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Clinical research
Corresponding author:
Aldona Pietrzak MD, PhD
Department of Dermatology,
Venereology and
Pediatric Dermatology
Medical University
of Lublin
13 Radziwiłłowska St
20-080 Lublin, Poland
Phone: +48607305 501
E-mail:
aldonkapietrzak@o2.pl
1
Department of Dermatology, Venereology and Pediatric Dermatology,
Medical University of Lublin, Lublin, Poland
2
Orthopedics and Traumatology Department, Medical University of Lublin, Lublin,
Poland
3
Department of Clinical Immunology and Immunotherapy, Medical University
of Lublin, Lublin, Poland
4
Department of Experimental Hematooncology, Medical University of Lublin, Lublin,
Poland
5
Department of Hematology, St. John’s Cancer Center, Lublin, Poland
6
Department of Surgical Oncology, Medical University of Lublin, Lublin, Poland
7
Department of Paediatric Orthopaedics and Rehabilitation, Medical University
of Lublin, Lublin, Poland
Submitted: 20 December 2017
Accepted: 20 January 2018
Arch Med Sci
DOI: https://doi.org/10.5114/aoms.2018.74021
Copyright © 2018 Termedia & Banach
Serum lipid metabolism in psoriasis and psoriatic
arthritis – an update
Aldona Pietrzak1, Paweł Chabros2, Ewelina Grywalska3, Paweł Kiciński4,5,
Kinga Franciszkiewicz-Pietrzak6, Dorota Krasowska1, Grzegorz Kandzierski7
Abstract
Introduction: Psoriasis and psoriatic arthritis (PSA) are chronic, inflamma-
tory, systemic diseases characterized by metabolic abnormalities, including
an increased cardiovascular risk and an oxidative imbalance. This study
assessed blood parameters of lipid metabolism and markers of oxidative
stress in patients with psoriasis and PSA.
Material and methods: The study included 93 patients with psoriasis
(31 patients with PSA and psoriasis, 62 patients with psoriasis vulgar-
is), and 60 healthy, age-matched controls. Serum concentrations of the
glucose and the following lipid metabolism parameters were measured:
triglycerides (TG), total cholesterol (TC), low-density lipoproteins (LDL),
very low-density lipoproteins (VLDL), high-density lipoproteins (HDL), and
apolipoproteins Aand B (ApoA, ApoB). Oxidative status was determined
as serum concentrations of ox-LDL/MDA Adduct. The Psoriasis Area and
Severity Index (PASI) was used to determine disease severity.
Results: Among the three studied groups, controls had the highest HDL con-
centration (p < 0.001), patients with PSA had the highest ApoB concentra-
tion (p < 0.05), ApoA : ApoB ratio (p < 0.05), ox-LDL/MDA adduct concen-
tration (p < 0.001), and TC: HDL and LDL : HDL ratios (accordingly p < 0.05,
p < 0.01). In patients with psoriasis or PSA, oxidative status correlated pos-
itively with TC and ApoB concentrations.
Conclusions: In line with previous research, among patients with psoriasis
and PSA, we found lipid metabolism abnormalities and an oxidative imbal-
ance, which might be due to chronic inflammation in these conditions. Ef-
fective treatment of patients with psoriasis or PSA could reduce the risk of
cardiovascular diseases.
Key words: oxidative stress, cholesterol, apolipoprotein, lipid metabolism.
Aldona Pietrzak, Paweł Chabros, Ewelina Grywalska, Paweł Kiciński, Kinga Franciszkiewicz-Pietrzak, Dorota Krasowska, Grzegorz Kandzierski
2 Arch Med Sci
Introduction
Psoriasis is a chronic, inflammatory, systemic
disease that has many clinical forms. Psoriasis
presents most commonly as plaque psoriasis, but
some patients have psoriatic arthritis (PSA) [1–5].
Psoriatic arthritis involves inflammatory changes
in the joints (arthritis) and ligament attachments
(enthesitis), which can precede or accompany
psoriatic lesions, or occur as the only symptom of
the disease [6]. Typically, the rheumatoid factor is
absent in patients with PSA, but the human leu-
kocyte antigens (HLA) b27 or cw6 are present. In
Poland, of 800,000–1,000,000 patients with psori-
asis, at least 13,600 have PSA [3, 4]. An increasing
number of pediatricpatients with different types
of PSA has also been observed [7].
