e-ISSN: 0976-822X, p-ISSN:2961-6042
A ailable online on h p://www.ijcp .com/
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1128
O iginal Resea ch A icle
S udy on Vi amin D Assay in Ch onic Non Choles a ic Li e Disease
A aya Chak abo y1, Kausik Mis a2, Binod Kuma Das3
1MBBS, DNB (Gene al Medicine), PDT (C i ical Ca e Medicine), Depa men o Gene al Medicine,
Manipal Hospi als Dhaku ia, Kolka a, Wes Bengal 700029
2Medical O ice (Specialis ), DCH, MD (Pulmona y Medicine), Depa men o Medicine, Manipal
Hospi als Dhaku ia, Kolka a, Wes Bengal 700029
3Medical O ice (Specialis ), MBBS,MD (Gene al Medicine), Depa men o Medicine, Manipal
Hospi als Dhaku ia, Kolka a, Wes Bengal 700029
Recei ed: 01-06-2025 / Re ised: 16-07-2025 / Accep ed: 19-08-2025
Co esponding Au ho : D A aya Chak abo y
Con lic o in e es : Nil
Abs ac
In oduc ion: Vi amin D is a secos e oid ho mone wi h pleio opic ac ions ha ex end beyond skele al
homeos asis o immunomodula o y, an i-in lamma o y and an i- ib o ic e ec s—pa hways ha a e highly
ele an o ch onic li e disease (CLD) o non-choles a icae iology, including me abolic dys unc ion-associa ed
s ea o ic li e disease (MASLD/NAFLD), alcohol- ela ed li e disease (ALD) and ch onic i al hepa i is.
Aims and Objec i es: To assay i amin D in pa ien s wi h non-choles a ic ch onic li e disease and o compa e
he pa ame e s o li e unc ion es (LFT) wi h i amin D le els and co ela e he wo i possible.
Ma e ials and Me hods: The p esen s udy was a desc ip i e obse a ional s udy wi h c oss sec ional design.
This S udy was conduc ed o e 1 yea pe iod om he da e o app o al o p o ocol a Nadia dis ic hospi al,
K ishnanaga , Wes Bengal.
Resul : In his s udy o pa ien s wi h ch onic non-choles a ic li e disease, se um i amin D s a us was
associa ed wi h a ia ions in li e unc ion and disease e iology. While age, sex, and BMI did no di e
signi ican ly ac oss i amin D g oups, an i-HCV posi i i y and unde lying e iology showed signi ican
associa ions, wi h alcohol- ela ed li e disease mo e common in pa ien s wi h lowe i amin D le els and NASH
p edomina ing in hose wi h su icien le els. Li e unc ion pa ame e s—including SGOT, SGPT, ALP, GGT,
bili ubin, albumin, and globulin—di e ed signi ican ly among he g oups, indica ing g ea e hepa ic
dys unc ion in pa ien s wi h i amin D de iciency o insu iciency.
Conclusion: This s udy highligh s a signi ican associa ion be ween se um i amin D s a us and bo h li e
unc ion and disease e iology in pa ien s wi h ch onic non-choles a ic li e disease. Pa ien s wi h lowe i amin
D le els ended o exhibi mo e p onounced al e a ions in li e unc ion ma ke s, including ele a ed li e
enzymes and educed se um albumin, sugges ing g ea e hepa ic dys unc ion.
Keywo ds: Vi amin D, Ch onic li e disease, Non-choles a ic li e disease, Li e unc ion es s.
This is an Open Access a icle ha uses a unding model which does no cha ge eade s o hei ins i u ions o access and dis ibu ed unde
he e ms o he C ea i e Commons A ibu ion License (h p://c ea i ecommons.o g/licenses/by/4.0) and he Budapes Open Access
Ini ia i e (h p://www.budapes openaccessini ia i e.o g/ ead), which pe mi un es ic ed use, dis ibu ion, and ep oduc ion in any medium,
p o ided o iginal wo k is p ope ly c edi ed.
