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Antioxidant Alpha Lipoic Acid

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By Jerry Ingram

NEW ORLEANS, LA -- June 20, 2003 -- The antioxidant alpha-lipoic acid administered over 3 weeks at a dose of 600 mg/day reduces symptomatic polyneuropathy in patients with diabetes, researchers reported here on June 15th at the 63Scientific Sessions of the American Diabetes Association.

We saw significant improvements in subjects and feel quite optimistic about the potential therapeutic use of this agent," said Dan Zeigler, MD, a clinical researcher at Heinrich Heine University in Dusseldorf, Germany.

Dr. Zeigler and colleagues conducted a meta-analysis of research from the database of VIATRIS GmbH, a pharmaceutical company based in Frankfurt, Germany, to determine the efficacy and safety of alpha-lipoic acid in diabetic patients with symptomatic polyneuropathy. All of the data came from randomized, double-masked, placebo-controlled, parallel-group trials using alpha-lipoic acid infusion.

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Chronic inflammatory demyelinating polyneuropathy (CIDP) may also be seen in patients with diabetes.

Krendel et al described 15 patients with non–insulin-dependent diabetes mellitus, studied by electrophysiologic and histologic analysis of nerve or muscle biopsy, with diabetic polyneuropathy, amyotrophy, or mononeuropathy multiplex. Perivascular and vascular lymphocytic infiltrates were noted in 7 patients. Neurological improvement with immunosuppressive therapy, often including IVIg, was also noted. Six additional patients in the study had electrophysiologic evidence of demyelinating neuropathy and lacked vascular inflammation on biopsy but did show onion bulbs, reflecting a chronic demyelinating process. These patients all had insulin-dependent diabetes mellitus and responded to immunosuppressive treatment. The authors postulated that these patients had CIDP and that type 1 diabetes mellitus may predispose patients to CIDP.

Patients with CIDP typically had a more chronic course (up to 180 months), did not lose weight, and were more likely to have a distal neuropathy, commonly involving the upper extremities. However, like that in inflammatory vasculopathy, the distribution was often asymmetric.

Unselected patients with type 1 diabetes rarely have demyelinating neuropathy as determined by nerve conduction studies. Neurologists see a population of patients with diabetes who have unusually severe neuropathy. Demyelination by nerve conduction studies should prompt suspicion of CIDP in patients with diabetes, just as it does in those without diabetes. Whether the autoimmune diathesis in patients with diabetes predisposes them to CIDP is unknown. The fact that demyelination has been found more often in association with type 1 diabetes than with type 2 diabetes makes this likely, since these patients more often have other associated autoimmune diseases.

Patients with demyelinating neuropathy by nerve conduction studies can reasonably be assumed to have CIDP. Although the weight of evidence to date suggests a role for empiric treatment with IVIg in patients with diabetes who have progressive disabling neuropathy presumably due to inflammatory vasculopathy or CIDP, considering nerve biopsy with immunohistochemistry to look for evidence of vasculitis or other causes of neuropathy is reasonable.
In summary, diabetes mellitus-CIDP differs from idiopathic CIDP in the following ways:

Older age at presentation in patients with diabetes

Imbalance a more common complaint in patients with diabetes

Duration of symptoms at the time of evaluation is longer in patients with diabetes

Prominent axonal loss in the diabetes group

Less response to therapy in the diabetes group

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