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Glial fibrillary acidic protein as a marker of axonal damage in chronic neuropathies
Author(s) -
Notturno Francesca,
Capasso Margherita,
Delauretis Angelo,
Carpo Marinella,
Uncini Antonino
Publication year - 2009
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.21323
Subject(s) - chronic inflammatory demyelinating polyneuropathy , glial fibrillary acidic protein , multifocal motor neuropathy , medicine , polyneuropathy , pathology , atrophy , endocrinology , mismatch negativity , gastroenterology , immunohistochemistry , immunology , antibody , electroencephalography , psychiatry
We evaluated serum glial fibrillary acidic protein (GFAP) levels by enzyme‐linked immunosorbent assay (ELISA) in controls ( n = 30) and in patients with chronic sensory‐motor axonal neuropathy (CSMAN) ( n = 30), chronic inflammatory demyelinating polyneuropathy (CIDP) ( n = 30), multifocal motor neuropathy (MMN) ( n = 30), and primary muscular spinal atrophy (PMSA) ( n = 15). GFAP levels, expressed as optical density, were increased in CSMAN (median = 1.05) compared to controls (median = 0.41; P < 0.05) and CIDP (median = 0.53, P < 0.05). They were also increased in PMSA (median = 0.99) compared to controls ( P < 0.05) and MMN (median = 0.66; P < 0.05). To differentiate CSMAN from CIDP and PMSA from MMN, we applied a cutoff of GFAP levels at 0.66, and we obtained good sensitivity and specificity. In neuropathies, serum GFAP correlated with summated sensory nerve action potential amplitudes ( r = −0.57; P = 0.0006) and disease severity ( r = 0.37; P = 0.0011). Thus, we propose serum GFAP as a marker of axonal damage and severity in chronic neuropathies. Muscle Nerve 40: 50–54, 2009