Autoantibodies in immune-mediated neuropathies.

PURPOSE OF REVIEW: Over the past 25 years, many autoantibodies directed against peripheral nerve glycan and protein antigens have been described. Principally through this area of research, significant advances have been achieved in the understanding of the pathophysiology of inflammatory neuropathies. More evidence constantly continues to emerge supporting the role of antibodies in pathogenesis. This review reports the recent studies highlighting the complex association between autoantibodies directed against various peripheral nerve antigens and immune polyneuropathies. RECENT FINDINGS: The discovery of serum antibodies directed against ganglioside and glycolipid complexes has generated huge interest in this area of research. The expectation that nodal proteins are important targets continues to be pursued in line with the improvements in detection methodology. Basic studies continue to support a direct role for autoantibodies in neuropathy pathogenesis. SUMMARY: Discovery of new target epitopes has not only raised hopes for further improvement in our understanding of pathophysiology and availability of new diagnostic markers, but also for future targeted therapies. Further studies are required to elucidate the precise pathological and clinical significance of these new antibodies.

Guillain-Barre syndrome 1N leprosy patients.

Leprosy commonly affects the peripheral and cranial nerves. This involvement often manifests with peripheral neuropathy, occurring as a result of direct invasion of the nerves by lepra bacilli. Immune-mediated neuropathy occurring in leprosy, as part of lepra reaction, has been described earlier. We report here two cases of Guillain-Barre syndrome occurring in patients with leprosy who did not have any obvious evidence of lepra reaction.

Leprosy with Guillain Barre Syndrome: a new neurologic manifestation?

A 19-year-old female patient of lepromatous leprosy with Type II reaction, on multidrug therapy and prednisolone, presented with acute onset flaccid quadriparesis. The cerebrospinal fluid examination revealed albumino-cytologic dissociation. Nerve biopsy showed infiltration with lepra bacilli, features of vasculitis, and demyelination. There were no other identifiable precipitating factors for Guillain Barre Syndrome in this patient. Her condition improved without any steroid therapy. This case emphasizes the hypothesis that cell injury caused by Type II reaction can expose neural antigens and incite an autoimmune reaction in the form of Guillain Barre Syndrome.