D Hemaka an Meena e al. A C oss-Sec ional S udy o E alua e Se um Magnesium Le el in Acu e Exace ba ion o
Ch onic Obs uc i e Pulmona y Disease Pa ien s a a Te ia y-Ca e Cen e in No h India. In . J Med. Pha m. Res., 6 (6):
535‐540, 2025
535
In e na ional Jou nal o Medical
and Pha maceu ical Resea ch
Online ISSN-2958-3683 | P in ISSN-2958-3675
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A ailable online on: h ps://ijmp .in/
O iginal A icle
A C oss-Sec ional S udy o E alua e Se um Magnesium Le el in Acu e
Exace ba ion o Ch onic Obs uc i e Pulmona y Disease Pa ien s a a
Te ia y-Ca e Cen e in No h India
D Hemaka an Meena1, D Mahend a Kuma Baina a2, D Ji end a Kuma Sha ma3
1 Junio Residen , Depa men o Respi a o y Medicine, Ins i u e o Respi a o y Disease, SMS Medical College, Jaipu
2 Senio P o esso , Depa men o Respi a o y Medicine, Ins i u e o Respi a o y Disease, SMS Medical College, Jaipu
3 Assis an P o esso , Ins i u e o Respi a o y Diseases, SMS Medical College, Jaipu
A B S T R A C T
Co esponding Au ho :
D Ji end a Kuma Sha ma
Assis an P o esso , Ins i u e o
Respi a o y Diseases, SMS Medical
College, Jaipu .
Recei ed: 15-10-2025
Accep ed: 13-11-2025
A ailable online: 18-11-2025
Backg ound: Ch onic obs uc i e pulmona y disease (COPD) is a majo global
cause o mo bidi y and mo ali y, wi h acu e exace ba ions ep esen ing c i ical
e en s ha accele a e lung- unc ion decline and aise heal hca e bu den.
Magnesium (Mg²⁺) egula es b onchial smoo h-muscle one, neu omuscula
ansmission, and in lamma ion. Hypomagnesaemia has been p oposed as a
modi iable biochemical ac o in luencing he se e i y and ou come o COPD
exace ba ions. This s udy e alua ed he p e alence o hypomagnesaemia and i s
associa ion wi h disease se e i y and hospi al ou comes in pa ien s p esen ing wi h
acu e exace ba ion o COPD (AECOPD) a a e ia y-ca e cen e in No h India.
Me hods: A hospi al-based c oss-sec ional s udy en olled 50 consecu i e pa ien s
≥40 yea s wi h spi ome y-con i med COPD p esen ing in acu e exace ba ion.
Se um magnesium was measu ed on admission. Demog aphic, clinical,
adiological, and biochemical da a we e analysed. Associa ions be ween
magnesium s a us and du a ion o s ay, ou come, and GOLD se e i y we e es ed
using chi-squa e and es s.
Resul s: Mean age was 61 ± 9 yea s; 60 % we e male. Hypomagnesaemia (< 1.7
mg dL⁻¹) occu ed in 58 % (n = 29). Pa ien s wi h low magnesium had signi ican ly
longe hospi al s ays > 7 days (79.3 % s 42.9 %, p = 0.018) and a highe , hough
no s a is ically signi ican , mo ali y (10.3 % s 4.8 %). The p e alence o
hypomagnesaemia ose p og essi ely wi h GOLD s age (15 % in mild → 87 % in
e y se e e).
Conclusion: Hypomagnesaemia is common in AECOPD and co ela es wi h
inc easing ai low limi a ion and p olonged hospi alisa ion. Rou ine magnesium
moni o ing a admission may help iden i y high- isk pa ien s and guide ea ly
supplemen a ion ials.
Copy igh © In e na ional Jou nal o
Medical and Pha maceu ical Resea ch
Keywo ds: COPD, acu e exace ba ion, se um magnesium, hypomagnesaemia,
p ognosis, b onchodila ion.
INTRODUCTION
Ch onic obs uc i e pulmona y disease (COPD) is a he e ogenous condi ion cha ac e ised by pe sis en espi a o y
symp oms and ai low limi a ion a ising om ai way and/o al eola abno mali ies (GOLD 2025 upda e [1]). I anks
among he op h ee global causes o dea h, accoun ing o 3.7 million a ali ies annually, and i s bu den con inues o ise
in low- and middle-income coun ies [2, 3]. In India, pooled spi ome y-based communi y su eys es ima e COPD
p e alence be ween 7 and 8 % among adul s ≥ 30 yea s [4], wi h subs an ial in e s a e he e ogenei y.
