低镁血症:糖尿病和糖尿病周围神经病变的深奥敌人

Manoj Saluja, P. Sen, Prasad Balachandran, D. Pillai, Saurabh Chittora, Komal Saluja
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摘要

背景:糖尿病是印度发病率的主要原因之一,糖尿病性神经病变是其主要并发症,导致生活质量下降。除慢性高血糖外,胰岛素抵抗和神经元损伤的非血糖病理生理是开发诸如纠正血清镁等新型糖尿病管理策略的关键。目的:我们旨在分析低镁血症及其与糖尿病和糖尿病周围神经病变的关系。材料和方法:我们在Kota GMC进行了一项横断面研究,收集了一年(2019-2020)的数据。血清镁与HbA1C、血清镁与神经传导参数Pearson相关。根据有无神经病变分类的患者,使用未配对t检验比较各种生化参数,并进行Welch校正。结果:Pearson相关性显示低镁血症与高血糖(HbA1c)呈负相关(r = -0.5568;P < 0.001),与神经病变无关。低镁血症与DPN有显著相关性,低血镁与神经振幅(所有被测神经)和传导速度(感觉神经)呈正相关。在我们的研究中,DPN的模式主要是感觉运动轴索多发性神经病。感觉神经有轴突和脱髓鞘混合病变。血清镁浓度对周围神经潜伏期无影响。伴有神经病变的T2DM患者血清镁含量明显低于无DPN患者,HbA1C和血清肌酐含量明显高于无DPN患者。结论:除控制高血糖外,非血糖矫正也需要控制糖尿病并发症。血清镁及其与疾病严重程度、轴突和脱髓鞘神经元损伤的相关性为这种策略提供了有趣的见解。需要进一步的研究来确定补充镁的可能作用及其对2型糖尿病的益处。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hypomagnesaemia: The esoteric foe in diabetes and diabetic peripheral neuropathy
Background: Diabetes is one of the leading causes of morbidity in India, and diabetic neuropathy is its major complication causing a reduced quality of life. Besides chronic hyperglycaemia, non-glycaemic pathophysiology of insulin resistance and neuronal damage are key to developing novel diabetes management strategies like correcting serum magnesium. Aims: We aimed to analyse hypomagnesemia and its correlation with diabetes and diabetic peripheral neuropathy. Materials and Methods: We conducted a cross sectional study, collecting data for a year (2019-2020) in GMC, Kota. Pearson correlation was performed between serum Magnesium and HbA1C, as well as serum magnesium and nerve conduction parameters. Patients classified based on the absence or presence of neuropathy were compared for various biochemical parameters using Unpaired t-tests, with Welch's correction. Results: Pearson correlation indicates an inverse relationship between hypomagnesemia and hyperglycaemia (HbA1c) (r = -0.5568; P < 0.001), irrespective of neuropathy. Hypomagnesemia has a significant correlation with DPN, such that low serum magnesium has a positive correlation with nerve amplitude (in all the tested nerves) and conduction velocity (in sensory nerves). The pattern of DPN in our study was predominantly sensorimotor axonal polyneuropathy. Mixed axonal and demyelinating neuropathy was seen in sensory nerves. Latency was not affected by serum magnesium concentration in any peripheral nerve tested. T2DM patients with neuropathy had significantly lower serum magnesium, higher HbA1C and serum creatinine than in patients without DPN. Conclusions: Apart from controlling hyperglycaemia, non-glycaemic corrections are also needed to manage the diabetic complications. Serum magnesium and its correlation with disease severity, axonal and demyelinating neuronal injury provides an interesting insight into one such strategy. Further studies are needed to establish the probable role of magnesium supplementation and its benefits in T2DM.
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