and younger patients tended to benefit more from the treatment in terms of nervous conduction velocity improvement. In conclusion, alpha-lipoic acid seems to be efficient and safe in the treatment of diabetic peripheral neuropathy, improving both clinical manifestations and nerve conduction velocity. Placebo controlled clinical trials are needed to further define the role of this new medication in the treatment of diabetic neuropathies.

COPYRIGHT 2005 Thorne Research Inc.
COPYRIGHT 2005 Gale Group

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