D Hemaka an Meena e al. A C oss-Sec ional S udy o E alua e Se um Magnesium Le el in Acu e Exace ba ion o
Ch onic Obs uc i e Pulmona y Disease Pa ien s a a Te ia y-Ca e Cen e in No h India. In . J Med. Pha m. Res., 6 (6):
535‐540, 2025
536
Acu e exace ba ions—episodes o wo sening dyspnoea, cough, and spu um wi hin ≤ 14 days— ep esen he mos
dynamic phase o he disease, o en p ecipi a ed by in ec ion o ai -pollu ion su ges [5]. Each hospi alised exace ba ion
accele a es FEV₁ decline by 20–30 mL pe yea and inc eases one-yea mo ali y by 30–40 % [6].
Du ing hese episodes, mul iple me abolic ac o s ampli y he espi a o y bu den: inc eased muscle wo k, co icos e oid-
induced enal losses, β₂-agonis he apy, and educed die a y in ake all deple e magnesium s o es [7, 8]. Magnesium is
he second-mos abundan in acellula ca ion and a co ac o in o e 300 enzyma ic eac ions ha egula e ene gy
me abolism, calcium anspo , and cell signalling [9]. Wi hin he espi a o y sys em, Mg²⁺ media es b onchodila ion ia
an agonism o calcium-dependen ai way-smoo h-muscle con ac ion, inhibi s ace ylcholine elease a agal e minals,
s abilises mas cells, and suppo s diaph agma ic con ac ili y [10, 11].
Clinical e idence linking magnesium o obs uc i e ai way disease has g own s eadily. Ea ly s udies demons a ed ha
hypomagnesaemia accompanies acu e exace ba ions and co ela es wi h ai low limi a ion [12–14]. P ospec i e coho s
in India epo ed hypomagnesaemia in 40–70 % o hospi alised AECOPD cases, wi h signi ican associa ions wi h
disease se e i y and eadmission [15–17]. A Coch ane Re iew (2022) showed ha in a enous magnesium sulpha e
modes ly educes eme gency-depa men admissions and sho ens leng h o s ay [18], and a 2025 me a-analysis
ea i med i s sa e y and apid b onchodila o y e ec [19]. La ge-scale epidemiological da a om he U.S. NHANES
(2005–2018) u he link low magnesium o high magnesium-deple ion sco es o inc eased COPD p e alence and
sys emic in lamma ion [20, 21].
Despi e such biological plausibili y, Indian da a emain spa se and he e ogeneous. Mos s udies a e single-cen e, employ
di e ing cu -o s o magnesium de iciency, and a ely inco po a e spi ome ic s aging o ou come analyses. The p esen
c oss-sec ional s udy was he e o e unde aken o es ima e he p e alence o hypomagnesaemia among pa ien s admi ed
wi h AECOPD in No h India and o co ela e magnesium le els wi h disease se e i y and sho - e m clinical ou comes.
MATERIALS AND METHODS
S udy design and se ing
A hospi al-based, obse a ional c oss-sec ional s udy was conduc ed a a e ia y-ca e cen e in No h India o e one
yea . E hical app o al was ob ained om he ins i u ional e iew boa d, and w i en in o med consen was secu ed om
all pa icipan s.
Pa icipan s
Fi y consecu i e adul s (≥ 40 yea s) wi h spi ome y-con i med COPD p esen ing in acu e exace ba ion (AECOPD)
we e included. Exclusion c i e ia comp ised need o immedia e in asi e en ila ion, majo como bidi ies likely o al e
se um magnesium (e.g., myoca dial in a c ion, s oke, enal ailu e), and use o d ugs a ec ing magnesium me abolism
(e.g., digoxin, aminoglycosides, loop diu e ics).
De ini ions
• COPD/AECOPD: Diagnosed acco ding o GOLD 2025 c i e ia [1].
• Hypomagnesaemia: Se um Mg < 1.7 mg dL⁻¹ (ins i u ional e e ence ange).
• Ou come a iables: Du a ion o hospi al s ay (≤ 7 days s > 7 days) and discha ge o dea h.
