A Cross-Sectional Study to Evaluate Serum Magnesium Level in Acute Exacerbation of Chronic Obstructive Pulmonary Disease Patients at a Tertiary-Care Centre in North India

Dr Hemakaran Meena et al. A Cross-Sectional Study to Evaluate Serum Magnesium Level in Acute Exacerbation of Chronic Obstructive Pulmonary Disease Patients at a Tertiary-Care Centre in North India. Int. J Med. Pharm. Res., 6 (6): 535‐540, 2025 535 International Journal of Medical and Pharmaceutical Research Online ISSN-2958-3683 | Print ISSN-2958-3675 Frequency: Bi-Monthly Available online on: https://ijmpr.in/ Original Article A Cross-Sectional Study to Evaluate Serum Magnesium Level in Acute Exacerbation of Chronic Obstructive Pulmonary Disease Patients at a Tertiary-Care Centre in North India Dr Hemakaran Meena1, Dr Mahendra Kumar Bainara2, Dr Jitendra Kumar Sharma3 1 Junior Resident, Department of Respiratory Medicine, Institute of Respiratory Disease, SMS Medical College, Jaipur 2 Senior Professor, Department of Respiratory Medicine, Institute of Respiratory Disease, SMS Medical College, Jaipur 3 Assistant Professor, Institute of Respiratory Diseases, SMS Medical College, Jaipur A B S T R A C T Corresponding Author: Dr Jitendra Kumar Sharma Assistant Professor, Institute of Respiratory Diseases, SMS Medical College, Jaipur. Received: 15-10-2025 Accepted: 13-11-2025 Available online: 18-11-2025 Background: Chronic obstructive pulmonary disease (COPD) is a major global cause of morbidity and mortality, with acute exacerbations representing critical events that accelerate lung-function decline and raise healthcare burden. Magnesium (Mg²⁺) regulates bronchial smooth-muscle tone, neuromuscular transmission, and inflammation. Hypomagnesaemia has been proposed as a modifiable biochemical factor influencing the severity and outcome of COPD exacerbations. This study evaluated the prevalence of hypomagnesaemia and its association with disease severity and hospital outcomes in patients presenting with acute exacerbation of COPD (AECOPD) at a tertiary-care centre in North India. Methods: A hospital-based cross-sectional study enrolled 50 consecutive patients ≥40 years with spirometry-confirmed COPD presenting in acute exacerbation. Serum magnesium was measured on admission. Demographic, clinical, radiological, and biochemical data were analysed. Associations between magnesium status and duration of stay, outcome, and GOLD severity were tested using chi-square and t tests. Results: Mean age was 61 ± 9 years; 60 % were male. Hypomagnesaemia (< 1.7 mg dL⁻¹) occurred in 58 % (n = 29). Patients with low magnesium had significantly longer hospital stays > 7 days (79.3 % vs 42.9 %, p = 0.018) and a higher, though not statistically significant, mortality (10.3 % vs 4.8 %). The prevalence of hypomagnesaemia rose progressively with GOLD stage (15 % in mild → 87 % in very severe). Conclusion: Hypomagnesaemia is common in AECOPD and correlates with increasing airflow limitation and prolonged hospitalisation. Routine magnesium monitoring at admission may help identify high-risk patients and guide early supplementation trials. Copyright © International Journal of Medical and Pharmaceutical Research Keywords: COPD, acute exacerbation, serum magnesium, hypomagnesaemia, prognosis, bronchodilation. INTRODUCTION Chronic obstructive pulmonary disease (COPD) is a heterogenous condition characterised by persistent respiratory symptoms and airflow limitation arising from airway and/or alveolar abnormalities (GOLD 2025 update [1]). It ranks among the top three global causes of death, accounting for 3.7 million fatalities annually, and its burden continues to rise in lowand middle-income countries [2, 3]. In India, pooled spirometry-based community surveys estimate COPD prevalence between 7 and 8 % among adults ≥ 30 years [4], with substantial interstate heterogeneity. Dr Hemakaran Meena et al. A Cross-Sectional Study to Evaluate Serum Magnesium Level in Acute Exacerbation of Chronic Obstructive Pulmonary Disease Patients at a Tertiary-Care Centre in North India. Int. J Med. Pharm. Res., 6 (6): 535‐540, 2025 536 Acute exacerbations—episodes of worsening dyspnoea, cough, and sputum within ≤ 14 days—represent the most dynamic phase of the disease, often precipitated by infection or air-pollution surges [5]. Each hospitalised exacerbation accelerates FEV₁ decline by 20–30 mL per year and increases one-year mortality by 30–40 % [6]. During these episodes, multiple