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Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) In Diabetes: Two Different Patterns Of Response To IV IG
Author(s) -
Cocito D,
Ciaramitaro P,
Isoardo G,
Pipieri A,
Barbero P,
Durelli L.
Publication year - 2001
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1046/j.1529-8027.2001.01007-14.x
Subject(s) - chronic inflammatory demyelinating polyneuropathy , medicine , polyneuropathy , antibody , gastroenterology , diabetes mellitus , polyradiculoneuropathy , immunology , endocrinology , guillain barre syndrome
OBJECTIVE: The finding of predominantly demyelinating polyneuropathies has been considered unusual in diabetic patients, however recent studies reported polyneuropathies satisfying electrophysiological criteria for diagnosis of CIDP (Gorson et al., 2000; Rotta et al., 2000) can be detected in diabetic patients. It is uncertain if this type of PN shows similar response to immunomodulating treatment as compared to other CIDP. In this study we evaluated response to IV IG in 10 diabetic patients with predominantly demyelinating polyneuropathy. PATIENTS AND METHODS: We included all diabetic patients with CIDP evaluated in our department from July 1999 to November 2000. 13 patients were found to be affected with predominantly demyelinating polyneuropathy; 3 of them refused IV IG. Sensory and motor disturbances according to Van Dijk et al. (1999) and nerve conduction studies (NCS) according to standard techniques were performed before IV IG treatment (T0) and 1 month (T1) and 6 months (T2) after IV IG. All patients underwent CSF examination and anti‐MAG, anti‐sulphatide and anti‐GM1 antibody assay. RESULTS: Increased CSF protein levels were found in 6 patients. No patients were positive for anti‐MAG, anti‐sulphatide or anti‐GM1 antibody assay. We did not detect significant clinical improvement after IV IG treatment, however there was improvement of motor deficit in 2 patients and of sensory score in 3. Six patients, 3 with increased CSF proteins level, had improvement on NCS, however there was not overall significant improvement of NCS abnormalities at T1. Patients with normal CSF protein levels had greater, although not significant, improvement on NCS than patients with increased protein levels. All patients with increased CSF protein levels deteriorated clinically or on NCS before T2. All patients with normal CSF protein levels remained stable on both items at T2. DISCUSSION: Our results confirmed low response of diabetic patients with demyelinating polyneuropathy to immunomodulating treatment, outlined by Gorson et al. (2000). In our study patients with normal CSF protein levels seem to have a better response to IV IG treatment probably reflecting a different pathogenesis as compared to patients with increased CSF protein levels. On the other hand, the high rate of relapse after IV IG treatment in patients with increased CSF protein levels seems to confirm the association of diabetes mellitus and CIDP in some patients.