Da a collec ion
A s uc u ed case- eco d o m cap u ed demog aphic p o ile, smoking his o y, symp oms, physical indings, adiog aphic
pa e n, a e ial blood gases (as a ailable), and se um magnesium a admission. Ches X- ays we e ead by wo
espi a o y physicians blinded o magnesium s a us.
S a is ical analysis
Da a we e analysed using s anda d s a is ical so wa e. Con inuous a iables we e exp essed as mean ± SD; ca ego ical
a iables as equencies (%). G oup compa isons employed S uden ’s o Mann–Whi ney U es s o con inuous da a and
Chi-squa e o Fishe ’s exac es s o ca ego ical a iables. Co ela ions we e explo ed using Spea man’s ρ. A wo- ailed
p ≤ 0.05 was deemed signi ican .
RESULTS
Age dis ibu ion
Mos pa ien s (34 %) we e aged 60–69 yea s, ollowed by 26 % in 50–59 yea s. COPD exace ba ions hus clus e ed in
olde adul s (Table 1)
Table 1. Age dis ibu ion o AECOPD pa ien s
Age g oup
N
%
D Hemaka an Meena e al. A C oss-Sec ional S udy o E alua e Se um Magnesium Le el in Acu e Exace ba ion o
Ch onic Obs uc i e Pulmona y Disease Pa ien s a a Te ia y-Ca e Cen e in No h India. In . J Med. Pha m. Res., 6 (6):
535‐540, 2025
537
40-49
11
22
50-59
13
26
60-69
17
34
≥ 70
9
18
To al
50
100
Sex dis ibu ion
Males cons i u ed 60 % (n = 30) and emales 40 % (n = 20) (Table 2)
Table 2. Sex dis ibu ion
Sex
N
%
Male
30
60
Female
20
40
Figu e 2. Sex dis ibu ion o AECOPD cases.
Place o esidence
U ban esiden s ou numbe ed u al (60 % s 40 %), e lec ing he hospi al’s ca chmen (Table 3).
Table 3. Residence dis ibu ion
Residence
N
%
U ban
30
60
Ru al
20
40
Figu e 3. U ban- u al dis ibu ion o pa icipan s.
Smoking s a us
Fi y-eigh pe cen we e ex-smoke s, 32 % cu en smoke s, and 10 % ne e -smoke s (Table 4).
Table 4. Smoking s a us
S a us
N
%
Ex-smoke
29
58
Cu en smoke
16
32
Ne e smoke
5
10
Figu e 4. Smoking s a us among AECOPD pa ien s.
Symp om p o ile
All pa ien s (100 %) p esen ed wi h b ea hlessness; cough occu ed in 70 %, expec o a ion 50 %, wheeze 36 %, and e e
30 % (Table 5).
Table 5. Symp om dis ibu ion
Symp om
N
%
B ea hlessness
50
100%
Cough
35
70
Expec o a ion
25
50
Wheeze
18
36
Fe e
15
30
Figu e 5. Clinical symp om equencies.
Radiological indings
Emphysema was he p edominan adiog aphic ea u e (28 %), ollowed by hype in la ion (22 %) and consolida ion (20
%) (Table 6).
Table 6. Ches -X- ay inding
Figu e 6. Common adiological indings in AECOPD.
Findings
N
%
Emphysema
14
28
Hype in la edlung
11
22
Consolida ion
10
20
In il a es
9
18
Ca diomegaly
6
12
D Hemaka an Meena e al. A C oss-Sec ional S udy o E alua e Se um Magnesium Le el in Acu e Exace ba ion o
Ch onic Obs uc i e Pulmona y Disease Pa ien s a a Te ia y-Ca e Cen e in No h India. In . J Med. Pha m. Res., 6 (6):
535‐540, 2025
538
Se um magnesium and hospi al s ay
Hypomagnesaemia was documen ed in 58 % (n = 29). A signi ican ly la ge p opo ion o hese pa ien s equi ed
hospi aliza ion > 7 days compa ed wi h hose wi h no mal Mg (79.3 % s 42.9 %; p = 0.0187) (Table 7).
Table 7. Du a ion o s ay s se um magnesium le el
Hospi al s ay |
Hypomagnesaemia (n = 29
No momagnesaemia (n = 21
To al
≤ 7 days
6 (20.7 %)
12 (57.1 %)
18
> 7 days
23 (79.3 %)
9 (42.9 %)
32
p = 0.0187.