In oduc ion
Vi amin D is a secos e oid ho mone wi h
pleio opic ac ions ha ex end beyond skele al
homeos asis o immunomodula o y, an i-
in lamma o y and an i- ib o ic e ec s—pa hways
ha a e highly ele an o ch onic li e disease
(CLD) o non-choles a icae iology, including
me abolic dys unc ion-associa ed s ea o ic li e
disease (MASLD/NAFLD), alcohol- ela ed li e
disease (ALD) and ch onic i al hepa i is. Hepa ic
25-hyd oxyla ion (p incipally ia CYP2R1)
gene a es 25-hyd oxy i amin D [25(OH)D], he
accep ed bioma ke o i amin D s a us, which
ci cula es la gely bound o i amin D–binding
p o ein and albumin; hus, hepa ocellula
dys unc ion, educed p o ein syn hesis,
malnu i ion and limi ed sunligh exposu e
equen ly con e ge o p oduce low o al 25(OH)D
in CLD [1,2]. Obse a ional coho s and e iews
consis en ly epo a high p e alence o i amin D
insu iciency/de iciency ac oss CLD se e i ies,
wi h le els declining as ib osis and syn he ic
ailu e p og ess, and in e se co ela ions wi h
Child–Pugh and MELD sco es ha e been desc ibed
[1,3,4,5]. In NAFLD, low 25(OH)D has been
associa ed wi h s ea osis, nec oin lamma ion and
ib osis in se e al popula ions, and Mendelian-
andomisa ion analyses sugges an in e se
ela ionship be ween gene ically p edic ed i amin
D s a us and NAFLD isk, al hough causali y o
his ological imp o emen emains deba ed [5,6].
Me a-analyses o supplemen a ion ials in NAFLD
demons a e eliable eple ion o se um 25(OH)D
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Chak abo y e al. In e na ional Jou nal o Cu en Pha maceu ical Re iew and Resea ch
1129
and modes lipid p o ile bene i s, bu inconsis en
e ec s on amino ans e ases and glycaemic indices,
unde sco ing biological plausibili y wi hou
de ini i e he apeu ic p oo o li e endpoin s [6].
In ch onic hepa i is C, mul iple s udies epo an
associa ion be ween low 25(OH)D and ad anced
ib osis, wi h mechanis ic wo k implica ing i amin
D ecep o signalling in s ella e-cell ac i a ion and
ma ix emodelling [2,4]. Beyond ib osis,
de iciency has been linked o in ec ions, hepa ic
encephalopa hy and mo ali y in ci hosis,
sugges ing p ognos ic alue ha may anscend
bone ou comes [1,5]. These clinicopa hological
links aise impo an ques ions o labo a o ies and
clinicians: which assay, wha h eshold, and in
whom should we es ? Assay me hodology a ies—
au oma ed compe i i e immunoassays,
adioimmunoassay and liquid ch oma og aphy–
andem mass spec ome y (LC-MS/MS) a e all
used—wi h no able in e -me hod bias, a iable
c oss- eac i i y o 25(OH)D₂/D₃, and ma ix
e ec s; con empo a y endoc ine and labo a o y
consensus documen s emphasises anda disa ion
(e.g., VDSP alignmen ) and ecognise ongoing
con o e sy a ound “op imal” cu -o s (20 s 30
ng/mL) [7,8]. In ci hosis, low albumin and
binding-p o ein concen a ions may
disp opo iona ely dep ess o al 25(OH)D while
ee/bioa ailable ac ions emain less a ec ed, a
nuance ha could in luence in e p e a ion when
compa ing ac oss disease se e i ies and assays
[1,7]. Guideline pe spec i es ha e shi ed: he 2024
Endoc ine Socie y guideline ad ises agains ou ine
25(OH)D sc eening o disease p e en ion in
o he wise unselec ed popula ions, e lec ing
ou come-based e idence gaps; none heless, high-
isk g oups and es ablished indica ions emain
app op ia e con ex s o measu emen and
ea men [7].
