Mixed or immune complex cryoglobulinaemia and neuropathy

Cream, J. J.; Hern, Jaclyn; Hughes, R. A. C.; Mackenzie, Ian C.

doi:10.1136/jnnp.37.1.82

Cited by 45 publications

(10 citation statements)

References 9 publications

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“…Fifteen patients (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15) were retrospectively selected in the neurology and internal medicine departments of our university hospital on the basis of (1) a peripheral neuropathy based on clinical and electrophysiological findings and (2) essential mixed cryoglobulinaemia diagnosed as described later. We included only the patients with positive mixed cryoglobulinaemia (corresponding to types II and III) on two successive determinations, with a serum concentration higher than 0 05 g/l.…”

Section: Patientsmentioning

confidence: 99%

Peripheral neuropathy associated with essential mixed cryoglobulinaemia: a role for hepatitis C virus infection?

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Musset

et al. 1996

Journal of Neurology, Neurosurgery & Psychiatry

102

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Background-The prevalence of hepatitis C virus (HCV) infection has been estimated at 43 to 84% in patients with essential mixed cryoglobulinaemia in recent large series. Some of these cases have been successfully treated with interferona. The objective was to evaluate the prevalence and the possible role of HCV infection in essential mixed cryoglobulinaemia. Methods-Fifteen patients (eight men and seven women; mean age: 612 (SD 16.5) years) with peripheral neuropathy (10 polyneuropathies and five multifocal mononeuropathies) and essential mixed cryoglobulinaemia were tested for serum anti-HCV antibodies. Results-Antibodies were found in 10 of 15 patients involving either polyneuropathies (seven patients) or multifocal mononeuropathies (three patients). Electrophysiological studies and teased nerve fibre studies (in seven patients) allowed neuropathies to be classified as predominantly sensory axonopathies. Compared with HCV-negative (HCV -) patients, HCV-positive (HCV +) patients had a more pronounced and more widespread motor deficit; motor nerve conduction velocities in peroneal and median nerves were more impaired in HCV + patients, although significance was not reached except for the mean value of the amplitude of the compound muscle action potentials of the median nerves (P < 0-05); necrotising vasculitis was found in two of nine nerve biopsies from the HCV + patients studied and in none of the three HCV -patients. In addition, HCV + patients had more frequent cryoglobulin related cutaneous signs, higher aminotransferase and serum cryoglobulin concentrations, lower total haemolytic complement concentrations, and more frequent presence of rheumatoid factor. A liver biopsy performed in eight HCV + patients disclosed a range of lesions, from chronic active hepatitis (six patients) to persistent hepatitis (two patients). Lastly, treatment with interferon-a conducted over six months in two patients seemed to improve the peripheral neuropathy. Conclusions-Patients with peripheral neuropathy and essential mixed cryoglobulinaemia should be tested for anti-HCV antibodies to determine the appropriate treatment.

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Section: Patientsmentioning

confidence: 99%

Peripheral neuropathy associated with essential mixed cryoglobulinaemia: a role for hepatitis C virus infection?

Apartis

Léger

Musset

et al. 1996

Journal of Neurology, Neurosurgery & Psychiatry

102

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“…The association of peripheral neuropathy with paraproteinaemia is well-established and has been described with cryoglobulinaemia (Abramsky et al, 1974;Cream et al, 1974;Reza et al, 1974), primary and secondary amyloidosis (Benson et al, 1975), Waldenstrom's macroglobulinaemia (Dayan and Lewis, 1966;Iwashita et al, 1974;Propp et al, 1975), multiple myeloma (Victor et al, 1958;Silverstein and Doniger, 1963), and benign IgM paraproteinaemia (Hobbs et al, 1976). Peripheral neuropathy has also been described in association with raised levels of polyclonal immunoglobulins (Whitaker et al, 1973;Hobbs et al, 1976;Iwabuchi et al, 1976), especially IgM.…”

mentioning

confidence: 99%

Peripheral neuropathy and benign IgG paraproteinaemia.

Read¹,

Vanhegan²,

Matthews³

1978

Journal of Neurology, Neurosurgery & Psychiatry

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“…151618 Our study demonstrated a high prevalence of peripheral neuropathy in EMC (56-8%) and a more common occurrence of polyneuropathy (51 4%) than of mononeuropathy and multiple mononeuropathy (21-6%), with association of both in 16-2%. Peripheral neuropathy was the presenting manifestation of EMC in 18 9% of cases, more often than previously reported (12- 16 EMC patients, and five out of seven patients with peripheral neuropathy had a severe hepatopathy, which may be a cause of polyneuropathy. 36 In the other prevalence studies,' 21 23 neurological data were not detailed, so that the features of peripheral neuropathy and the respective occurrence of polyneuropathy or mononeuropathy and multiple mononeuropathy cannot be deduced.…”

Section: Discussionmentioning

confidence: 72%