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