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Immunosuppression, IVIG, and Diabetic Lumbosacral Plexopathy
Abstract & Commentary
Source: Zochodne DW, et al. Failure of immunotherapy tp prevent, arrest or reverse diabetic lumbosacral plexopathy. Acta Neurol Scand. 2003;107:299-301.
Intravenous immunoglobulin (IVIG) is an expensive but powerful and useful therapeutic tool in the neurologist’s armamentarium. Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, Lambert-Eaton myasthenic syndrome, and dermatomyositis have all been shown, in controlled clinical trials, to benefit from IVIG. Recurrent shortages of IVIG, however, underscore the notion that IVIG is being overused in instances where science has yet to document its use. Diabetic plexopathy may be one of those instances.
Three male diabetics, including a cardiac allograft recipient on cyclosporine and mycophenolate mofetil (CellCept) for immunosuppression, developed asymmetric proximal leg pain, weakness, atrophy, and areflexia consistent with a diagnosis of diabetic lumbosacral plexopathy. Nerve conduction studies and electromyography supported the diagnosis. Imaging studies, including MRI and computerized tomography of the lumbar spine, failed to demonstrate any secondary confounding structural lesion. IVIG was of no benefit in the 2 nonimmunosuppressed patients, and progression of weakness and disability occurred in all 3. Results such as these raise questions as to the use of immunosuppression for this condition and, indeed, cast doubt on whether the underlying etiology is autoimmune microvasculitis.
Proper management of these patients, as for all diabetic neuropathies, begins with strict control of hyperglycemia, which can reduce the prevalence of neuropathy by 50% at 5 years.1 Tolrestat, an aldose reductase inhibitor (ARI), improves autonomic function and vibration perception, but ARIs alone will not likely alter the progression of neuropathy.2 Alpha lipoic acid is currently being investigated in a 4-year international multicenter trial, and interim (2-year) results are expected to be announced this month at the American Diabetes Association meeting. Gamma-linoleic acid resulted in clinical and electrophysiological improvement,3 but human aminoguanidine trials were discontinued due to toxicity. Nerve growth factor did not deliver on its initial promise, and further trials with this agent are on hold. IVIG is appropriate and may be effective when autoimmunity underlies neuropathy, but the prevalence of neuropathy in diabetes and over-interpretation of electrodiagnostic results invite overuse. Controlled trials of IVIG for some forms of diabetic neuropathy are an idea whose time has come. — Michael Rubin
Dr. Rubin is Professor of Clinical Neurology, New York Presbyterian Hospital - Cornell Campus.
1. N Engl J Med. 1993;329:977-986.
2. Didangelos TP, et al. J Diabetes Complications. 1998;12:201-207.
3. Keen H, et al. Diabetes Care. 1993;16:8-15.