Fo hepa ology, whe e ac u e isk, sa copenia,
in ec ion suscep ibili y and encephalopa hy ca y
p ognos ic weigh , a ge ed assessmen may s ill be
clinically jus i ied, pa icula ly in decompensa ed
disease, ALD, malnu i ion, and p e- ansplan
e alua ions [1,3,5,9,10]. Agains his backg ound, a
ocused “S udy on Vi amin D Assay in Ch onic
Non-Choles a ic Li e Disease” is imely. I can
quan i y he bu den o hypo i aminosis D by a
s anda dised me hod, examine conco dance o bias
ac oss commonly used assays, and explo e
co ela ions be ween 25(OH)D and alida ed
measu es o li e se e i y (e.g., ib osis su oga es,
Child–Pugh, MELD), nu i ion and ex a-hepa ic
ou comes. By in eg a ing igo ous p e-analy ical
con ol (season, la i ude, BMI, diabe es, alcohol
and supplemen use), me hod selec ion (p e e ably
LC-MS/MS o a VDSP-aligned immunoassay), and
clinically meaning ul h esholds p especi ied om
consensus s a emen s, such a s udy can cla i y he
in e p e i e landscape o hepa ology se ices.
Ul ima ely, delinea ing how assay choice and
disease- ela ed binding-p o ein pe u ba ions shape
25(OH)D eadou s will help de e mine when and
how i amin D es ing should in o m isk
s a i ica ion and managemen in non-choles a ic
CLD [1–10].
Ma e ials and Me hods
S udy A ea: Nadia dis ic hospi al, K ishnanaga ,
Wes Bengal.
S udy Popula ion: Pa ien s wi h he diagnosis o
non-choles a ic li e disease a ending hei
depa men we e included.
All he pa ien s we e explained in de ail abou he
s udy, and an in o med consen was aken.
S udy Design: Desc ip i e obse a ional s udy
wi h c oss sec ional design.
S udy Du a ion: 1 yea pe iod om he da e o
app o al o p o ocol.
Inclusion C i e ia: De ailed his o y and clinical
e alua ion done.
The inclusion c i e ia o he pa ien s in his s udy
we e:
All he pa ien s diagnosed wi h non choles a ic
ch onic li e disease diagnosed wi h he help o
USG (ul asonog aphy) andLFT (Li e unc ion
es ) (USG sugges i e o ch onic li e disease is
inc eased echo ex u e and LFT wi h low albumin
and mildly aised li e enzymes)
Exclusion C i e ia
1. Pa ien s wi h choles a ic li e disease
2. Pa ien s who we e on calcium supplemen s and
i amin D
3. Pa ien s on medica ions which a ec bone
mine al densi y
4. Pos menopausal women
5. Pa ien s wi h coexis en ch onic kidney disease
Sample Size: 55 Pa ien s wi h ch onic non-
choles a ic li e disease.
S udy Tools
1. P e designed and p e es ed Ques ionnai e
2. USG machine
3. Rele an in es iga ion eco ds
S a is ical Analysis: Fo s a is ical analysis, da a
we e ini ially en e ed in o a Mic oso Excel
sp eadshee and hen analysed using SPSS ( e sion
27.0; SPSS Inc., Chicago, IL, USA) and G aphPad
P ism ( e sion 5). Nume ical a iables we e
summa ized using means and s anda d de ia ions,
while Da a we e en e ed in o Excel and analyzed
using SPSS and G aphPad P ism. Nume ical
a iables we e summa ized using means and
s anda d de ia ions, while ca ego ical a iables
In e na ional Jou nal o Cu en Pha maceu ical Re iew and Resea ch e-ISSN: 0976-822X, p-ISSN: 2961-6042
Chak abo y e al. In e na ional Jou nal o Cu en Pha maceu ical Re iew and Resea ch
1130
we e desc ibed wi h coun s and pe cen ages. Two-
sample - es s we e used o compa e independen
g oups, while pai ed - es s accoun ed o
co ela ions in pai ed da a. Chi-squa e es s
(including Fishe ’s exac es o small sample
sizes) we e used o ca ego ical da a compa isons.