In psoriasis, chronic inflammation may lead to
oxidative stress and other metabolic alterations.
For instance, in patients with psoriasis, leukocyte
enzymes, such as proteolytic enzymes or myelop-
eroxidase, produce an excess of reactive oxygen
species (ROS), which leads to oxidative stress.
In the epidermis and psoriatic plaques, ROS oxi-
dize lipids, proteins, and low-density lipoproteins
(LDLs), which results in cell damage [2]. Notably, in
contrast to normal skin, the skin of patients with
psoriasis contains oxidized LDLs (oxLDLs) [8]. Be-
cause LDL oxidation is one of the earliest stages of
atherosclerosis, oxLDLs, which contain hundreds
of different oxidized lipoproteins, can serve as ath-
erosclerosis markers [1, 5, 9].
In addition to oxidative stress, metabolic risk
factors such as atherosclerosis, hyperlipidemia,
or insulin resistance are common among patients
with psoriasis [1, 10–15]. In patients with psoriasis
or PSA, several groups have found numerous lipid
alterations, including changes in concentrations of
total cholesterol (TC), low-density lipoprotein cho-
lesterol (LDL-C), triglycerides (TG), or lipoprotein
Lp(a), or decreased concentrations of high-density
lipoprotein cholesterol (HDL-C) [5, 16, 17]. More-
over, patients with psoriasis or PSA have dysfunc-
tional LDLs or HDLs, low-volume LDLs, and LDL ef-
flux disturbances [5, 11, 18]. Additionally, patients
with PSA might have apolipoprotein or oxLDL ab-
normalities, and PSA severity could be related to
the concentration of small, dense LDLs [9].
Dyslipidemia is the most widespread cardio-
vascular (CV) risk factor. Available results of sci-
entific research point to adirect link between the
concentrations of TC, LDL-C and non-HDL-C (total
cholesterol concentration minus HDL cholesterol
concentration) and the risk of myocardial infarc-
tion (MI), stroke and fatal cardiovascular disease
(CVD) [19]. Pol-SCORE is auseful tool used for the
estimation of total CV risk of patients in primary
prevention. The VARO study demonstrated im-
proved identification of high-risk individuals and
greater adherence to current treatment guidelines
and modern drug therapy [20]. Psoriasis is afac-
tor increasing CV risk which is not included in Pol-
SCORE. Patients with these diseases have higher
CV morbidity and mortality rates compared with
the general population [19].
It is worth noting that in the general population
children of parents who had coronary heart dis-
ease (CHD) had significantly higher levels of TC,
low-density LDL-C, glucose, and body weight as
compared to those without aparental history. This
emphasizes the need for greater attention to be
paid to primary prevention efforts to control risk
factors in children of CHD patients [21], especially
with coexisting psoriasis.
Because oxidative stress and lipid alterations
can co-occur in psoriasis or PSA, this study inves-
tigated parameters of lipid metabolism and oxida-
tive stress in patients with psoriasis and PSA [22].
Material and methods
Participants
This study was approved by our local Bioethics
Committee. All participants signed informed con-
sent before enrolment to the study. The study con-
sisted of 31 patients with PSA and 62 patients with
psoriasis. The control group comprised 60 healthy,
age-matched volunteers without psoriasis or oth-
er systemic diseases. We excluded participants
who received medications that could affect lipid
metabolism (thiazides, β-blockers, local or system-
ic hormonal formulations, statins, fibrates). Pa-
tients did not receive local retinoids or dithranol.
PSA was diagnosed according to the “Classifica-
tion Criteria for Psoriatic Arthritis” (CASPAR). The
Psoriasis Area Severity Index (PASI) was used to
determine the severity of psoriatic skin lesions in
patients with psoriasis or PSA. The percentage of
skin affected by psoriatic lesions was determined
with an assumption that apatient’s hand repre-
sented 1% of the total body surface area.
Laboratory studies
Blood samples were collected after an over-
night fast (12–14 h) and deposited in additive-free
vacutainer tubes to obtain serum by low-speed
centrifugation at 4°C. Lipid and glucose concen-
trations were determined in fresh serum samples.
