title: The characteristics of chronic inflammatory demyelinating polyneuropathy in patients with and without diabetes--an observational study.
abstract: BACKGROUND
  We aimed to determine whether the clinical characteristics and electrodiagnostic classification of nerve injury, and response to treatment differed in patients diagnosed with chronic inflammatory demyelinating polyneuropathy (CIDP) with and without diabetes.
  
  
  METHODS
  CIDP patients with diabetes (CIDP+DM) (n = 67) and without diabetes (CIDP-DM) (n = 67) underwent clinical examination and nerve conduction studies (NCS). CIDP-DM patients were selected using age and gender matching with the existing CIDP+DM cohort. Patients treated with immunotherapies were classified as responders (R) (n = 46) or non-responders (NR) (n = 54) based on clinical response to treatment. The groups were compared using analysis of variance, contingency tables and Kruskal-Wallis analyses.
  
  
  RESULTS
  CIDP+DM subjects had more severe neuropathy based on higher lower limb vibration potential thresholds (VPT)(p = 0.004), higher Toronto Clinical Neuropathy Score (TCNS) (p = 0.0009), more proximal weakness (p = 0.03), more gait abnormality (p = 0.03) and more abnormal NCS. CIDP+DM subjects had more abnormal sural NCS with lower sural sensory nerve action potential amplitudes (2.4±3.0 µV, 6.6±6.0 µV, p<0.0001) and slower sural nerve conduction velocities (38.6±5.4 m/s, 41.0±5.3 m/s, p = 0.04). CIDP-DM subjects were more likely to receive immune therapies (93% vs 57%, p = <0.0001), despite no significant differences in treatment responder rates (p = 0.71). Patients who responded to therapy had shorter duration of CIDP than non-responders (8.0±6.0 y vs 11.9±7.6 y, p = 0.004).
  
  
  CONCLUSIONS
  The clinical phenotype and electrophysiological profile of CIDP patients differs according to the presence or absence of diabetes. Despite CIDP+DM patients having more severe clinical and electrophysiological neuropathy, they are less likely to receive disease-modifying/specific therapy, yet have similar response rates to treatment as those without diabetes. Specifically, the duration of neuropathy - not diabetes status - was associated with treatment response.
authors.affiliation: Division of Neurology, Department of Medicine, University of Toronto, Toronto, Canada.
authors.forename: Samantha K
authors.initials: SK
authors.lastname: Dunnigan
authors.affiliation: Division of Neurology, Department of Medicine, University of Toronto, Toronto, Canada.
authors.forename: Hamid
authors.initials: H
authors.lastname: Ebadi
authors.affiliation: Division of Neurology, Department of Medicine, University of Toronto, Toronto, Canada.
authors.forename: Ari
authors.initials: A
authors.lastname: Breiner
authors.affiliation: Division of Neurology, Department of Medicine, University of Toronto, Toronto, Canada.
authors.forename: Hans D
authors.initials: HD
authors.lastname: Katzberg
authors.affiliation: Division of Neurology, Department of Medicine, University of Toronto, Toronto, Canada.
authors.forename: Carolina
authors.initials: C
authors.lastname: Barnett
authors.affiliation: Division of Endocrinology and Metabolism, Department of Medicine, University of Toronto, Toronto, Canada.
authors.forename: Bruce A
authors.initials: BA
authors.lastname: Perkins
authors.affiliation: Division of Neurology, Department of Medicine, University of Toronto, Toronto, Canada.
authors.forename: Vera
authors.initials: V
authors.lastname: Bril
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000367:Age Factors; D000704:Analysis of Variance; D048909:Diabetes Complications / Q000503:physiopathology*; D006801:Humans; D009431:Neural Conduction / Q000502:physiology; D020277:Polyradiculoneuropathy, Chronic Inflammatory Demyelinating / Q000150:complications* / Q000503:physiopathology*; D012737:Sex Factors; D018709:Statistics, Nonparametric