Souayah Nizar, Chen Hongxin, Chong Zhao Zhong, Patel Tejas, Pahwa Ankit, Menkes Daniel L, Cunningham Timothy
New Jersey Medical School, 90 Bergen Street DOC 8100, Newark, NJ, 07101, USA.
SMR Consulting, 407 Elmwood Avenue, Sharon Hill, PA, 19079, USA.
Heliyon. 2024 Apr 26;10(9):e30419. doi: 10.1016/j.heliyon.2024.e30419. eCollection 2024 May 15.
To develop a novel strategy for identifying acquired demyelination in diabetic distal symmetrical polyneuropathy (DSP).
Motor nerve conduction velocity (CV) slowing in diabetic DSP exceeds expectations for pure axonal loss thus implicating superimposed acquired demyelination.
After establishing demyelination confidence intervals by regression analysis of nerve conduction data from chronic inflammatory demyelinating polyneuropathy (CIDP), we prospectively studied CV slowing in 90 diabetic DSP patients with and without at least one motor nerve exhibiting CV slowing (groups A and B) into the demyelination range by American Academy of Neurology (AAN) criteria respectively and 95 amyotrophic lateral sclerosis (ALS) patients. Simultaneously, secretory phospholipase A2 (sPLA2) activity was assessed in both diabetic groups and 46 healthy controls.
No ALS patient exhibited CV slowing in more than two motor nerves based on AAN criteria or the confidence intervals. Group A demonstrated a significantly higher percentage of patients as compared to group B fulfilling the above criteria, with an additional criterion of at least one motor nerve exhibiting CV slowing in the demyelinating range and a corresponding F response in the demyelinating range by AAN criteria (70.3 % 1.9 %; p < 0.0001). Urine sPLA2 activity was increased significantly in diabetic groups as compared to healthy controls (942.9 ± 978.0 591.6 ± 390.2 pmol/min/ml, p < 0.05), and in group A compared to Group B (1328.3 ± 1274.2 673.8 ± 576.9 pmol/min/ml, p < 0.01). More patients with elevated sPLA2 activity and more than 2 motor nerves with CV slowing in the AAN or the confidence intervals were identified in group A as compared to group B (35.1 % 5.7 %, p < 0.001). Furthermore, 13.5 % of patients in diabetic DSP Group A, and no patients in diabetic DSP Group B, fulfilled an additional criterion of more than one motor nerve with CV slowing into the demyelinating range with its corresponding F response into the demyelinating range by AAN criteria.
A combination of regression analysis of electrodiagnostic data and a urine biological marker of systemic inflammation identifies a subgroup of diabetic DSP with superimposed acquired demyelination that may respond favorably to immunomodulatory therapy.
制定一种识别糖尿病性远端对称性多发性神经病（DSP）中获得性脱髓鞘的新策略。
糖尿病性DSP中运动神经传导速度（CV）减慢超出了单纯轴突损失的预期，因此提示存在叠加的获得性脱髓鞘。
通过对慢性炎症性脱髓鞘性多发性神经病（CIDP）的神经传导数据进行回归分析建立脱髓鞘置信区间后，我们前瞻性研究了90例糖尿病性DSP患者（有和没有至少一条运动神经CV减慢，分别为A组和B组），根据美国神经病学学会（AAN）标准，其CV减慢进入脱髓鞘范围，以及95例肌萎缩侧索硬化（ALS）患者。同时，在两个糖尿病组和46名健康对照中评估分泌型磷脂酶A2（sPLA2）活性。
根据AAN标准或置信区间，没有ALS患者表现出超过两条运动神经的CV减慢。与B组相比，A组符合上述标准的患者百分比显著更高，还有一个额外标准，即至少一条运动神经的CV减慢进入脱髓鞘范围且AAN标准下相应的F波反应也在脱髓鞘范围内（70.3%±1.9%；p<0.0001）。与健康对照相比，糖尿病组尿sPLA2活性显著升高（942.9±978.0对591.6±390.2pmol/min/ml，p<0.05），A组与B组相比也是如此（1328.3±1274.2对673.8±576.9pmol/min/ml，p<0.01）。与B组相比，A组中sPLA2活性升高且超过两条运动神经CV减慢在AAN标准或置信区间内的患者更多（35.1%对5.7%，p<0.001）。此外，糖尿病性DSP A组中13.5%的患者符合另一个额外标准，即超过一条运动神经的CV减慢进入脱髓鞘范围且其相应的F波反应也在AAN标准下的脱髓鞘范围内，而糖尿病性DSP B组中没有患者符合该标准。
电诊断数据的回归分析与全身炎症的尿生物标志物相结合，可识别出伴有叠加获得性脱髓鞘的糖尿病性DSP亚组，该亚组可能对免疫调节治疗有良好反应。
