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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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Thioctic acid & diabetic neuropathy - Shorts
From Townsend Letter for Doctors and Patients, 8/1/03 by Jule Klotter

In Germany, thioctic acid, also known as alpha-lipoic acid, is an approved therapy for diabetic neuropathy. The sulphur-containing compound, found in mitochondria, is necessary for converting food into energy. It also regenerates oxidized vitamins E & C, allowing the body to use the antioxidants again. When given as a supplement, thioctic acid works as an antioxidant that is both fat- and water-soluble. Thioctic acid is also known to chelate heavy metals from the body.

In their review of botanicals and dietary supplements that have undergone randomized controlled trials for diabetic neuropathy (J AM Board Fam Pract 16(1): 47-57, 2003), Kathleen M. Halat and Cathi E. Dennehy, PharmD, state that "[t]reatment with alpha-lipoic acid improves nerve blood flow and distal nerve conduction and increases endoneurial glucose uptake and energy metabolism in animals." Four randomized, double-blind, placebo-controlled studies entitled ALADIN (Alpha Lipoic Acid in Diabetic Neuropathy), ALADINII, ALADINIII, & ORPIL (Oral Pilot) have indicated that supplementation with alpha-lipoic acid reduces neuropathic deficits and symptoms.

Short-term parenteral use (IV) appears to be more effective than long-term oral use, although some clinical trials have shown improvement in nerve conduction velocity using oral doses of 600 to 1,200 mg/day for 2 years.

Adverse side effects of thioctic acid include headache, skin rash, stomach upset (at doses >600 mg/day), and possible hypoglycemia. Because thioctic acid is a chelating agent, Halat and Dennehy warn that iron levels need to be monitored as mineral deficiencies may occur. It may also chelate some medications, such as antacids, so thioctic acid should be taken at least 2 hours away from these.

Halat, Kathleen M. & Dennehy, Cathi E., PharmD. Botanicals and Dietary Supplements in Diabetic Perpheral Neuropathy. J Am Board Fam Pract 16(1):47-57, 2003

Passwater, Richard A., PhD. Lipoic Acid Basics--Interview with Dr. Jim Clark. www.healthy.net/asp/templates/interview.asp?PageType=Interview&ID=160

COPYRIGHT 2003 The Townsend Letter Group
COPYRIGHT 2003 Gale Group

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