Two female patients aged 64 and 54 were studied, affected by a progressive, distal sensori-motor mononeuritis multiplex. A nerve biopsy specimen from the first patient, suffering from chronic active hepatitis without detectable serum hepatitis B surface antigen (HBsAg) or antibody (anti-HBs), showed segmental demyelination and widespread inflammatory and necrotizing vasculitis and perivasculitis. The second patient, affected by a localized, caeseating tuberculous infection of the right kidney, refused to undergo a nerve biopsy. Serum levels of circulating immune complexes, detected by C1q BA binding method were strongly positive in both subjects; activation of the complement system (decreased serum level of C3 and/or C4) was also present. The course of the peripheral neuropathy was progressive and worsened in the first patient whose circulating immune complexes were always detectable. On the contrary the second patient showed improvement after the nephrectomy, which coincided with a quick disappearance of the circulating immune complexes. The findings may suggest in these two patients an immune complex mediated pathogenetic mechanism like the one recently accepted for the peripheral neuropathies in the course of chronic hepatitis B.