P- alues ≤ 0.05 we e conside ed
s a is ically signi ican .
Resul
Table 1: Dis ibu ion o Age and Sex ac oss Se um Vi amin D S a us in Ch onic Non-Choles a ic Li e
Disease Pa ien s
Se um Vi amin D G oup
De iciency
Insu iciency
Su iciency
To al
P- alue
Age in
G oup
≤50
2(6.3%)
1(6.3%)
0(0%)
3(5.5%)
0.2808
51-60
2(6.3%)
5(31.3%)
0(0%)
7(12.7%)
61-70
11(34.4%)
4(25%)
4(57.1%)
19(34.5%)
71-80
10(31.3%)
5(31.3%)
2(28.6%)
17(30.9%)
81-90
7(21.9%)
1(6.3%)
1(14.3%)
9(16.4%)
To al
32(100%)
16(100%)
7(100%)
55(100%)
Sex
Female
13(40.6%)
5(31.3%)
5(71.4%)
23(41.8%)
0.1944
Male
19(59.4%)
11(68.8%)
2(28.6%)
32(58.2%)
To al
32(100%)
16(100%)
7(100%)
55(100%)
Table 2: Dis ibu ion o Vi al Se ology and E iology ac oss Se um Vi amin D S a us in Ch onic Non-
Choles a ic Li e Disease Pa ien s
Se um Vi amin D G oup
De iciency
Insu iciency
Su iciency
To al
P- alue
An i HCV
Nega i e
32(100%)
12(75.0%)
7(100%)
51(92.7%)
0.0052
Posi i e
0(0%)
4(25%)
0(0%)
4(7.3%)
To al
32(100%)
16(100%)
7(100%)
55(100%)
Hepa i is B se ology
Nega i e
31(96.9%)
16(100%)
7(100%)
54(98.2%)
0.6935
Posi i e
1(3.1%)
0(0%)
0(0%)
1(1.8%)
To al
32(100%)
16(100%)
7(100%)
55(100%)
E iology
Alcohol
12(37.5%)
12(75%)
0(0%)
24(43.6%)
<0.0001
Hepa i is C ela ed
1(3.1%)
4(25%)
0(0%)
5(9.1%)
Nash ela ed
19(59.4%)
0(0%)
7(100%)
26(47.3%)
To al
32(100%)
16(100%)
7(100%)
55(100%)
Table 3: Compa ison o Demog aphic, An h opome ic, and Biochemical Pa ame e s ac oss Vi amin D
S a us in Ch onic Non-Choles asis Li e Disease Pa ien s
Numbe
Mean
SD
Minimum
Maxim
um
Medi
an
p-
alue
Age (y )
De iciency
32
71.4375
10.4633
48
90
72.5
0.2825
Insu iciency
16
66.6875
9.4919
49
81
67.5
Su iciency
7
71
6.4031
62
82
70
BMI (kg/m2)
De iciency
32
27.9219
2.4033
24.5
32
27
0.4288
Insu iciency
16
27.0625
2.3585
25.5
33
26.5
Su iciency
7
28
0
28
28
28
Size o po al
ein (in mm)
De iciency
32
15.6406
0.7853
14
16.5
16
<0.0001
Insu iciency
16
14.5
0.8944
14
16
14
Su iciency
7
16
0
16
16
16
Se um i amin
D(OH) assay
(ng/ml)
De iciency
32
13.8
3.3884
3
19
15
<0.0001
Insu iciency
16
22.675
1.2969
20.5
23.4
23.4
Su iciency
7
32
0
32
32
32
To al bili ubin
(mg/dl)
De iciency
32
3.0494
1.1174
1.6
4.22
3.1
<0.0001
Insu iciency
16
1.7175
0.0939
1.56
1.77
1.77
Su iciency
7
2.3
0
2.3
2.3
2.3
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Chak abo y e al. In e na ional Jou nal o Cu en Pha maceu ical Re iew and Resea ch
1131
Table 4: Compa ison o Li e Func ion Pa ame e s ac oss Vi amin D S a us Ca ego ies in Ch onic Non-
