Severe hepatitis C virus‐related cryoglobulinaemic sensory–motor polyneuropathy treated with pegylated interferon‐a2b and ribavirin: clinical, laboratory and neurophysiological study

Koskinas, John; Kilidireas, Constantinos; Karandreas, Nikolaos; Kountouras, Dimitrios; Savvas, S.; Hadziyannis, Emilia; Archimandritis, Athanasios

doi:10.1111/j.1478-3231.2006.01436.x

Cited by 11 publications

(6 citation statements)

References 28 publications

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“…Antiviral therapy has often been prescribed to patients with HCV-associated cryoglobulinemia with vasculitis [16,24,27]. However, the results of studies involving antiviral therapy in neuropathic patients-mainly consisting of small cohorts-are controversial [2,17]. De novo appearance or worsening of HCV-related cryoglobulinemic neuropathy has been reported within 6 months of interferon therapy [6,14,20], even though similar effects were not reported in a prospective study using pegylated interferon [7].…”

Section: Discussionmentioning

confidence: 98%

Rituximab in cryoglobulinemic peripheral neuropathy

et al. 2009

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Type II mixed cryoglobulinemia is sustained by an oligoclonal production of IgM sharing rheumatoid activity and can be associated with renal, cutaneous, rheumatologic or neurological manifestations. Peripheral neuropathy is a major cause of morbidity in hepatitis C virus-associated mixed cryoglobulinemia and is often refractory to any treatment. Rituximab induces a selective depletion of IgM-producing B cells, and both case reports on monoclonal IgM-related polyneuropathy as well as studies on small series of patients with interferon alpha-resistant mixed cryoglobulinemia have suggested that it may be beneficial. Thirteen patients affected by type II mixed cryoglobulinemia with polyneuropathy were treated. Rituximab was administered intravenously at a dose of 375 mg/m(2) on days 1, 8, 15 and 22. Two more doses were given 1 and 2 months later. No other immunosuppressive drugs were added. Response was evaluated by assessing the changes in the clinical neurological condition, in electromyographic indices and in laboratory parameters (including cryocrit, viral load, complement levels and rheumatoid factor) over at least 12 months. Sensory symptoms disappeared or improved following treatment. A significant improvement in the clinical neuropathy disability score was observed. Electromyography examination revealed that the amplitude of compound motor action potential had increased. Viral load did not significantly change. Side effects were negligible. In this open prospective study, rituximab appeared to be effective and safe in the treatment of patients with type II cryoglobulinemia-associated neuropathy.

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Section: Discussionmentioning

confidence: 98%

Rituximab in cryoglobulinemic peripheral neuropathy

et al. 2009

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“…On one hand, cryoglobulins are thought to be related to vasculitis, consecutively affecting small vessels with infiltration of perivascular regions leading to peripheral nerve damage [21,23]. On the other hand, a direct neurotoxic effect of HCV leading to neuropathy was suggested previously [7,9,12,34].…”

Section: Discussionmentioning

confidence: 99%

“…(1) neurotoxicity of the virus itself [7,9,12,34], (2) HCV infection associated cryoglobulinaemia [21,23] and (3) treatment with interferon [4,22]. The prevalence of HCV associated neuropathy has been evaluated in previous studies by clinical assessment alone or in combination with standard nerve conduction studies [5,29,34].…”

mentioning

confidence: 99%

Sensory neuropathy in patients with cryoglobulin negative hepatitis-C infection

et al. 2010

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There is growing evidence that hepatitis-C virus (HCV) infection might cause peripheral neuropathy. We aimed to investigate the prevalence, clinical and electrophysiological features of sensory neuropathy in patients with cryoglobulin negative HCV infection. We studied 46 consecutive cryoglobulin negative HCV positive patients (24 of them with and 22 without neuropathic symptoms, NS) and compared to 28 age and gender matched controls. In all patients and controls, clinical neuropathy symptom (NSS) and neuropathy deficit scores (NDS) were assessed and standard nerve conduction velocity (SNCV) and pain related-evoked potentials (PREP) were recorded. Both, SNCV and PREP were abnormal in 13 NS positive patients (13/46, 28%). Abnormal PREP but normal SNCV were found in 5 (5/46, 11%) NS positive and in 2 NS negative patients (2/46, 4%). PREP abnormalities correlated positive with both clinical neuropathy scores (NSS r=0.62; p<0.001; NDS r=0.57; p<0.001), but not with the duration of the disease, current viral load, or the virus subtype. PREP abnormalities were more frequent (16/33, 48.5%) in HCV patients treated with interferon than in therapy naïve patients (4/13, 30.8%); the difference was, however, not significant. In our present study (1) all virus subtypes are capable of inducing neuropathy, (2) no differences were found between interferon therapy and treatment naive patients, (3) the prevalence of peripheral sensory neuropathy including small sensory fibers (20/46, 43.5%) is higher than previously reported and (4) we found that detection of HCV associated neuropathy depends on the evaluation method.

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“…In CIDP, DCs are probably initially recruited to inflamed spinal nerve roots and adjacent meninges to take up released antigens (13 (14). There have been several reports indicating an association between HCV infection and neuropathy (15,16).…”

Section: To Our Knowledge This Is the First Report To Demonstrate mentioning

confidence: 99%