Gutmann L, Martin J D, Welton W
Neurology. 1976 Jun;26(6 PT 1):514-6. doi: 10.1212/wnl.26.6.514.
Dapsone produces a potentially reversible toxic neuropathy, with its primary effect on the soma and axons of motor neurons as opposed to myelin. There is very little evidence to suggest involvement of sensory axons in most cases; if present, it would appear minimal. A "dying back" of motor axons is postulated to produce the clinical features of primarily distal weakness and wasting. Recovery appears to occur via axon regeneration and peripheral sprouting. The sporadic occurrence of this neuropathy may be due to slow acetylation of dapsone in some patients.
氨苯砜可导致一种潜在可逆的中毒性神经病，其主要作用于运动神经元的胞体和轴突，而非髓鞘。在大多数情况下，几乎没有证据表明感觉轴突受累；若有感觉轴突受累，其程度似乎也很轻微。推测运动轴突的“逆行性死亡”会导致主要为远端肌无力和消瘦的临床特征。恢复似乎是通过轴突再生和周围神经芽生实现的。这种神经病的散发性发生可能是由于一些患者体内氨苯砜的乙酰化缓慢所致。