Choles a ic Li e Disease Pa ien s
Numbe
Mean
SD
Minimum
Maximum
Median
p- alue
SGOT(U/
L)
De iciency
32
68.4375
25.3885
25
111
67
<0.0001
Insu iciency
16
140.75
23.7023
101
154
154
Su iciency
7
35
0
35
35
35
SGPT
(U/L)
De iciency
32
37.7188
10.5195
25
65
34
<0.0001
Insu iciency
16
102.5
13.4164
80
110
110
Su iciency
7
27
0
27
27
27
ALP(U/L)
De iciency
32
65.25
18.2968
45
90
66
<0.0001
Insu iciency
16
101.75
22.8079
89
140
89
Su iciency
7
78
0
78
78
78
Albumin
(g/dl)
De iciency
32
2.8625
0.3867
2.1
3.5
2.9
0.0034
Insu iciency
16
3.25
0.4472
3
4
3
Su iciency
7
3.2
0
3.2
3.2
3.2
Globulin(g
/dl)
De iciency
32
4.3469
0.4174
3.5
4.9
4.4
0.0004
Insu iciency
16
3.925
0.1342
3.7
4
4
Su iciency
7
4.1
0
4.1
4.1
4.1
Table 5: Dis ibu ion o mean Gama GT(U/L): Se um i amin D G oup
Numbe
Mean
SD
Minimum
Maximum
Median
p- alue
Gama
GT(U/L)
De iciency
32
73.8125
22.3079
49.0000
110.0000
70.0000
<0.0001
Insu iciency
16
122.2500
1.3416
120.0000
123.0000
123.0000
Su iciency
7
60.0000
.0000
60.0000
60.0000
60.0000
Figu e 1: Dis ibu ion o Vi al Se ology and E iology ac oss Se um Vi amin D S a us in Ch onic Non-
Choles a ic Li e Disease Pa ien s
Figu e 2: Dis ibu ion o mean Gama GT(U/L): Se um i amin D G oup
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Chak abo y e al. In e na ional Jou nal o Cu en Pha maceu ical Re iew and Resea ch
1132
In his s udy o 55 pa ien s wi h ch onic non-
choles a ic li e disease, he dis ibu ion o age
ac oss se um i amin D g oups showed ha he
majo i y o pa ien s in he de iciency g oup we e
aged 61–70 yea s (34.4%) and 71–80 yea s
(31.3%), while in he insu iciency g oup, mos
we e be ween 51–60 yea s (31.3%) and 71–80
yea s (31.3%). In he su iciency g oup, 57.1%
we e aged 61–70 yea s, wi h smalle p opo ions in
he 71–80 (28.6%) and 81–90 yea s (14.3%)
ca ego ies. The di e ence in age dis ibu ion
among i amin D g oups was no s a is ically
signi ican (p = 0.2808). Rega ding sex
dis ibu ion, males p edomina ed in he de iciency
(59.4%) and insu iciency (68.8%) g oups, whe eas
emales comp ised a majo i y in he su iciency
g oup (71.4%). This di e ence was also no
s a is ically signi ican (p = 0.1944).
Among he 55 pa ien s, an i-HCV se ology showed
ha all pa ien s in he i amin D de iciency (100%)
and su iciency (100%) g oups we e nega i e,
while 75% o pa ien s in he insu iciency g oup
we e nega i e and 25% we e posi i e. This
di e ence was s a is ically signi ican (p = 0.0052).