Figu e 7. Rela ionship be ween magnesium s a us and du a ion o hospi al s ay.
Ou come
Fou dea hs occu ed (8 % o e all). Mo ali y was highe among hypomagnesaemic pa ien s (10.3 %)
Table 8. Ou come s se um magnesium
Ou come
Hypomagnesemia
No momagnesemia
To al
Discha ged
26(89.7%)
20(95.2%)
46
Deceased
3(10.3%)
1(4.8%)
4
han no momagnesaemic (4.8 %), hough he di e ence was no signi ican (p = 0.85) (Table 8).
Figu e 8. Ou come dis ibu ion acco ding o magnesium s a us.
COPD se e i y and magnesium s a us
The equency o hypomagnesaemia ose s eadily wi h GOLD s age— om 15 % in mild o 87 % in e y se e e disease
(Table 9).
Table 9. GOLD se e i y s se um magnesium s a us
GOLD S age
N
Hypomagnesaemia
no momagnesemia
I mild
13
2
11
II mode a e
17
10
7
III se e e
15
13
2
IV e y se e e
5
4
1
Figu e 9. T end o declining magnesium le els wi h ad ancing GOLD s age.
Summa y o key indings:
• Mean age ≈ 61 yea s; male- o- emale a io 3:2.
• Hypomagnesaemia p e alence ≈ 58 %.
• S ong co ela ion be ween low Mg²⁺ and bo h ad anced ai low limi a ion and p olonged s ay.
• Mo ali y signal highe in low-Mg g oup, hough no s a is ically signi ican .
DISCUSSION
The p esen s udy demons a es ha hypomagnesaemia is common (58 %) among hospi alised pa ien s wi h acu e
exace ba ion o COPD (AECOPD) and ha i co ela es signi ican ly wi h bo h disease se e i y and p olonged hospi al
s ay. Al hough mo ali y was no s a is ically highe , he consis en downwa d end in se um magnesium wi h ad ancing
GOLD s age unde sco es magnesium’s po en ial pa hophysiological and p ognos ic ele ance.
Age and gende pa e n
Mos admissions clus e ed be ween 50 and 69 yea s—an age band whe e cumula i e inhala ional inju y,
immunosenescence, and declining espi a o y-muscle ese e con e ge o igge exace ba ions [1, 2]. Simila
dis ibu ions we e epo ed by Makwana e al (2022) [15] and An in e al (2023) [24]. Male p edominance (60 %) e lec s
pe sis en ly highe smoking p e alence among men; howe e , he 40 % emale ep esen a ion highligh s a na owing
gende gap a ibu ed o biomass smoke exposu e and passi e smoking in domes ic se ings [25].
Smoking s a us
D Hemaka an Meena e al. A C oss-Sec ional S udy o E alua e Se um Magnesium Le el in Acu e Exace ba ion o
Ch onic Obs uc i e Pulmona y Disease Pa ien s a a Te ia y-Ca e Cen e in No h India. In . J Med. Pha m. Res., 6 (6):
535‐540, 2025
539
Nea ly one- hi d o subjec s we e ac i e smoke s, echoing ecen Indian egis y da a showing 28–35 % con inued
obacco use despi e p io hospi alisa ion [26]. Con inued smoking accele a es FEV₁ decline and aises exace ba ion
equency by in ensi ying ai way and sys emic in lamma ion. S uc u ed cessa ion counselling wi h pha macologic
he apy ( a enicline, bup opion, o combina ion NRT) should he e o e be embedded in o AECOPD ca e pa hways [27].
Clinical p esen a ion and adiology
Dyspnoea was uni e sal, while cough and expec o a ion we e less consis en . This a ia ion mi o s seasonal and
ea men - ela ed di e ences epo ed ac oss Indian e ia y-ca e se ies [28]. Radiologically, emphysema and
hype in la ion p edomina ed—consis en wi h he obs uc i e pheno ype—bu one- i h o pa ien s exhibi ed
consolida ion, sugges ing in ec ious igge s o exace ba ion, also no ed by Kshi saga and Pa il (2021) [16].
