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自身免疫与糖尿病性神经病变

Autoimmunity and diabetic neuropathy.

作者信息

Canal N, Nemni R

机构信息

Dept. of Neurology, Scientific Institute S. Raffaele, Milan, Italy.

出版信息

Clin Neurosci. 1997;4(6):371-3.

PMID:9358982
Abstract

Autoimmunity has been implicated in the pathogenesis of diabetic neuropathy. A number of putative target antigens have been investigated in the attempt to find a relationship between the presence of autoantibodies and the presence of neuropathy. Attention has been given to antibodies against nerve growth factor, adrenal medulla, sympathetic and parasympathetic structures, glutamic acid decarboxylase and phospholipids. Data in the literature do not support a clear-cut difference in frequency of positivity or titres between patients with or without diabetic neuropathy. Moreover, it is not clear whether autoantibodies to the above-mentioned antigens, whenever present, play a role in causing nerve damage or if they simply reflect the presence of nerve damage. Longitudinal studies are needed to clarify some conflicting data in the literature.

摘要

自身免疫已被认为与糖尿病性神经病变的发病机制有关。为了找出自身抗体的存在与神经病变的存在之间的关系,人们对许多假定的靶抗原进行了研究。针对神经生长因子、肾上腺髓质、交感和副交感神经结构、谷氨酸脱羧酶和磷脂的抗体已受到关注。文献中的数据并不支持糖尿病神经病变患者与无糖尿病神经病变患者在阳性频率或滴度上存在明显差异。此外,尚不清楚针对上述抗原的自身抗体,无论何时出现,是在导致神经损伤中起作用,还是仅仅反映了神经损伤的存在。需要进行纵向研究以澄清文献中一些相互矛盾的数据。

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