Fo hepa i is B se ology, nea ly all pa ien s we e
nega i e ac oss all i amin D g oups, wi h only one
pa ien (3.1%) in he de iciency g oup es ing
posi i e, showing no signi ican di e ence be ween
g oups (p = 0.6935). Rega ding e iology, alcohol-
ela ed li e disease was p edominan in he
insu iciency g oup (75%) and common in he
de iciency g oup (37.5%) bu absen in he
su iciency g oup. Hepa i is C– ela ed li e disease
was obse ed in 25% o he insu iciency g oup
and 3.1% o he de iciency g oup, while non-
alcoholic s ea ohepa i is (NASH) was mos
equen in he su iciency g oup (100%) and in
59.4% o he de iciency g oup. These di e ences in
e iology ac oss i amin D g oups we e highly
signi ican (p < 0.0001).
In his s udy o 55 pa ien s wi h ch onic non-
choles a ic li e disease, he mean age did no
di e signi ican ly ac oss se um i amin D g oups,
wi h he de iciency, insu iciency, and su iciency
g oups ha ing mean ages o 71.44 ± 10.46, 66.69 ±
9.49, and 71 ± 6.40 yea s, espec i ely (p =
0.2825). Simila ly, body mass index (BMI) showed
no signi ican di e ences be ween g oups (27.92 ±
2.40 s. 27.06 ± 2.36 s. 28 ± 0 kg/m²; p = 0.4288).
The size o he po al ein, howe e , a ied
signi ican ly among he g oups, wi h he de iciency
g oup showing a mean diame e o 15.64 ± 0.79
mm, insu iciency 14.5 ± 0.89 mm, and su iciency
16 ± 0 mm (p < 0.0001). Se um 25-hyd oxy i amin
D le els di e ed signi ican ly, as expec ed, wi h
mean le els o 13.8 ± 3.39 ng/mL in he de iciency
g oup, 22.68 ± 1.30 ng/mL in he insu iciency
g oup, and 32 ± 0 ng/mL in he su iciency g oup
(p < 0.0001). To al bili ubin le els also
demons a ed signi ican di e ences, wi h he
de iciency g oup showing he highes mean alue
(3.05 ± 1.12 mg/dL), ollowed by he su iciency
(2.3 ± 0 mg/dL) and insu iciency g oups (1.72 ±
0.09 mg/dL) (p < 0.0001).
The analysis o li e unc ion pa ame e s ac oss
se um i amin D g oups e ealed signi ican
di e ences among he de iciency, insu iciency,
and su iciency ca ego ies. Mean SGOT le els
we e highes in he insu iciency g oup (140.75 ±
23.70 U/L) compa ed o he de iciency (68.44 ±
25.39 U/L) and su iciency g oups (35 ± 0 U/L) (p
< 0.0001). Simila ly, SGPT le els we e
signi ican ly ele a ed in he insu iciency g oup
(102.5 ± 13.42 U/L) ela i e o he de iciency
(37.72 ± 10.52 U/L) and su iciency g oups (27 ± 0
U/L) (p < 0.0001). ALP le els also di e ed
ma kedly, wi h he insu iciency g oup showing he
highes mean (101.75 ± 22.81 U/L), ollowed by
su iciency (78 ± 0 U/L) and de iciency g oups
(65.25 ± 18.30 U/L) (p < 0.0001). Se um albumin
was signi ican ly lowe in he de iciency g oup
(2.86 ± 0.39 g/dL) compa ed o he insu iciency
(3.25 ± 0.45 g/dL) and su iciency g oups (3.2 ± 0
g/dL) (p = 0.0034). Con e sely, globulin le els
we e highe in he de iciency g oup (4.35 ± 0.42
g/dL) han in he insu iciency (3.93 ± 0.13 g/dL)
and su iciency g oups (4.1 ± 0 g/dL) (p = 0.0004).
The se um gamma-glu amyl ans e ase (GGT)
le els di e ed signi ican ly ac oss he i amin D
g oups. The mean GGT was highes in he
insu iciency g oup (122.25 ± 1.34 U/L), ollowed
by he de iciency g oup (73.81 ± 22.31 U/L), and
lowes in he su iciency g oup (60 ± 0 U/L) (p <
0.0001).