Se um magnesium and ou comes
The cen al obse a ion was a s a is ically signi ican link be ween hypomagnesaemia and p olonged hospi al s ay
(> 7 days, p = 0.018). This aligns wi h p e ious Indian da a by Makwana e al (2022) [18] and Kuma e al (2025) [22],
bo h o which iden i ied low admission Mg²⁺ as an independen p edic o o longe s ay and need o non-in asi e
en ila ion. Simila ends we e con i med in e na ionally by Gumus e al (2014) and in he Coch ane e iew (Powell e
al 2022) [19], whe e in a enous magnesium sho ened mean hospi alisa ion by ≈ 2.7 days.
Hypomagnesaemia’s mechanis ic plausibili y is well suppo ed:
• B onchial smoo h-muscle one: low Mg²⁺ emo es inhibi o y con ol on calcium in lux, ampli ying cons ic ion
[10].
• Neu omuscula pe o mance: Mg-ATP deple ion p ecipi a es ea ly espi a o y-muscle a igue [7, 9].
• In lamma o y modula ion: de iciency enhances NF-κB ac i a ion and cy okine elease [11].
Collec i ely, hese pa hways explain why e en modes se um Mg²⁺ dec emen s wo sen ai low limi a ion and p olong
eco e y.
Compa ison wi h ea lie s udies
Bha e al (2008) [15] i s epo ed magnesium as an independen p edic o o eadmission equency; Kshi saga and
Pa il (2021) [16] obse ed hypomagnesaemia in 72 % du ing exace ba ion e sus 1 % a s abili y, con i ming i s dynamic
all du ing acu e illness. Me a-analyses (Heida i e al 2025 [23]) now consolida e hese obse a ions, showing pooled
odds 0.45 o hospi al admission wi h IV MgSO₄ and no excess ad e se e en s. Mo eo e , he NHANES-de i ed
Magnesium Deple ion Sco e (Zhang e al 2024 [21]) e ealed a g aded associa ion be ween sys emic magnesium de ici
and COPD p e alence, emphasising i s ole beyond acu e la es.
Clinical implica ions
Rou ine es ima ion o se um magnesium a AECOPD admission p o ides a apid, low-cos p ognos ic ool
complemen ing ABG and eosinophil coun s. Iden i ying hypomagnesaemia ea ly allows imely supplemen a ion—ei he
o al (400–600 mg/day elemen al Mg) o in a enous (1–2 g MgSO₄ o e 20 min in se e e b onchospasm)—as suppo ed
by con olled ials [17–19]. Co ec ion may sho en s ay, imp o e b onchodila ion, and p e en ecu ence.
F om a policy pe spec i e, inco po a ing se um magnesium measu emen in o s anda d COPD admission panels could
meaning ully enhance iage and bed-day u ilisa ion in high- olume go e nmen hospi als.
Limi a ions
The s udy’s single-cen e design and modes sample size limi gene alisabili y. Magnesium in ake, diu e ic exposu e, and
ollow-up eadmissions we e no eco ded. Ne e heless, obus in e nal alidi y, uni o m measu emen p o ocols, and
consis ency wi h mul i-cen e da a s eng hen c edibili y.
Fu u e di ec ions
P ospec i e mul icen e ials should es whe he magnesium eple ion du ing AECOPD measu ably educes en ila ion
equi emen , elapse a e, o mo ali y. Pa allel communi y-based s udies e alua ing die a y magnesium and ch onic
supplemen a ion may cla i y i s p e en i e po en ial.
CONCLUSION
Hypomagnesaemia was obse ed in o e hal o hospi alised AECOPD pa ien s and co ela ed wi h bo h ai low-
limi a ion se e i y and p olonged hospi al s ay. Al hough mo ali y di e ences we e no signi ican , he consis en end
sugges s magnesium plays a clinically meaning ul ole in disease exace ba ion and eco e y. Rou ine magnesium
moni o ing and a ge ed co ec ion should be conside ed as pa o comp ehensi e COPD managemen , while la ge
p ospec i e s udies a e wa an ed o de ine causali y and he apeu ic bene i .
D Hemaka an Meena e al. A C oss-Sec ional S udy o E alua e Se um Magnesium Le el in Acu e Exace ba ion o
Ch onic Obs uc i e Pulmona y Disease Pa ien s a a Te ia y-Ca e Cen e in No h India. In . J Med. Pha m. Res., 6 (6):
535‐540, 2025
540
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