metabolic factors amplify the respiratory burden: increased muscle work, corticosteroidinduced renal losses, β₂-agonist therapy, and reduced dietary intake all deplete magnesium stores [7, 8]. Magnesium is the second-most abundant intracellular cation and a cofactor in over 300 enzymatic reactions that regulate energy metabolism, calcium transport, and cell signalling [9]. Within the respiratory system, Mg²⁺ mediates bronchodilation via antagonism of calcium-dependent airway-smooth-muscle contraction, inhibits acetylcholine release at vagal terminals, stabilises mast cells, and supports diaphragmatic contractility [10, 11]. Clinical evidence linking magnesium to obstructive airway disease has grown steadily. Early studies demonstrated that hypomagnesaemia accompanies acute exacerbations and correlates with airflow limitation [12–14]. Prospective cohorts in India reported hypomagnesaemia in 40–70 % of hospitalised AECOPD cases, with significant associations with disease severity and readmission [15–17]. A Cochrane Review (2022) showed that intravenous magnesium sulphate modestly reduces emergency-department admissions and shortens length of stay [18], and a 2025 meta-analysis reaffirmed its safety and rapid bronchodilatory effect [19]. Large-scale epidemiological data from the U.S. NHANES (2005–2018) further link low magnesium or high magnesium-depletion scores to increased COPD prevalence and systemic inflammation [20, 21]. Despite such biological plausibility, Indian data remain sparse and heterogeneous. Most studies are single-centre, employ differing cut-offs for magnesium deficiency, and rarely incorporate spirometric staging or outcome analyses. The present cross-sectional study was therefore undertaken to estimate the prevalence of hypomagnesaemia among patients admitted with AECOPD in North India and to correlate magnesium levels with disease severity and short-term clinical outcomes. MATERIALS AND METHODS Study design and setting A hospital-based, observational cross-sectional study was conducted at a tertiary-care centre in North India over one year. Ethical approval was obtained from the institutional review board, and written informed consent was secured from all participants. Participants Fifty consecutive adults (≥ 40 years) with spirometry-confirmed COPD presenting in acute exacerbation (AECOPD) were included. Exclusion criteria comprised need for immediate invasive ventilation, major comorbidities likely to alter serum magnesium (e.g., myocardial infarction, stroke, renal failure), and use of drugs affecting magnesium metabolism (e.g., digoxin, aminoglycosides, loop diuretics). Definitions • COPD/AECOPD: Diagnosed according to GOLD 2025 criteria [1]. • Hypomagnesaemia: Serum Mg < 1.7 mg dL⁻¹ (institutional reference range). • Outcome variables: Duration of hospital stay (≤ 7 days vs > 7 days) and discharge or death. Data collection A structured case-record form captured demographic profile, smoking history, symptoms, physical findings, radiographic pattern, arterial blood gases (as available), and serum magnesium at admission. Chest X-rays were read by two respiratory physicians blinded to magnesium status. Statistical analysis Data were analysed using standard statistical software. Continuous variables were expressed as mean ± SD; categorical variables as frequencies (%). Group comparisons employed Student’s t or Mann–Whitney U tests for continuous data and Chi-square or Fisher’s exact tests for categorical variables. Correlations were explored using Spearman’s ρ. A two-tailed p ≤ 0.05 was deemed significant. RESULTS Age distribution Most patients (34 %) were aged 60–69 years, followed by 26 % in 50–59 years. COPD exacerbations thus clustered in older adults (Table 1) Table 1. Age distribution of AECOPD patients Age group N % Dr Hemakaran Meena et al. A Cross-Sectional Study to Evaluate Serum Magnesium Level in Acute Exacerbation of Chronic Obstructive Pulmonary Disease Patients at a Tertiary-Care Centre in North India. Int. J Med. Pharm. Res., 6 (6): 535‐540, 2025 537 40-49 11 22 50-59 13 26 60-69 17 34 ≥ 70 9 18 Total 50 100 Sex distribution Males constituted 60 % (n = 30) and females 40 % (n = 20) (Table 2) Table 2. Sex distribution Sex N % Male 30 60 Female 20 40 Figure 2. Sex distribution of AECOPD cases. Place of residence Urban residents outnumbered rural (60 % vs 40 %), reflecting the hospital’s catchment (Table 3). Table 3. Residence distribution Residence N % Urban 30 