Anti-sulphatide antibodies in peripheral neuropathy.

Berg, Leonard H van den; Lankamp, C. L. A. M.; Jager, A.E.J. de; Notermans, N. C.; Sodaar, P.; Marrink, J; Jong, H. de; Bär, P.R.; Wokke, John H. J.

doi:10.1136/jnnp.56.11.1164

Cited by 75 publications

(37 citation statements)

References 13 publications

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“…It is therefore likely that anti-sulfatide IgM antibodies binding to sensory axons and dorsal root ganglia produce a sensory axonal nerve lesion, whereas in patients with demyelinating neuropathy these antibodies may be directed against sulfatide in the myelin. Morphological studies showed wide myelin lamellae and deposits of IgM on myelin sheets [2,21].…”

Section: Discussionmentioning

confidence: 99%

Polyneuropathy attributes: a comparison between patients with anti-MAG and anti-sulfatide antibodies

Erb

Ferracin

Fuhr

et al. 2000

Journal of Neurology

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Thirty-two patients with a peripheral neuropathy and paraproteinemia were tested for IgM antibodies against myelin-associated protein (MAG) and sulfatide by means of enzyme-linked immunosorbent assay. Nine patients (28 %) had increased anti-sulfatide IgM antibodies and showed a chronic, slowly progressive, distally pronounced, and symmetric polyneuropathy with sensory to sensory-motor impairment, ataxia, hyporeflexia, and axonal involvement in electrophysiological studies. Ten patients (31 %) with increased anti-MAG antibodies had a similar, homogeneous polyneuropathy syndrome but presented with demyelinating features. A weak cross-reactivity between anti-MAG and anti-sulfatide antibodies was present in only three patients. In conclusion, although the two neuropathy groups clearly differed in their electrophysiological features, their clinical presentation was rather similar.

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Section: Discussionmentioning

confidence: 99%

Polyneuropathy attributes: a comparison between patients with anti-MAG and anti-sulfatide antibodies

Erb

Ferracin

Fuhr

et al. 2000

Journal of Neurology

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“…Both axonal and demyelinating neuropathies have been described. 19,30,109 The antibodies are most often polyclonal but also occur as IgM monoclonal gammopathies, except in the small-fiber neuropathies, in which they are invariably polyclonal. 19 Some antisulfatide antibodies crossreact with MAG, P0, or chondroitin sulfate A or C. 19 Passive transfer of antisulfatide antibodies into rabbits or immunization of guinea pigs with sulfatide results in experimental neuropathy.…”

Section: Differential Diagnosismentioning

confidence: 99%

Clinical features and pathophysiological basis of sensory neuronopathies (ganglionopathies)

Antoine²,

2004

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Sensory ganglionopathies have a frequent association with neoplastic disorders (paraneoplastic subacute sensory neuronopathy, or SSN) or dysimmune disorders (Sjögren's syndrome, SS; Miller Fisher syndrome; and Bickerstaff's brainstem encephalitis, BBE), with drugs, such as cisplatin or pyridoxine, and with inherited disorders with degeneration of dorsal root ganglion cells. Unsteady gait and pseudoathetoid movements of the hand are the distinctive signs encountered in these disorders. The chronic disorders are characterized by non-length-dependent abnormalities of sensory nerve action potentials (SNAPs) and differ from other sensory neuropathies in showing a global, rather than distal, decrease in SNAP amplitudes. This review focuses on recent advances in defining the mechanisms involved in sensory ganglionopathies. Specific topics include a summary of their clinical features, pathological findings, and immunopathology. In SSN, early diagnosis by the detection of anti-Hu antibodies and early treatment of the cancer gives the best chance of stabilizing the disorder. In SS sensory ganglionitis, response to treatment has been disappointing, but immunomodulating treatments are emerging. The immunological profile common to BBE and Fisher syndrome supports a common pathogenesis. In toxic sensory neuronopathy, no treatment is available. The differential diagnosis involves separating sensory ganglionopathies from other ataxic polyneuropathies, such as infectious neuropathies, sensory neuropathies with various autoantibodies, and the neuropathies seen in celiac disease.

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“…Similarly, we found no elevated reactivity to sulphatide, although this has also been a target of antibody in neuropathy. 41 CIDP patients had increased T cell reactivity to the gangliosides GM1, GM3, GD3 and possibly GQ1b more frequently than healthy controls and ON patients but the differences were not statistically significant. The proportions of CIDP patients with increased T cell reactivity to gangliosides may be an underestimate, as it is possible that the level of this reactivity may fluctuate with the disease course of CIDP, as we have demonstrated for T cell reactivity to myelin antigens in multiple sclerosis.…”

Section: Discussionmentioning

confidence: 88%

Increased circulating T cell reactivity to GM1 ganglioside in patients with Guillain–Barré syndrome

Csurhes

Sullivan

Green

et al. 2005

Journal of Clinical Neuroscience

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This study was performed to determine whether increased ganglioside-specific T cell reactivity can be detected in the peripheral blood of patients with Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). T cell responsiveness to the gangliosides GM1, GM3, GD1a, GD1b, GD3, GT1b, GQ1b and sulphatide was assessed in peripheral blood mononuclear cells from untreated GBS patients (57), CIDP patients (43), patients with other peripheral neuropathies (55) and healthy control subjects (74) in a standard 6-day proliferation assay. Increased T cell reactivity to GM1 occurred in GBS patients compared to healthy controls and patients with other neuropathies. There was increased reactivity to GM3 in GBS patients compared to patients with other neuropathies but not compared to healthy controls. The frequencies of increased T cell reactivity to GM1 and GM3 in CIDP patients were intermediate between those of GBS patients and controls. We suggest that T cell reactivity to gangliosides might play a contributory role in the pathogenesis of GBS and perhaps CIDP.

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Anti-sulphatide antibodies in peripheral neuropathy.

Cited by 75 publications

References 13 publications

Polyneuropathy attributes: a comparison between patients with anti-MAG and anti-sulfatide antibodies

Polyneuropathy attributes: a comparison between patients with anti-MAG and anti-sulfatide antibodies

Clinical features and pathophysiological basis of sensory neuronopathies (ganglionopathies)

Increased circulating T cell reactivity to GM1 ganglioside in patients with Guillain–Barré syndrome

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