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1 nt antioxidant that is used in patients with diabetic polyneuropathy.
2  a significant beneficial effect of rhNGF on diabetic polyneuropathy.
3  have been implicated in the pathogenesis of diabetic polyneuropathy.
4 ar endothelial growth factor (VEGF) to treat diabetic polyneuropathy.
5 CI: 1, 3); multiple sclerosis, 2 (CI: 2, 3); diabetic polyneuropathy, 2 (CI: 1, 3); compressive monon
6 CI: 183, 230); shingles, 140 (CI: 104, 184); diabetic polyneuropathy, 54 (CI: 33, 83); compressive ne
7 n-derived NGF influences the presentation of diabetic polyneuropathy, although metabolic or vascular
8 tin receptor deficient mouse (dbdb) model of diabetic polyneuropathy and 2) superoxide dismutase 1 kn
9 fied sensory and autonomic function in early diabetic polyneuropathy and correlated changes with leve
10 to minimizing the prevalence and severity of diabetic polyneuropathy and makes research into the dele
11 rmacologic therapies for neuropathic pain in diabetic polyneuropathy appear promising.
12  diagnosis of and differential diagnosis for diabetic polyneuropathy are reviewed herein.
13 d-stage kidney disease prevents worsening of diabetic polyneuropathy, but neuropathic improvement is
14 ts the progression and improves the signs of diabetic polyneuropathy by restoration of a normoglycemi
15 ntify alterations of nerve microstructure in diabetic polyneuropathy (DPN) by magnetic resonance (MR)
16 of the metabolic syndrome that contribute to diabetic polyneuropathy (DPN) in type 2 diabetes mellitu
17                                  Large-fiber diabetic polyneuropathy (DPN) leads to balance and gait
18 omote nerve regeneration, early diagnosis of diabetic polyneuropathy, followed by tight glycemic cont
19 e should be useful as a measure of change in diabetic polyneuropathy for purposes of medical practice
20 nomena are major expressions of varieties of diabetic polyneuropathies needing improved assessments f
21            In general, treatment options for diabetic polyneuropathy remain primarily symptomatic.
22  an important measure of overall severity of diabetic polyneuropathy, taking into account both sympto
23 e by which to diagnose and grade severity of diabetic polyneuropathy than does the use of individual
24 erstanding of chronic symmetric sensorimotor diabetic polyneuropathy, the most common and problematic
25                      To estimate severity of diabetic polyneuropathy, the results of the neurological
26 s may address some of the challenges of past diabetic polyneuropathy trials.
27 le to adequately characterize and quantitate diabetic polyneuropathies using only one or two clinical

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