Article

Prevalence and characteristics of peripheral neuropathy in hepatitis C virus population

Dipartimento di Scienze Neurologiche, Università degli Studi di Napoli Federico II, Via Sergio Pansini 5, 80131 Napoli, and Department of Neurology, Hospital Maggiore, Lodi, Italy.
Journal of Neurology Neurosurgery & Psychiatry (Impact Factor: 5.58). 05/2006; 77(5):626-9. DOI: 10.1136/jnnp.2005.081570
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ABSTRACT To assess the prevalence of peripheral neuropathy (PN) and its correlation with cryoglobulinemia (CG) in an unselected, untreated referral hepatitis C virus (HCV) population.
Two hundred and thirty four patients (120 women and 114 men) with untreated HCV infection were consecutively enrolled by seven Italian centres. Clinical neuropathy was diagnosed when symptoms and signs of peripheral sensory or motor involvement were present. Median, ulnar, peroneal, and sural nerves were explored in all patients and distal symmetric polyneuropathy was diagnosed when all explored nerves or both lower limb nerves were affected. Mononeuropathy and mononeuropathy multiplex were diagnosed when one nerve or two non-contiguous nerves with asymmetrical distribution were affected. Screening for CG was done in 191 unselected patients.
Clinical signs of PN were observed in 25 of the 234 patients (10.6%). Electrophysiological PN was found in 36 (15.3%). CG was present in 56/191 patients (29.3%). The prevalence of CG increased significantly with age (p<0.001) and disease duration (p<0.05). PN was present in 12/56 (21%) patients with CG and 18/135 (13%) without CG (p=NS). PN increased significantly with age (p<0.001) and logistic regression analysis confirmed age as the only independent predictor of PN (OR 1.10 for each year; 95% CI 1.04 to 1.15; p<0.001).
Electrophysiological examination detected subclinical neuropathy in 11 patients (4.7%). Statistical analysis showed that CG was not a risk factor for PN whereas PN prevalence increased significantly with age.

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    • "The pathophysiology of HCV related PN remains largely speculative; vascular deposition of HCV-RNA containing cryoglobulins (CGs), direct viral infection or perivascular mononuclear inflammatory cells may be at the origin of HCV associated inflammatory vascular lesions. However, it is likely that HCV neuropathy results from virus triggered immune mediated mechanisms rather than from direct nerve infection and in situ replication [13]. "
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