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To the Editor: Drs Sheetz and King¹ stated that "[a]nimal models of diabetes support the importance of hyperglycemia as a causative factor in diabetic neuropathy. . . . " However, models in which the animal is made hyperglycemic do not reproduce the essential neuropathologic features of human diabetic neuropathy, especially the loss of unmyelinated C fibers.² It is damage to fibers mediating pain that is responsible for trophic ulcers, damage to metatarsal heads, and Charcot joints.

In an autoimmune model designed to reproduce acute sensory loss occurring in human leprosy,³ there was a selective diminution in the amplitude of the slower component of C fibers, but A fibers were unaffected.⁴ If the lack of a neurotrophic factor is involved in the pathogenesis of diabetic neuropathy, it is unlikely to be nerve growth factor (NGF), because when antibodies to NGF are injected into newborn rats there is a specific loss of . . . [Full Text of this Article]

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