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SPECIFIC DISORDERS 155 Nichols WC, Gregg RE, Brewer BH, Benson MD A mutation in apolipoprotein A1 Iowa type of familial amyloidotic polyneuropathy Genomics 1990;8:318 323 156 Meretoja J Familial systemic paramyloidosis with lattice dystrophy of the cornea, progressive cranial neuropathy, skin changes and various internal symptoms Ann Clin Res 1969;1:314 324 157 Haltia M, Levy E, Meretohi J, Fernandez-Madrid I, Koivunene O, Frangione B Gelsolin gene mutation at codon 187 in familial amyloidosis, Finnish: DNAdiagnostic assay Am J Med 1992;42:357 359 158 Kiuru-Enari S, Somer H, Seppalainen AM, Notkola IL, Haltia M Neuromuscular pathology in hereditary gelsolin amyloidosis J Neuropathol Exp Neurol 2002;61(6):565 571 159 Gorevic PD, Munoz PC, Gorgone G, et al Amyloidosis due to a mutation in the gelsolin gene in an American family with lattice corneal dystrophy type II N Engl J Med 1991;325:1780 1785 160 Kiuru S Gelsolin-related familial amyloidosis, Finnish type (FAF), and its variants found worldwide Amyloid 1998;5:55 66 161 Maury CP, Liljestrom M, Boysen G, Tornroth T, de la Chapelle A, Nurmiaho-Lassila EL Danish type gelsolin related amyloidosis: 654G-T mutation is associated with a disease pathogenetically and clinically similar to that caused by the 654G-A mutation (familial amyloidosis of the Finnish type) J Clin Pathol 2000;53(2):95 99
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147 Briemberg HR, Amato AA Transthyretin amyloidosis presenting with multifocal demyelinating mononeuropathies Muscle Nerve 2004;29(2):318 22 148 Anrade C A peculiar form of peripheral neuropathy Brain 1952;75:408 426 149 Plante-Bordeneuve V, Lalu T, Misrahi M, et al Genotypic phenotypic variations in a series of 65 patients with familial amyloid polyneuropathy Neurology 1998;51:708 714 150 Plant -Bordeneuve V, Ferreira A, Lalu T, Zaros C, Lacroix e C, Adams D, Said G Diagnostic pitfalls in sporadic transthyretin familial amyloid polyneuropathy (TTR-FAP) Neurology 2007 Aug 14;69(7):693 698 151 Bergethon PR, Sabin TD, Lewis D, Simms RW, Cohen AS, Skinner M Improvement in the polyneuropathy associated with familial amyloid polyneuropathy after liver transplantation Neurology 1996;47:944 951 152 Adams D, Samule D, Goulin-Goeau C, et al The course and prognostic factors of familial amyloid polyneuropathy after liver transplantation Brain 2000;123:1495 1504 153 Van Allen MW, Frolich JA, Davis JR Inherited predisposition to generalized amyloidosis Neurology 1969;19:10 25 154 Joy T, Wang J, Hahn A, Hegele RA APOA1 related amyloidosis: A case report and literature review Clin Biochem 2003;36:641 645
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Neuropathies can develop as a direct result of various bacterial and viral infections, as well as an indirect or parainfectious autoimmune response to the infection (Table 15 1) Neuropathies as a consequence of parainfectious responses (eg, Gullain Barre syndrome associated with various infections and vasculitis associated with hepatitis) are discussed in detail in other chapters As in the tuberculoid form, there is a predilection for involvement of cooler regions of the body In ltration of the organism in the face leads to the loss of eyebrows and eyelashes and exaggeration of the natural skin folds, leading to the so-called leonine facies Super cial cutaneous nerves of the ears and distal limbs are also commonly affected A slowly progressive symmetric sensorimotor polyneuropathy gradually develops due to widespread invasion of the bacilli into the epi-, peri-, and endoneurium Distal extremity weakness may be seen, but large sensory ber modalities and muscle stretch re exes are relatively spared Involvement of nerve trunks leads to superimposed mononeuropathies, including facial neuropathy Neuropathies are most common in patients with borderline leprosy1,2,4 Patients can develop generalized symmetric sensorimotor polyneuropathies, mononeuropathies, and mononeuropathy multiplex, including multiple mononeuropathies in atypical locations, such as the brachial plexus Borderline leprosy is associated with clinical and histological features of both the lepromatous and the tuberculoid forms of leprosy (Table 15 2, Fig 15 3) There is partial impairment in cellular immunity in patients with borderline leprosy such that there is some degree of mycobacterial spread as well as an in ammatory response The immunological state is considered unstable in patients with borderline leprosy in that the immune response and clinical manifestations can shift up and down the spectrum Patients with leprosy may present with isolated peripheral neuropathy without skin lesions, particularly in endemic areas5,6 Most cases of the so-called pure neuritic leprosy have the tuberculoid or borderline tuberculoid subtypes of the disease
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