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  Vol. 289 No. 14, April 9, 2003 TABLE OF CONTENTS
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Animal Models of Human Diabetic Polyneuropathy—Reply

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

In Reply: In response to Drs Crawford and Hardwicke, the etiology of diabetic peripheral polyneuropathy is complex and hyperglycemia may not cause all the pathologic features in all forms of the disease.1-2 However, a great deal of clinical evidence supports hyperglycemia as being a major independent risk factor for diabetic polyneuropathy and glycemic control is a key element in its treatment.3-4 Since patients with both type 1 and 2 diabetes may experience peripheral polyneuropathy, it is unlikely that autoimmune mechanisms play a major role.

We agree that animal models of diabetes may not mimic all neuronal and vascular pathologies of diabetic polyneuropathy since many differences such as age, duration of disease, body size, and others exist between patients with diabetes and animal models of diabetes. We also agree that NGF may not have a critical pathogenic role. Nonetheless, it is likely that abnormalities of nerve trophic factors contribute significantly to . . . [Full Text of this Article]



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RELATED ARTICLE

Animal Models of Human Diabetic Polyneuropathy
Colin L. Crawford and Peter Hardwicke
JAMA. 2003;289(14):1779-1780.
EXTRACT | FULL TEXT  


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