Background In contrast to cutaneous vasculitis, the morphology of which is well known, that of peripheral nerve lesions in HCV-positive mixed cryoglobulinemia (MC) patients are still under debate.1,2
Objectives To evaluate the pathological processes underlying the peripheral nerve damage in HCV-infected patients, with and without MC.
Methods From 14 HCV-infected patients (10 with MC and 4 without), all with clinically peripheral neuropathy, a sural nerve biopsy was obtained. Diseases other than HCV infection were excluded. The tissue samples were processed according to standard methods to perform morphologic and morphometric evaluation, on light and electronmicroscopic study. An immunohistochemical evaluation was carried out using labelled antisera against immunoglobulins (IgA, IgG, IgM), complement proteins (C1q, C3, terminal complex C5–9), and cellular antigens (CD3, CD11a-b-c, CD20, CD45, CD68).
Results In all nerve biopsies an axonal involvement without a distinctive vasculitis was found. Scarce perivascular infiltration by monuclear cells was observed, particularly around perineural blood vessels; extravasation of red cells was also found in the endoneurial vessels. Immunohistochemical study pointed out deposits of immunoglobulins and complement in sub-perineurial vessels, and infiltrations by mononuclear cells, mainly macrophages and CD4 T cells. Demyelinating neuropathy was only observed in patients without MC.
Conclusion Our data suggest that in HCV-infected patients different physiopathological processes are involved in induction of peripheral nerve damage. A potential direct pathogenic role of HCV should be investigated.
Bonetti B, et al. J Neuroimmunol. 1997;73:145
Bonetti B, et al. Virchows Arch. 1999;434:533
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