{'fraction_non_alphanumeric': 0.02491349480968858, 'fraction_numerical': 0.001384083044982699, 'mean_word_length': 5.426666666666667, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Leprous neuropathy--observation from the standpoint vasculitis].

Pathogenesis of leprous neuropathy was studied from the standpoint of vasculitis. In vasculitic syndrome, mononeuritis multiplex is the most specific peripheral nerve injury. It occurs most frequently in small vessel vasculitis. Among them, the incidence is highest in microscopic polyangitis (MPO), Churg-Strauss Syndrome (CSS), and Wegener's granulomatosis (WG). All of them are categorized as ANCA associated disease. Because the disease activity is parallel with ANCA titer and ANCA is related directory to the pathogenesis of necrotizing vasculitis as well as the occurrence of peripheral neuropathy. Other small vessel vasculitis, such as lupus or rheumatoid vasculitis which are believed to occur by immune complex mechanism, are accompanied seldom by peripheral neuropathy. In WG, there are granulomatous lesions in upper and lower respiratory tracts which are supposed to be induced by Th1 dominant CD4 T cell infiltration. In cases of leprosy, if peripheral neuropathy were related to small vessel vasculitis, there might be two different pathogenesis. One is granulomatous vasculitis like WG in tuberculoid type. The other is immune complex type necrotizing vasculitis like SLE in lepromatous type, especially ENL. The site of these events may be small vessel in epineurium. Further immunologic studies are needed to clarify detailed mechanisms of leprous neuropathy.