营养不良诱发的以反复晕厥肌无力为表现的糖尿病多发神经病变1例并文献复习
A Case of Diabetic Multiple Neuropathy Induced by Malnutrition Manifested by Recurrent Syncope Muscle Weakness and Literature Review
DOI: 10.12677/ACM.2024.143748, PDF,   
作者: 刘 震:青岛大学医学部,山东 青岛;邓玉杰, 赵宇航, 李成乾*:青岛大学附属医院内分泌与代谢性疾病科,山东 青岛
关键词: 糖尿病神经病变直立性低血压营养不良低碳水饮食Diabetic Neuropathy Orthostatic Hypotension Malnutrition Low-Carbon Diet
摘要: 糖尿病神经病变(Diabetic Neuropathy)是糖尿病最常见的慢性并发症,常见周围神经及自主神经受累,其中自主神经病变因其临床表现的隐匿和多样化而容易被忽略。糖尿病心血管自主神经病变是糖尿病神经病变中最严重的一种,被认为是糖尿病心血管疾病相关死亡的强独立预测因子,但因其临床表现的多样性及隐匿性常常不易引起重视,且缺乏满意的临床治疗效果,从而显著增加了糖尿病患者死亡率。对于糖尿病自主神经病变的诱发因素及治疗管理策略目前没有统一的定论,本文通过介绍分析1例以反复体位性晕厥、肌无力为表现的糖尿病多发神经病变患者的诊疗过程,结合其饮食结构、营养状况及研究进展对该类疾病发病机制、危险因素及治疗管理进行探讨,旨在提高临床医师对特殊临床表现类型的糖尿病神经病变及其危险因素的认识和临床治疗管理能力。
Abstract: Diabetic neuropathy is the most common chronic complication of diabetes, involving peripheral nerves and autonomic nerves, among which autonomic neuropathy is easily ignored due to its in-sidious and diverse clinical manifestations. Diabetic cardiovascular autonomic neuropathy is the most serious type of diabetic neuropathy and is considered to be a strong independent predictor of diabetic cardiovascular disease-related mortality, but it is often not easy to pay attention to due to the diversity and insidiousness of its clinical manifestations, and lacks satisfactory clinical treat-ment effects, which significantly increases the mortality rate of diabetic patients. This article intro-duces and analyzes the diagnosis and treatment process of a patient with diabetic polyneuropathy manifested by recurrent orthostatic syncope and muscle weakness, and discusses the pathogenesis, risk factors and treatment management of this type of disease based on his dietary structure, nutri-tional status and research progress, aiming to improve clinicians’ understanding of special clinical manifestations of diabetic neuropathy and its risk factors, as well as the clinical treatment and management ability.
文章引用:刘震, 邓玉杰, 赵宇航, 李成乾. 营养不良诱发的以反复晕厥肌无力为表现的糖尿病多发神经病变1例并文献复习[J]. 临床医学进展, 2024, 14(3): 624-631. https://doi.org/10.12677/ACM.2024.143748

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