A Controlled Study of Medial Arterial Calcification of Legs

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Abstract
Neuropathies associated with diabetes mellitus (DM) are of several varieties and caused by different underlying mechanisms.1,2 Large artery and microvessel alterations are more prevalent in patients with DM than in healthy subjects (HS) and may be involved in the pathogenesis of some diabetic neuropathies.3-5 Early reports suggested that peripheral arterial disease (PAD) caused infarctions in nerves.6 However, these so-called infarctions were later recognized as Renaut bodies, structures described earlier and known to occur in normal nerves without causing fiber degeneration.7-9 It has been increasingly recognized that PAD is not a precursor condition of distal, length-dependent sensorimotor polyneuropathy (DSPN) in most patients with DM. It might play a role in late progression of this polyneuropathy, and we consider that issue here. Distal, length-dependent sensorimotor polyneuropathy, the most common variety of diabetic neuropathies, develops on a background of long-standing hyperglycemia, associated metabolic derangements (increased polyol flux, accumulation of advanced glycation end products, oxidative stress, and altered metabolism of lipids, among others2,10-14), and microvessel alterations.2,15,16 It has been suggested that PAD may influence the expression and severity of diabetic polyneuropathies, perhaps late in its course.5 It is possible and perhaps even likely that severe symptomatic PAD can worsen DSPN by causing ischemic damage of nerves. It is known that ischemic gangrene causes distal infarction of all tissues, including that of peripheral nerves.17

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