The TC concentration was measured with acol-
orimetric method with cholesterol esterase and
oxidase, the HDL-C concentration was measured
with adirect enzymatic-colorimetric method with
polyethylene glycol (PEG)-modified cholesterol es-
terase and oxidase, and the triglyceride (TG) con-
centration was measured with an enzymatic-col-
orimetric method with phosphoglycerol oxidase.
The LDL-C concentration was calculated according
Serum lipid metabolism in psoriasis and psoriatic arthritis – an update
Arch Med Sci 3
to the Friedewald formula. We used the Cobas
Integra 400 analyzer with commercially available
reagents (Roche Diagnostics, Japan).
The remaining measurements were performed
in frozen serum samples, which were stored at
–80°C before use. Serum levels of apolipoproteins
Aand B (ApoA and ApoB) were determined by an
immunonephelometric method in aBehring neph-
elometer (BNA) and ox-LDL/MDA Adduct concen-
tration was measured with an enzyme-linked im-
munosorbent assay (ox-LDL/MDA Adduct ELISA
Kit, Immundiagnostik AG, Germany).
Moreover, the following cardiovascular risk
parameters were calculated: the TC : HDL ratio
(Castelli index I); the LDL-C : HDL-C ratio (Cas-
telli index II), the ApoB : ApoA ratio, the LDL-C :
ApoB ratio, and the Atherogenic Index of Plasma
(AIP) calculated according to astandard formula:
log(TG : HDL-C) [22].
Statistical analysis
The Shapiro-Wilk test was used to test for nor-
mality. For comparisons between two groups, Stu-
dent’s t-test or the Mann-Whitney test was used
depending on data distribution. For comparisons
among more than two groups, the Kruskal-Wallis
test was used, and the multiple comparisons of
mean ranks test was used for post hoc compar-
isons when significant differences were found
in the Kruskal-Wallis test. Correlations were as-
sessed with the Spearman rank correlation coef-
ficient. P-value < 0.05 was considered significant.
The Statistica 10.0 software was used for all cal-
culations.
Results
Table Ipresents the mean age, body mass index
(BMI), and systolic and diastolic blood pressure in
patients with psoriasis, patients with PSA, and
controls.
Table II presents clinical characteristics of pa-
tients with psoriasis and patients with PSA. Dis-
ease duration and disease severity, assessed with
the PASI, were statistical important greater in pa-
tients with PSA than in patients with psoriasis (Ta-
ble II). Among the three studied groups, controls
had the highest HDL-C concentration (p < 0.001)
and patients with PSA had the highest ApoB con-
centration (p < 0.05), ApoA:ApoB ratio and ox-
LDL/MDA Adduct concentration (respectively p <
0.05, p < 0.001). The studied groups did not differ
significantly with respect to the remaining labo-
ratory parameters (Table III). Moreover, patients
with PSA had the highest TC : HDL-C and LDL-C
: HDL-C ratios (respectively p < 0.05, p < 0.01; Ta -
ble IV). In the combined group including patients
with psoriasis and PSA, the ox-LDL/MDA Adduct,
indicating the oxidative status, correlated with the
TC (Rs = 0.34; p < 0.05) and ApoB concentrations
(Rs = 0.39; p < 0.01; Table V). These correlations
were non-significant in controls.
Table I. Mean age, body mass index, and systolic and diastolic blood pressure in the studied groups
Parameter Psoriatic arthritis
(n = 31)
Psoriasis vulgaris
(n = 62)
Controls
(n = 60)
P-value
Mean Standard
deviation
Mean Standard
deviation
Mean Standard
deviation
Age [years] 40.68 7.38 40.87 11.05 41.02 9.84 0.9880
BMI [kg/m2]27.52 4.13 26.48 4.34 26.31 4.08 0.2514
SBP [mm Hg] 126.71 16.39 126.34 16.57 127.15 11.39 0.6119
DBP [mm Hg] 83.35 10.63 79.82 14.60 82.33 8.11 0.3689
BMI – body mass index, SBP – systolic blood pressure, DBP – diastolic blood pressure.
Table II. Clinical features of patients with psoriasis and psoriatic arthritis
Parameter Psoriatic arthritis
(n = 31)
Psoriasis vulgaris
(n = 62)
P-value
Mean Standard
deviation
Mean Standard
deviation
Duration of psoriasis vulgaris [years] 16.75 13.19 9.25 10.12 < 0.001
Duration of psoriatic arthritis [months] 10.35 12.91 –––
PASI 28.07 5.87 26.00 6.54 < 0.05
% of total body surface affected by
psoriatic lesions
38.64 13.95 35.83 15.59 0.2438
PASI – Psoriasis Area Severity Index.
