Hoffman-Snyder Charlene, Smith Benn E, Ross Mark A, Hernandez Jose, Bosch E Peter
Department of Neurology, Mayo Clinic Scottsdale, 13400 E. Shea Boulevard, Scottsdale, AZ 85259, USA.
Arch Neurol. 2006 Aug;63(8):1075-9. doi: 10.1001/archneur.63.8.noc50336. Epub 2006 Jun 12.
An underlying cause is found in only 7% to 30% of patients with chronic idiopathic axonal polyneuropathy (CIAP). Diabetes mellitus, inherited disorders, toxin exposure, and primary amyloidosis are the most common identified causes of sensory neuropathies affecting both large and small myelinated fibers. Undiagnosed impaired fasting glucose metabolism has been associated with CIAP at a higher frequency rate than in the general population. This increased prevalence rate was identified using the 2-hour oral glucose tolerance test (2h-OGTT) and a previous version of the American Diabetes Association (ADA) guidelines.
To determine the prevalence of abnormal fasting glucose metabolism in patients with CIAP and to compare the value of determining fasting plasma glucose levels using revised (2003) ADA criteria with the 2h-OGTT for predicting abnormal fasting glucose metabolism.
In this 24-month retrospective study, 100 consecutive patients were identified with no known cause for CIAP, including diabetes mellitus, between January 2003 and January 2005. All had both a fasting plasma glucose test and a 2h-OGTT in addition to a complete neurological examination. Neurophysiological studies, computer-assisted sensory examination, and quantitative sudomotor axonal reflex testing were used to classify CIAP into subtypes according to nerve fiber involvement.
The prevalence of undiagnosed abnormal fasting glucose metabolism was found to be nearly 2-fold higher (62%) in patients with CIAP than in similar age-matched general population groups (33%). Using the 2003 revised ADA criteria, 39 patients (39%) had abnormal fasting plasma glucose metabolism (36 with impaired fasting glucose, 3 with diabetes mellitus), while the 2h-OGTT provided an even higher diagnostic rate of 62% (62 patients; P<.001) of impaired fasting glucose metabolism (38 with impaired glucose tolerance, 24 with diabetes mellitus). The abnormal glucose metabolism rates were found to be similar across the 3 subtypes (sensorimotor, pure sensory, and small-fiber neuropathy) of CIAP (P = .60, .72, and .61).
This study adds to emerging evidence that abnormal glucose metabolism may be a risk factor for CIAP. Even with revised (2003) ADA criteria, the 2h-OGTT provides additional diagnostic information to the health care professional in the evaluation of CIAP. Subtypes of CIAP are equally likely to have abnormal glucose metabolism.
在慢性特发性轴索性多神经病（CIAP）患者中，仅7%至30%能找到潜在病因。糖尿病、遗传性疾病、毒素暴露及原发性淀粉样变性是影响大小有髓纤维的感觉神经病最常见的已确定病因。与普通人群相比，未诊断出的空腹血糖代谢受损与CIAP的关联频率更高。这一较高的患病率是通过2小时口服葡萄糖耐量试验（2h - OGTT）及美国糖尿病协会（ADA）先前版本的指南确定的。
确定CIAP患者中空腹血糖代谢异常的患病率，并比较使用修订后的（2003年）ADA标准测定空腹血糖水平与2h - OGTT在预测空腹血糖代谢异常方面的价值。
在这项为期24个月的回顾性研究中纳入了2003年1月至2005年1月期间连续100例无CIAP已知病因（包括糖尿病）的患者。除了进行全面的神经系统检查外，所有患者均接受了空腹血糖检测和2h - OGTT。神经生理学研究、计算机辅助感觉检查及定量汗腺轴突反射测试用于根据神经纤维受累情况将CIAP分为不同亚型。
发现CIAP患者中未诊断出的空腹血糖代谢异常患病率（62%）几乎是年龄匹配的普通人群组（33%）的2倍。使用2003年修订的ADA标准，39例患者（39%）存在空腹血糖代谢异常（36例空腹血糖受损，3例患有糖尿病），而2h - OGTT对空腹血糖代谢受损的诊断率更高，为62%（62例患者；P <.001）（38例糖耐量受损，24例患有糖尿病）。在CIAP的3种亚型（感觉运动型、纯感觉型和小纤维神经病型）中，异常糖代谢率相似（P =.60、.72和.61）。
本研究进一步证明异常糖代谢可能是CIAP的一个危险因素。即使采用修订后的（2003年）ADA标准，2h - OGTT在CIAP评估中也能为医护人员提供额外的诊断信息。CIAP的各亚型出现糖代谢异常的可能性相同。
