Delayed apperance of anti–myelin‐associated glycoprotein antibodies in a patient with chronic demyelinating polyneuropathy

Valldeoriola, Francesc; Graus, Francesc; Steck, Andreas; Muñoz, Eva; Fuente, Miguel A. de la; Gallart, Teresa; Ribalta, Teresa; Bombí, J. A.; Tolosa, Eduard

doi:10.1002/ana.410340314

Cited by 22 publications

(7 citation statements)

References 12 publications

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“…In contrast, our patient 4 who worsened after PBSCT had atypical CIDP with a paraprotein and was old and not responsive to IVIg and had not responded to other agents apart from a slight response to corticosteroids. Although he developed an IgM paraprotein late in the course of his disease, as has been described ( Valldeoriola et al, 1993 ), our surrogate test for antibodies to MAG was negative and the clinical picture resembled CIDP rather than IgM paraproteinemic demyelinating neuropathy associated with antibodies to MAG.…”

Section: Discussionsupporting

confidence: 61%

Autologous peripheral blood stem cell transplantation for chronic acquired demyelinating neuropathy

Mahdi-Rogers

Kazmi

Ferner

et al. 2009

J Peripheral Nervous Sys

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Six patients with chronic acquired demyelinating neuropathy (CADP) were treated with autologous peripheral blood stem cell transplantation (PBSCT). Two with polyneuropathy, organomegaly, endocrinopathy, M-protein, and skin changes (POEMS) syndrome improved-improvement was sustained in one but relapsed and required repeat transplant in the other. Two of the three with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and one with an IgM paraprotein and antibodies to nerve improved--of the responders, one relapsed after 18 months and the other was in remission after 6 months. Four developed neutropenic septicemia and pneumonia. The role of PBSCT in CADP refractory to other treatment deserves further investigation but the serious adverse events and lack of sustained response in some patients emphasize the need for caution.

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Section: Discussionsupporting

confidence: 61%

Autologous peripheral blood stem cell transplantation for chronic acquired demyelinating neuropathy

Mahdi-Rogers

Kazmi

Ferner

et al. 2009

J Peripheral Nervous Sys

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“…The paraprotein was detected in the blood only on repeating the test approximately 1 year after the first examination in three cases, but immunofixation had not been carried out on the first occasion. 17,54 Four patients (IgM case nos Neurophysiological Findings. All patients had a sensorimotor neuropathy at their last follow-up (Tables 1, 2, and 4).…”

Section: Resultsmentioning

confidence: 99%

Long-term clinical and neurophysiological follow-up of patients with peripheral, neuropathy associated with benign monoclonal gammopathy

Ponsford¹,

Willison

Veitch

et al. 2000

Muscle Nerve

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The incidence of hematological malignancy in patients with monoclonal gammopathy of undetermined significance (MGUS) has been assessed as 17% to 25%. To ascertain whether this is true of neuropathy associated with MGUS, a long‐term (5–42 years) retrospective clinical and neurophysiological follow‐up was conducted in 50 cases (immunoglobulin M [IgM], n = 38; IgG, n = 11; IgA, n = 1). Only three patients developed hematological malignancy. Of 25 survivors with IgM paraproteinemia, 7 had myelin‐associated glycoprotein antibodies with typical clinical features. Evoked distal muscle amplitudes were significantly smaller than for the other paraprotein classes. Preferential distal demyelination manifested by relative prolongation of distal motor latency was not apparent in the cases of long duration. Two patients with IgM antidisialosyl antibodies and cold agglutinating activity had a large fiber neuropathy with intermittent oculofacial involvement. Both responded to intravenous immunoglobulin. Findings in the remaining patients were varied. Recognition of IgM subgroups is important both for prognosis and possible response to treatment. © 2000 John Wiley & Sons, Inc. Muscle Nerve 23: 164–174, 2000.

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“…The fact that many of the neural antigens which react with monoclonal antibodies also react with polyclonal antibodies in some patients with inflammatory PN substantiates this opinion (56). Moreover, delayed appearance of monoclonal anti-MAG antibodies was reported in a patient with CIDP (74).…”

Section: Introductionmentioning

confidence: 77%

Paraproteinemic Neuropathies

Vital¹

2001

Brain Pathology

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The occurrence of a peripheral neuropathy (PN) in association with a monoclonal gammopathy is quite common and suggests that monoclonal proteins may play a pathogenetic role in peripheral nervous system damage. In fact, paraproteinemic PN constitute an heterogeneous group of disorders related to various pathogenetic factors, and the histopathologic features in peripheral nerve biopsies differ from one condition to another. In several well defined disorders, the responsibility of the monoclonal component in the development of the PN has been evidenced. This is the case for most of the PN associated with an IgM monoclonal gammopathy, either a monoclonal gammopathy of undetermined significance (MGUS) or Waldenstrom's macroglobulinemia. The responsibility of the monoclonal protein in the occurrence of amyloid neuropathy related to multiple myeloma is also recognized. However, most IgG or IgA MGUS, as well as the monoclonal component in POEMS syndrome, have an uncertain causal relationship with the neuropathy. PN associated with monoclonal cryoglobulin (type 1) are occasional and differ from those associated with mixed cryoglobulins (types 2 or 3).

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Delayed apperance of anti–myelin‐associated glycoprotein antibodies in a patient with chronic demyelinating polyneuropathy

Cited by 22 publications

References 12 publications

Autologous peripheral blood stem cell transplantation for chronic acquired demyelinating neuropathy

Autologous peripheral blood stem cell transplantation for chronic acquired demyelinating neuropathy

Long-term clinical and neurophysiological follow-up of patients with peripheral, neuropathy associated with benign monoclonal gammopathy

Paraproteinemic Neuropathies

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