Polyneuropathy in Waldenström's macroglobulinaemia

Iwashita, Hiroshi; Argyrakis, A.; Lowitzsch, К.; Spaar, F. W.

doi:10.1016/0022-510x(74)90178-6

Cited by 67 publications

(21 citation statements)

References 19 publications

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“…Moreover, experience has shown that immunohistochemistry fails to demonstrate immunoglobulin deposits in paraffin-embedded samples. However, deposits may be seen as diffuse deposits of an amorphous, hyaline-like substance in the endoneurium as in our patients 1 and 4 and in the case reported by Iwashita et al 2 Specific staining and the absence of multifocal distribution can rule out amyloid deposits. Only direct immunofluorescence on frozen sections can demonstrate multiple specific deposits in the endoneurium that stain by fluorescein isothiocyanate (FITC)-conjugated antibodies to light and heavy chains of the monoclonal dysglobulinemia.…”

Section: Discussionmentioning

confidence: 62%

Intranervous immunoglobulin deposits: An underestimated mechanism of neuropathy

et al. 2008

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There are several pathogenic mechanisms of peripheral nerve involvement in patients with monoclonal dysglobulinemia. Intranervous proliferation of malignant cells, immunoglobulin, or amyloid deposits in the endoneurial space can only be determined by examination of nerve biopsy specimens. We present clinical, electrophysiological, and histological data from seven patients whose polyneuropathy was induced by immunoglobulin deposits in the endoneurial space. As these lesions cannot be demonstrated on clinical and electrophysiological grounds, the indication for nerve biopsy derives from careful analysis of each patient presenting with a polyneuropathy and a monoclonal dysglobulinemia. To visualize and clearly characterize these deposits, electron microscopic examination is indispensable. Immunocytochemical methods using both light and electron microscopy for ultrastructural analysis are of great value. Demonstration of endoneurial immunoglobulin deposits may have major therapeutic consequences. Indeed, identification of these deposits prompted the use of aggressive treatment, which was quite effective in five of our seven patients.

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Section: Discussionmentioning

confidence: 62%

Intranervous immunoglobulin deposits: An underestimated mechanism of neuropathy

et al. 2008

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“…12,18 Most commonly, peripheral nerve involvement consists of a chronic, progressive, symmetrical sensorimotor polyneuropathy that affects both arms and legs. 5,15,22 Other forms of neuropathy include sensory 17 and motor 14 polyneuropathies, mononeuritis, 14 and mononeuritis multiplex. 13 Pathogenetic mechanisms include an autoimmune demyelinating process associated with anti-MAG antibodies or antibodies directed against another neural component, 3 endoneurial immunoglobulin deposition, 27 vasculitis, 25 amyloid deposition, 2 infiltration by malignant cells, 15 and serum hyperviscosity.…”

Section: Discussionmentioning

confidence: 99%

“…5,15,22 Other forms of neuropathy include sensory 17 and motor 14 polyneuropathies, mononeuritis, 14 and mononeuritis multiplex. 13 Pathogenetic mechanisms include an autoimmune demyelinating process associated with anti-MAG antibodies or antibodies directed against another neural component, 3 endoneurial immunoglobulin deposition, 27 vasculitis, 25 amyloid deposition, 2 infiltration by malignant cells, 15 and serum hyperviscosity. 12 Severe neuropathy is an indication for consideration of therapy.…”

Section: Discussionmentioning

confidence: 99%

Nineteen‐year follow‐up of Waldenström's‐associated neuropathy and Bing–Neel syndrome

et al. 2008

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We describe the follow-up of a patient with Waldenström's macroglobulinemia who developed mild predominantly sensory peripheral neuropathy, Bing-Neel syndrome, and, after 17 years, acute mononeuropathy multiplex associated with increasing paraprotein levels. Nerve biopsy demonstrated deposition of IgM in the endoneurium and perineurium. Magnetic resonance imaging showed extension of the cerebral white-matter abnormality. We suggest that the pathogenetic mechanism of the mononeuropathy multiplex may include direct IgM deposition. Late peripheral nerve complications appeared to be related to the paraprotein level.

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“…Neurological complications develop in 50% of patients with WM and generally consist of symmetrical sensorimotor peripheral neuropathy, whereas mononeuritis or mononeuritis multiplex are less common [3,4]. The pathogenetic mechanisms of IgM-related neuropathy are heterogeneous, including an autoimmune demyelinating process associated with anti-MAG (myelin associated glycoprotein) antibodies [5], endoneurial deposition of immunoglobulins or light chains [6,7], vasculitis [8], amyloid deposition [9] and infiltration by malignant cells [10].…”

Section: Introductionmentioning

confidence: 99%