Aldona Pietrzak, Paweł Chabros, Ewelina Grywalska, Paweł Kiciński, Kinga Franciszkiewicz-Pietrzak, Dorota Krasowska, Grzegorz Kandzierski
4 Arch Med Sci
Discussion
Our study confirmed that patients with psori-
asis or PSA have lipid metabolism alterations and
an oxidative imbalance. In our study, we found
significant alterations of the HDL-C, ApoB, and ox-
LDL/MDA Adduct concentrations, which were ele-
vated in patients with psoriasis or PSA. Moreover,
among patients with psoriasis or PSA, oxidative
stress was associated with higher TC and ApoB
concentrations.
Psoriasis and PSA are systemic diseases asso-
ciated with an increased risk of metabolic syn-
drome, cardiovascular diseases, and major cardio-
vascular events [1–3, 5, 10, 12, 15–17, 19, 23–25].
In the 1920s, Ishimaru and Lortat-Jacob described
lipid metabolism abnormalities among patients
with psoriasis and showed how these abnormal-
ities influenced the disease course. In the 1930s,
Grutz and Burger hypothesized that lipid intesti-
nal absorption might be related to skin function,
and they referred to psoriasis as “lipoidosis”. In
1963, Melczer described arelationship between
the progression of psoriasis and lipid metabolism
[26]. Subsequent research confirmed that patients
with psoriasis or PSA have numerous lipid profile
alterations, with increased serum concentrations
of TC, LDL-C, and TG being the most frequent
abnormalities. Moreover, patients with psoria-
sis tend to have reduced HDL-C, ApoA, and ApoB
concentrations [8, 10, 17, 16]. In a recent study
performed in Spain among 358 patients with pso-
riasis (disease length, 10–25 years), 41.6% had
hypercholesterolemia, including 65 patients who
received lipid-lowering medications; moreover,
47.6% of patients with PSA had hypercholester-
olemia, compared to 39.8% of patients with pso-
riasis. In addition, in that study, 20.7% of patients
had documented prior cardiovascular events [12].
Table III. Laboratory characteristics in the studied groups
Parameter Psoriatic arthritis
(n = 31)
Psoriasis vulgaris
(n = 62)
Controls
(n = 60)
P-value
Mean Standard
deviation
Mean Standard
deviation
Mean Standard
deviation
Glucose [mg/dl] 89.97 14.77 83.55 11.06 81.65 11.06 0.0519
TC [mg/dl] 214.27 40.08 193.54 39.75 203.42 39.23 0.0637
HDL-C [mg/dl] 45.69 11.59 48.40 12.15 53.07 11.69 < 0.001
LDL-C [mg/dl] 129.56 32.92 112.92 27.93 118.31 35.23 0.0798
VLDL [mg/dl] 33.00 19.25 25.09 10.42 25.50 15.47 0.1268
TG [mg/dl] 157.21 98.01 127.70 52.95 132.17 84.70 0.4156
ApoA [mg/dl] 1.31 0.40 1.31 0.41 1.26 0.40 0.7500
ApoB [mg/dl] 1.13 0.42 0.98 0.33 0.90 0.27 < 0.05
ApoA : ApoB ratio 0.90 0.27 0.24 0.76 0.76 0.27 < 0.05
Ox-LDL [µmol/l] 420.79 335.79 390.26 311.04 84.99 83.81 < 0.001
TC – total cholesterol, HDL-C – high-density lipoprotein cholesterol, LDL-C – low-density lipoprotein cholesterol, VLDL – very low-density
lipoprotein, TG – triglycerides, ApoA – apolipoprotein A, ApoB – apolipoprotein B, Ox-LDL – oxidized LDL.