60 Rural 20 40 Figure 3. Urban-rural distribution of participants. Smoking status Fifty-eight percent were ex-smokers, 32 % current smokers, and 10 % never-smokers (Table 4). Table 4. Smoking status Status N % Ex-smoker 29 58 Current smoker 16 32 Never smoker 5 10 Figure 4. Smoking status among AECOPD patients. Symptom profile All patients (100 %) presented with breathlessness; cough occurred in 70 %, expectoration 50 %, wheeze 36 %, and fever 30 % (Table 5). Table 5. Symptom distribution Symptom N % Breathlessness 50 100% Cough 35 70 Expectoration 25 50 Wheeze 18 36 Fever 15 30 Figure 5. Clinical symptom frequencies. Radiological findings Emphysema was the predominant radiographic feature (28 %), followed by hyperinflation (22 %) and consolidation (20 %) (Table 6). Table 6. Chest-X-ray finding Figure 6. Common radiological findings in AECOPD. Findings N % Emphysema 14 28 Hyperinflatedlung 11 22 Consolidation 10 20 Infiltrates 9 18 Cardiomegaly 6 12 Dr Hemakaran Meena et al. A Cross-Sectional Study to Evaluate Serum Magnesium Level in Acute Exacerbation of Chronic Obstructive Pulmonary Disease Patients at a Tertiary-Care Centre in North India. Int. J Med. Pharm. Res., 6 (6): 535‐540, 2025 538 Serum magnesium and hospital stay Hypomagnesaemia was documented in 58 % (n = 29). A significantly larger proportion of these patients required hospitalization > 7 days compared with those with normal Mg (79.3 % vs 42.9 %; p = 0.0187) (Table 7). Table 7. Duration of stay vs serum magnesium level Hospital stay | Hypomagnesaemia (n = 29 Normomagnesaemia (n = 21 Total ≤ 7 days 6 (20.7 %) 12 (57.1 %) 18 > 7 days 23 (79.3 %) 9 (42.9 %) 32 p = 0.0187. Figure 7. Relationship between magnesium status and duration of hospital stay. Outcome Four deaths occurred (8 % overall). Mortality was higher among hypomagnesaemic patients (10.3 %) Table 8. Outcome vs serum magnesium Outcome Hypomagnesemia Normomagnesemia Total Discharged 26(89.7%) 20(95.2%) 46 Deceased 3(10.3%) 1(4.8%) 4 than normomagnesaemic (4.8 %), though the difference was not significant (p = 0.85) (Table 8). Figure 8. Outcome distribution according to magnesium status. COPD severity and magnesium status The frequency of hypomagnesaemia rose steadily with GOLD stage—from 15 % in mild to 87 % in very severe disease (Table 9). Table 9. GOLD severity vs serum magnesium status GOLD Stage N Hypomagnesaemia normomagnesemia I mild 13 2 11 II moderate 17 10 7 III severe 15 13 2 IV very severe 5 4 1 Figure 9. Trend of declining magnesium levels with advancing GOLD stage. Summary of key findings: • Mean age ≈ 61 years; male-to-female ratio 3:2. • Hypomagnesaemia prevalence ≈ 58 %. • Strong correlation between low Mg²⁺ and both advanced airflow limitation and prolonged stay. • Mortality signal higher in low-Mg group, though not statistically significant. DISCUSSION The present study demonstrates that hypomagnesaemia is common (58 %) among hospitalised patients with acute exacerbation of COPD (AECOPD) and that it correlates significantly with both disease severity and prolonged hospital stay. Although mortality was not statistically higher, the consistent downward trend in serum magnesium with advancing GOLD stage underscores magnesium’s potential pathophysiological and prognostic relevance. Age and gender pattern Most admissions clustered between 50 and 69 years—an age band where cumulative inhalational injury, immunosenescence, and declining respiratory-muscle reserve converge to trigger exacerbations [1, 2]. Similar distributions were reported by Makwana et al (2022) [15] and Antin et al (2023) [24]. Male predominance (60 %) reflects persistently higher smoking prevalence among men; however, the 40 % female representation highlights a narrowing gender gap attributed to biomass smoke exposure and passive smoking in domestic settings [25]. Smoking status Dr Hemakaran Meena et al. A Cross-Sectional Study to Evaluate Serum Magnesium Level in Acute Exacerbation of Chronic Obstructive Pulmonary Disease Patients at a Tertiary-Care Centre in North India. Int. J Med. Pharm. Res., 6 (6): 535‐540, 2025 539 Nearly one-third of subjects were active smokers, echoing recent Indian registry data showing 28–35 % continued tobacco use despite prior hospitalisation [26]. Continued smoking accelerates FEV₁ decline and raises exacerbation frequency by intensifying airway and systemic inflammation. Structured cessation counselling with pharmacologic therapy (varenicline, bupropion, or