The characteristics of chronic inflammatory demyelinating polyneuropathy in patients with and without diabetes--an observational study

• Published in: PloS one Vol. 9; no. 2; p. e89344
• Main Authors: Dunnigan, Samantha K, Ebadi, Hamid, Breiner, Ari, Katzberg, Hans D, Barnett, Carolina, Perkins, Bruce A, Bril, Vera
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 19.02.2014; Public Library of Science (PLoS)
• Subjects: Action potential; Action Potentials - physiology; Age Factors; Analysis of Variance; Biology; Care and treatment; Comparative analysis; Contingency; Demyelination; Diabetes; Diabetes Complications - physiopathology; Diabetes mellitus; Diabetic neuropathy; Diabetics; Electromyography; Gait; Glucose; Health aspects; Health care networks; Hemoglobin; Humans; Immunotherapy; Inflammation; Laboratories; Medical diagnosis; Medical research; Medicine; Nerve conduction; Neural Conduction - physiology; Neurology; Neuropathy; Neurophysiology; Observational studies; Patients; Polyneuropathies; Polyneuropathy; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating - complications; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating - physiopathology; Sex Factors; Statistics, Nonparametric; Sural nerve; Therapy; Type 2 diabetes; Variance analysis; Vibration; Canada
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0089344

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. 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. 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). 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.