Table IV. Cardiovascular risk parameters in the studied groups
Parameter Psoriatic arthritis
(n = 31)
Psoriasis
(n = 62)
Controls
(n = 60)
P-value
Mean Standard
deviation
Mean Standard
deviation
Mean Standard
deviation
TC : HDL-C ratio 5.00 1.68 4.17 1.15 4.01 1.15 < 0.05
AIP 0.48 0.31 0.40 0.22 0.33 0.31 0.0541
LDL-C : HDL-C ratio 3.03 1.07 2.47 0.87 2.33 0.89 < 0.01
ApoB : ApoA ratio 0.88 0.28 0.77 0.20 0.76 0.27 0.0534
LDL-C : ApoB ratio 125.33 43.57 125.76 41.12 144.41 47.01 0.0755
TC – total cholesterol, HDL-C – high-density lipoprotein cholesterol, LDL-C – low-density lipoprotein cholesterol, ApoB – apolipoprotein B,
ApoA – apolipoprotein A, AIP – atherogenic index of plasma.
Serum lipid metabolism in psoriasis and psoriatic arthritis – an update
Arch Med Sci 5
Astudy involving 246 patients with psoriasis, per-
formed in Poland, found that, compared to con-
trols, patients with psoriasis had an abnormal
concentration of HDL-C but not of other blood
lipids [14]. In a study performed among 15,484
patients from South Korea, 10.94% had dyslipid-
emia, including 14.88% of patients with PSA and
10.39% of patients with psoriasis [15]. In line with
previous research, our study found that patients
with PSA had more atherogenic lipid profiles than
patients with psoriasis [27, 28]. Moreover, in our
study, patients with PSA or psoriasis differed from
controls with respect to all the studied parame-
ters, except for the ApoA concentration.
Evidence shows that chronic inflammation
can cause structural protein changes, including
creation of neo-epitopes, which, in turn, triggers
autoantibody production and HDL alterations.
Moreover, patients with an increased cardiovas-
cular risk have elevated levels of autoantibod-
ies against HDLs and apolipoprotein AI [29, 30].
These autoantibodies are regarded as biomark-
ers of cardiovascular diseases among patients
with autoimmune disorders. Anti-aHDL and anti-
aApo-AI antibodies were also detected in patients
with psoriasis, and their presence correlated with
greater disease severity [18]. Moreover, these au-
toantibodies could be involved in atherosclerotic
plaque development in patients with psoriasis
[30, 31]. However, among the many lipid alter-
ations observed in psoriasis, it is difficult to dis-
tinguish between those specific to psoriasis and
those associated with dyslipidemia [31].
OxLDLs contribute to atherosclerosis progres-
sion because they activate monocyte infiltration
and smooth muscle cell proliferation. Numerous
studies have reported that patients with psoriasis
have elevated oxLDL levels. Among 45 patients
with moderate psoriasis severity (mean PASI: 14.0
±8.3), Sunitha et al. found acorrelation between
the PASI and anti-oxLDL and oxLDL concentrations.
Moreover, compared to controls, patients with pso-
riasis had ahigher anti-ox-LDL : oxLDL ratio, which
indicated greater oxidative stress [32]. Patients
with psoriasis were found to have oxLDLs in the
epidermis and serum [5, 8, 11, 24, 25, 32], as well
as antibodies against HDLs or apolipoprotein AI [30,
31]. Tekin et al. also found significantly elevated ox-
LDL and anti-oxLDL concentrations in patients with
psoriasis, particularly in the upper part of the epi-
dermis; in contrast, normal skin did not contain ox-
LDLs or anti-oxLDL antibodies [8]. Also, in patients
with psoriasis, the oxLDL concentration correlated
with the BMI. In contrast to most studies on lipid
alterations in psoriasis, Gerdes et al. and Gkalpa-
kiotis et al. did not find significant differences be-
tween patients with psoriasis and controls with
respect to the oxLDL concentration [24, 25].
