Manoj Saluja, P. Sen, Prasad Balachandran, D. Pillai, Saurabh Chittora, Komal Saluja
{"title":"Hypomagnesaemia: The esoteric foe in diabetes and diabetic peripheral neuropathy","authors":"Manoj Saluja, P. Sen, Prasad Balachandran, D. Pillai, Saurabh Chittora, Komal Saluja","doi":"10.4103/cmrp.cmrp_71_22","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":72736,"journal":{"name":"Current medicine research and practice","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current medicine research and practice","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4103/cmrp.cmrp_71_22","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
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.