combination NRT) should therefore be embedded into AECOPD care pathways [27]. Clinical presentation and radiology Dyspnoea was universal, while cough and expectoration were less consistent. This variation mirrors seasonal and treatment-related differences reported across Indian tertiary-care series [28]. Radiologically, emphysema and hyperinflation predominated—consistent with the obstructive phenotype—but one-fifth of patients exhibited consolidation, suggesting infectious triggers of exacerbation, also noted by Kshirsagar and Patil (2021) [16]. Serum magnesium and outcomes The central observation was a statistically significant link between hypomagnesaemia and prolonged hospital stay (> 7 days, p = 0.018). This aligns with previous Indian data by Makwana et al (2022) [18] and Kumar et al (2025) [22], both of which identified low admission Mg²⁺ as an independent predictor of longer stay and need for non-invasive ventilation. Similar trends were confirmed internationally by Gumus et al (2014) and in the Cochrane review (Powell et al 2022) [19], where intravenous magnesium shortened mean hospitalisation by ≈ 2.7 days. Hypomagnesaemia’s mechanistic plausibility is well supported: • Bronchial smooth-muscle tone: low Mg²⁺ removes inhibitory control on calcium influx, amplifying constriction [10]. • Neuromuscular performance: Mg-ATP depletion precipitates early respiratory-muscle fatigue [7, 9]. • Inflammatory modulation: deficiency enhances NF-κB activation and cytokine release [11]. Collectively, these pathways explain why even modest serum Mg²⁺ decrements worsen airflow limitation and prolong recovery. Comparison with earlier studies Bhatt et al (2008) [15] first reported magnesium as an independent predictor of readmission frequency; Kshirsagar and Patil (2021) [16] observed hypomagnesaemia in 72 % during exacerbation versus 1 % at stability, confirming its dynamic fall during acute illness. Meta-analyses (Heidari et al 2025 [23]) now consolidate these observations, showing pooled odds 0.45 for hospital admission with IV MgSO₄ and no excess adverse events. Moreover, the NHANES-derived Magnesium Depletion Score (Zhang et al 2024 [21]) revealed a graded association between systemic magnesium deficit and COPD prevalence, emphasising its role beyond acute flares. Clinical implications Routine estimation of serum magnesium at AECOPD admission provides a rapid, low-cost prognostic tool complementing ABG and eosinophil counts. Identifying hypomagnesaemia early allows timely supplementation—either oral (400–600 mg/day elemental Mg) or intravenous (1–2 g MgSO₄ over 20 min in severe bronchospasm)—as supported by controlled trials [17–19]. Correction may shorten stay, improve bronchodilation, and prevent recurrence. From a policy perspective, incorporating serum magnesium measurement into standard COPD admission panels could meaningfully enhance triage and bed-day utilisation in high-volume government hospitals. Limitations The study’s single-centre design and modest sample size limit generalisability. Magnesium intake, diuretic exposure, and follow-up readmissions were not recorded. Nevertheless, robust internal validity, uniform measurement protocols, and consistency with multi-centre data strengthen credibility. Future directions Prospective multicentre trials should test whether magnesium repletion during AECOPD measurably reduces ventilation requirement, relapse rate, or mortality. Parallel community-based studies evaluating dietary magnesium and chronic supplementation may clarify its preventive potential. CONCLUSION Hypomagnesaemia was observed in over half of hospitalised AECOPD patients and correlated with both airflowlimitation severity and prolonged hospital stay. Although mortality differences were not significant, the consistent trend suggests magnesium plays a clinically meaningful role in disease exacerbation and recovery. Routine magnesium monitoring and targeted correction should be considered as part of comprehensive COPD management, while larger prospective studies are warranted to define causality and therapeutic benefit. Dr Hemakaran Meena et al. A Cross-Sectional Study to Evaluate Serum Magnesium Level in Acute Exacerbation of Chronic Obstructive Pulmonary Disease Patients at a Tertiary-Care Centre in North India. Int. J Med. Pharm. Res., 6 (6): 535‐540, 2025 540 REFERENCES 1. Global Initiative for Chronic Obstructive Lung Disease (GOLD). 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