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Autoimmune reactions in patients with M‐component and peripheral neuropathy
Author(s) -
JøNSSON V.,
SCHRøDER H. D.,
TROJABORG W.,
JENSEN T. STAEHELIN,
HIPPE E.,
HANSEN M. MøRK
Publication year - 1992
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.1992.tb00570.x
Subject(s) - medicine , endoneurium , peripheral neuropathy , autoantibody , pathology , immunology , monoclonal gammopathy of undetermined significance , gammopathy , peripheral nervous system , connective tissue disease , autoimmune disease , immunoglobulin d , antibody , monoclonal , central nervous system , monoclonal antibody , b cell , endocrinology , sciatic nerve , diabetes mellitus
A study of 17 patients with autoimmune axonal or demyelinating peripheral neuropathy in combination with M‐component is described. The M‐component was associated with MGUS (monoclonal gammopathy of undetermined significance) in 12 patients, CLL in one patient, WaldenstrÖm's disease in one patient, and myeloma in three patients. Immunohistological examination with direct and indirect fluorescence showed binding of antibodies to nerve structures of the same class and light chain as seen in the M‐component. In five cases of IgM M‐component, the demyelinating neuropathy was caused by binding of the IgM M‐protein and complement C3b to myelin‐associated glycoproteins (MAG). In 12 cases with axonal neuropathy, binding of IgG to the connective tissue of the peri‐ and endoneurium was found in 50% of cases, IgM in five cases, and IgD in one case. None of the patients had central nervous system (CNS) symptoms. The clinical and therapeutic difficulties are discussed; only two patients with an acute course responded to immunosuppression. A marked co‐expression of other autoimmune phenomena is interpreted in the light of cross‐reactions between the autoantibody and similar tissue autoantigens.