It is hypothesized that an increased cardiovas-
cular risk among patients with autoimmune dis-
Table V. Correlation between oxidative activity and the studied parameters in patients with psoriasis or psoriatic
arthritis and in controls
Parameter Patients with psoriatic arthritis
or psoriasis
Controls
Rs P-value Rs P-value
TC 0.34 < 0.05 0.21 0.2549
HDL-C 0.23 0.1224 0.06 0.7384
LDL-C 0.23 0.1187 0.27 0.1316
VLDL –0.02 0.8896 0.18 0.3122
TG –0.07 0.6210 0.18 0.3122
ApoA 0.26 0.0900 0.12 0.5263
ApoB 0.39 < 0.01 –0.07 0.7091
ApoA : ApoB ratio 0.25 0.0939 –0.08 0.6582
TC : HDL-C ratio 0.08 0.5777 0.11 0.5618
API –0.15 0.3076 0.10 0.5878
LDL-C : HDL-C ratio 0.11 0.4475 0.12 0.5231
ApoB : ApoA ratio 0.24 0.1159 –0.10 0.6100
LDL-C : ApoB ratio –0.25 0.0934 0.28 0.1253
TC – total cholesterol, HDL-C – high-density lipoprotein cholesterol, LDL-C – low-density lipoprotein cholesterol, VLDL – very low-density
lipoprotein, TG – triglycerides, ApoA – apolipoprotein A, ApoB – apolipoprotein B, API – atherogenic index of plasma. Significant correlations
are marked in bold.
Aldona Pietrzak, Paweł Chabros, Ewelina Grywalska, Paweł Kiciński, Kinga Franciszkiewicz-Pietrzak, Dorota Krasowska, Grzegorz Kandzierski
6 Arch Med Sci
eases could be associated with the duration and
severity of inflammatory changes. For instance,
dyslipidemia affects mostly patients with severe
psoriasis or PSA [16]. However, in psoriasis, the
exact mechanisms that link chronic inflammation
to lipid metabolism alterations remain unknown.
Moreover, it remains unclear whether chronic in-
flammation is the cause or the effect of lipid metab-
olism alterations. To date, numerous studies have
investigated potential molecular mechanisms that
could underlie the association between psoriasis
and cardiovascular diseases, including shared ge-
netic factors or inflammatory pathways, secretion
of adipokines, insulin resistance, lipoprotein struc-
ture and function, angiogenesis, oxidative stress,
microparticles, and hypercoagulability. Moreover,
it is hypothesized that due to skin shedding with
psoriatic plaques, patients with psoriasis lose nu-
merous substances, such as interleukin 18 (hu-
man leukocyte elastase inhibitor), cathepsin G,
C5a/C5adesarg, and lipids (ca. 60 g each month)
[17, 33–36]. Moreover, compared to the non-le-
sioned skin, cholesterol concentration in psoriatic
plaques is 5 times as high. Among patients with
rheumatoid arthritis, Oliviero et al. found that the
levels of ApoAI and TC were reduced in serum but
elevated in the synovial membrane [37]. Those
authors suggested that HDLs may accumulate in
the inflamed joints, which can inhibit pro-inflam-
matory cytokine production. Alternatively, ApoAI
sequestration in the inflamed joints could lead to
low HDL serum levels, which would result in an
elevated cardiovascular risk among patients with
rheumatoid arthritis or PSA [37]. Orgaz-Molina et
al. found that vitamin D concentration correlated
with the levels of total cholesterol, LDLs, and TG
only in patients with psoriasis who did not have
joint involvement [27].
Currently, treatment targets in patients with
PSA include not only preservation of joint function
but also improvement of physical functioning, re-
duction of dactylitis, enthesitis, and reduction of
skin and nail changes [6]. The occurrence of au-
toimmune, rheumatic or inflammatory diseases,
such as psoriasis and PSA, is not an indication for
the preventive use of lipid-lowering drugs. Mea-
sures for the prevention and treatment of dys-
lipidemia do not differ from generally applicable
rules [19]. In view of current research, treating
lipid alterations should also become part of care
in patients with psoriasis. Studies show that mod-
erate physical exercise increases antioxidative
enzyme activity (e.g., superoxide dismutase) and
reduces serum concentrations of total cholesterol,
LDL-C, and oxidized lipids [38]. Because statins, in
addition to lowering lipid serum concentrations,
can reduce disease severity in psoriasis, some
patients with psoriasis could benefit from statin
treatment.
In conclusion, lipid metabolism abnormalities
and oxidative stress are common among patients
with psoriasis and PSA. Every patient should be
evaluated to determine total CV risk for the pur-
pose of ensuring appropriate patient education
and making decisions on the intensity of treat-
ment [19]. Effective treatment of patients with
psoriasis or PSA could reduce the risk of cardio-
vascular diseases.
Acknowledgments
The authors would like to express their grati-
tude to Proper Medical Writing Ltd. for assistance
in writing this manuscript.
Conflict of interest
The authors declare no conflict of interest.
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