Discussion
In his coho o 55 pa ien s wi h ch onic non-
choles a ic li e disease, i amin-D s a a acked
clinically meaning ul di e ences in i ology,
e iology, and li e biochemis y despi e b oadly
simila age and BMI dis ibu ions. The s ikingly
highe an i-HCV posi i i y con ined o he
insu iciency g oup (25%) mi o s p io wo k
showing ha lowe 25-hyd oxy i amin D
(25[OH]D) le els in HCV a e linked o g ea e
in lamma ion, ib osis, and poo e ea men
esponse, sugges ing ha e en “insu icien ” (no
ankly de icien ) s a us may ma e biologically in
i al hepa i is [13,20]. E iologic pa e ns also
aligned wi h con empo a y li e a u e: alcohol-
ela ed disease clus e ed in lowe i amin-D s a es,
consis en wi h high a es o hypo i aminosis D in
ALD and i s associa ion wi h wo se ou comes
[19,20], whe eas he 100% NASH p opo ion in he
su iciency g oup (wi h small n) con as s wi h he
usual in e se ela ionship be ween i amin D and
NAFLD isk/se e i y epo ed by se e al
analyses— hough disco dan indings exis and
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Chak abo y e al. In e na ional Jou nal o Cu en Pha maceu ical Re iew and Resea ch
1133
some s udies ind no his ologic g adien by
25(OH)D, unde sco ing he e ogenei y and po en ial
con ounding by adiposi y, season, and sampling
ame [17,18]. Biochemically, he insu iciency
g oup showed he highes mean SGOT, SGPT,
ALP, and GGT, while he de iciency g oup
exhibi ed he lowes albumin and highes
bili ubin— oge he echoing he b oad associa ion
be ween low i amin D and mo e ad anced hepa ic
dys unc ion no ed ac oss CLD (lowe albumin,
highe bili ubin, and wo se Child-Pugh/MELD)
[11,12,16].
Po al ein calibe di e ed ac oss g oups; al hough
di ec links be ween 25(OH)D and measu ed po al
p essu e a e mixed, lowe i amin-D s a us has
been ied o po al-hype ension complica ions and
decompensa ion isks in ci hosis, sugges ing ha
i amin D may be a ma ke —o modes media o —
o he pa hobiology d i ing po al hype ension
[12,14,15].
O e all, ou pa e n con e ges wi h “ano he
au ho ’s” se ies—A eh e al., who epo ed nea -
uni e sal i amin-D de iciency in CLD—while
ex ending i by showing ha g adien s ac oss
de iciency/insu iciency/su iciency map on o
dis inc i ologic and biochemical p o iles e en
when age/BMI a e balanced [11]. Clinically, hese
da a suppo ou ine i amin-D assessmen in CLD
and a ge ed co ec ion alongside disease-speci ic
managemen , pa icula ly o pa ien s wi h i al
hepa i is o alcohol- ela ed disease, whe e low
25(OH)D acks wi h ad e se pheno ypes and
ou comes [13–16,19,20].
Conclusion
This s udy highligh s a signi ican associa ion
be ween se um i amin D s a us and bo h li e
unc ion and disease e iology in pa ien s wi h
ch onic non-choles a ic li e disease. Pa ien s wi h
lowe i amin D le els ended o exhibi mo e
p onounced al e a ions in li e unc ion ma ke s,
including ele a ed li e enzymes and educed
se um albumin, sugges ing g ea e hepa ic
dys unc ion.
Addi ionally, i amin D s a us appea ed o co ela e
wi h he unde lying cause o li e disease, wi h
alcohol- ela ed li e disease mo e common among
hose wi h lowe i amin D le els, while non-
alcoholic a y li e disease was p edominan in
pa ien s wi h su icien le els.
These indings unde sco e he po en ial ole o
i amin D as a ma ke o li e heal h and disease
se e i y, sugges ing ha assessmen and co ec ion
o i amin D de iciency may be an impo an
conside a ion in he managemen o ch onic li e
disease. O e all, main aining adequa e i amin D
le els could ha e implica ions no only o gene al
heal h bu also o op imizing li e unc ion and
po en ially mi iga ing disease p og ession.
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