Khan Zarghuna, Habib Syed H, Al-Khlaiwi Thamir, Baseer Najma, Khalifa Mohammed M, Habib Syed S
Department of Physiology, Institute of Basic Medical Sciences, Khyber Medical University, Peshawar, Pakistan.
Department of Physiology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
J Family Med Prim Care. 2025 Jun;14(6):2358-2364. doi: 10.4103/jfmpc.jfmpc_1739_24. Epub 2025 Jun 30.
Data on the role of anti- and proinflammatory markers in diabetes and prediabetes and their associations with diabetic neuropathy are limited. Therefore, the aim of this study was to determine and compare the associations of inflammatory markers and nerve function with blood glucose levels among diabetic patients and prediabetic patients.
This was a cross-sectional study consisting of 80 participants (40 diabetic patients and 40 prediabetic patients). The assessment involved a detailed history and neurological examination, including neuropathy symptom scoring (NSS) and the neuropathy deficit score (NDS), to grade neuropathy if present. Baseline investigations were performed, and HbA1c values were assessed in all the subjects. Serum TNFα and IL-10 levels were measured via enzyme-linked immunosorbent assay (ELISA). Nerve function was evaluated through a nerve conduction study. The data were subjected to an independent sample test.
The results revealed a significant increase in the concentrations of IL-10 ( = 0.016) and TNFα ( < 0.001) in diabetic patients compared with prediabetic patients. Nerve conduction velocity in the sural nerve (right side, = 0.019; left side, = 0.001) and ulnar nerve (right side, = 0.007; left side, = 0.005) was also lower in both limbs of diabetic patients than in those of prediabetic patients. Latency was greater in diabetic patients than in prediabetic patients.
The inflammatory markers TNF-α and IL-10 were significantly elevated in patients with diabetes compared with those with prediabetes, and these markers might contribute to neuropathy in patients with diabetes. However, no associations were found between inflammatory markers and nerve function.
关于抗炎和促炎标志物在糖尿病及糖尿病前期中的作用及其与糖尿病神经病变的关联的数据有限。因此，本研究的目的是确定并比较糖尿病患者和糖尿病前期患者中炎症标志物及神经功能与血糖水平的关联。
这是一项横断面研究，包括80名参与者（40名糖尿病患者和40名糖尿病前期患者）。评估包括详细的病史和神经系统检查，包括神经病变症状评分（NSS）和神经病变缺损评分（NDS），以对存在的神经病变进行分级。进行了基线调查，并评估了所有受试者的糖化血红蛋白值。通过酶联免疫吸附测定（ELISA）测量血清肿瘤坏死因子α（TNFα）和白细胞介素10（IL-10）水平。通过神经传导研究评估神经功能。数据进行独立样本检验。
结果显示，与糖尿病前期患者相比，糖尿病患者的IL-10浓度显著升高（P = 0.016），TNFα浓度显著升高（P < 0.001）。糖尿病患者双侧腓肠神经（右侧，P = 0.019；左侧，P = 0.001）和尺神经（右侧，P = 0.007；左侧，P = 0.005）的神经传导速度也低于糖尿病前期患者。糖尿病患者的潜伏期比糖尿病前期患者更长。
与糖尿病前期患者相比，糖尿病患者的炎症标志物TNF-α和IL-10显著升高，这些标志物可能导致糖尿病患者发生神经病变。然而，未发现炎症标志物与神经功能之间存在关联。
