Serum zinc levels in seborrheic dermatitis: A case-control study

Abstract

Background/aim:
Malassezia colonization, sebaceous gland activity, hormones, immune system defects, environmental factors, and the interactions between these factors are thought to contribute to the pathogenesis of seborrheic dermatitis (SD). Zinc, an essential element, is involved in many biological processes including the ones that contribute to the development of SD. The aim of this study is to evaluate serum zinc levels in patients with SD.

Materials and methods:
Forty-three patients with SD and 41 healthy controls were enrolled in the study. Disease activity was assessed by the Seborrheic Dermatitis Area and Severity Index by a single dermatologist. Serum zinc levels of all subjects were evaluated.

Results:
Statistically significantly lower serum zinc levels were noted in SD patients than in the control group (79.16 ± 12.17 vs. 84.88 ± 13.59, respectively; P = 0.045).

Conclusion:
The results of the study demonstrated that patients who had SD had lower levels of serum zinc levels than healthy subjects.

Full text

1503
http://journals.tubitak.gov.tr/medical/
Turkish Journal of Medical Sciences
Turk J Med Sci
(2019) 49: 1503-1508
© TÜBİTAK
doi:10.3906/sag-1906-72
Serum zinc levels in seborrheic dermatitis: a case-control study
Ezgi AKTAŞ KARABAY1,*, Aslı AKSU ÇERMAN2
1Department of Dermatology and Venereology, Faculty of Medicine, Bahçeşehir University, İstanbul, Turkey
2Department of Dermatology and Venereology, Health Sciences University,
Şişli Hamidiye Etfal Training and Research Hospital, İstanbul, Turkey
* Correspondence: ezgiaktasmd@gmail.com
1. Introduction
Seborrheic dermatitis (SD) is a chronic inammatory
skin disease localized to areas rich in sebaceous glands,
such as the scalp, face, upper chest, and back [1]. Various
factors contribute to the pathogenesis of SD, including
hormonal factors, comorbidities (associated diseases),
individual immunological features, inammatory status,
and nutritional, environmental, and lifestyle factors, but
the exact etiology of the disease has not been claried [2].
Zinc is a mineral involved in many biological
processes, including immune functions and metabolic and
hormonal pathways. It may play a role in the dierent steps
of the cutaneous inammatory reactions, inhibiting the
chemotaxis of neutrophils, activating natural killer (NK)
cells, and modulating the production of proinammatory
cytokines. In addition, zinc displays antioxidant and
antiandrogen activity [3]. Zinc is considered a contributor
in the pathogenesis of several inammatory skin diseases
associated with innate immunity dysregulation, such as
inammatory acne, folliculitis decalvans, and hidradenitis
suppurativa (HS) [4]. It has been reported that patients
with severe acne and HS have lower serum zinc levels
than the healthy population [5–8]. Moreover, SD-like
dermatitis has also been reported to be associated with zinc
deciency [9,10]. Among many functions, zinc also plays a
role in some of the biological processes that contribute to
the development of SD. However, no reports are available
investigating serum zinc levels in patients with SD.
e aim of this study was to determine the association
between SD and serum zinc levels.
2. Materials and methods
e study was reviewed and approved by the local ethics
committee (protocol number: 22481095-020-1958, date
of approval: 19/09/2018), and all individuals gave written
informed consent. e study was carried out according to
the principles expressed in the Declaration of Helsinki.
A prospective case-control study was designed to
investigate the relationship between serum zinc levels and
SD. Forty-three patients diagnosed with SD by clinical
or histopathological examination were recruited from
a dermatology outpatient clinic. For comparison, 41
healthy age- and sex-matched controls with no evidence
of SD were recruited from among hospital sta volunteers.
Only those with a normal body mass index (BMI) (18.5–
25 kg/m2) were included. Subjects taking zinc salts or
Background/aim: Malassezia colonization, sebaceous gland activity, hormones, immune system defects, environmental factors, and
the interactions between these factors are thought to contribute to the pathogenesis of seborrheic dermatitis (SD). Zinc, an essential
element, is involved in many biological processes including the ones that contribute to the development of SD. e aim of this study is
to evaluate serum zinc levels in patients with SD.
Materials and methods: Forty-three patients with SD and 41 healthy controls were enrolled in the study. Disease activity was assessed
by the Seborrheic Dermatitis Area and Severity Index by a single dermatologist. Serum zinc levels of all subjects were evaluated.
Results: Statistically signicantly lower serum zinc levels were noted in SD patients than in the control group (79.16 ± 12.17 vs. 84.88
± 13.59, respectively; P = 0.045).
Conclusion: e results of the study demonstrated that patients who had SD had lower levels of serum zinc levels than healthy subjects.
Key words: Immune system, inammation, seborrheic dermatitis, zinc
Received: 13.06.2019 Accepted/Published Online: 18.08.2019 Final Version: 24.10.2019
Research Article
is work is licensed under a Creative Commons Attribution 4.0 International License.

1504
AKTAŞ KARABAY and AKSU ÇERMAN / Turk J Med Sci
multivitamins containing zinc, or under any systemic
treatment, including corticosteroids, retinoids, antifungal
agents, and immunosuppressants within 6 months of
the study, were excluded. Subjects with a history of any
disease or condition that can present with serum zinc
level alterations, such as inammatory acne, folliculitis
decalvans, enteropathic acrodermatitis, malabsorptive
diseases, malnutrition, strict diet, or high alcohol
consumption (more than 20g/day for women and more
than 30g/day for men) [11], were also excluded. Subjects
with any inammatory conditions that may be associated
with immune disruption, such as inammatory bowel
disease, rheumatoid arthritis, ankylosing spondylitis,
psoriasis, and any other systemic diseases (e.g., diabetes
mellitus, parathyroid or thyroid disorders, autoimmune
diseases, anemia, atopy, chronic renal or liver disease, and
malignancy), as well as currently pregnant or lactating
females and smokers, were also excluded. e data on
smoking relied on self-reports.
e data on baseline demographics, clinical
characteristics, and blood test results were obtained on
the same day. Serum zinc levels were measured in all
subjects using fasting venous blood samples. Venous
blood samples were drawn from the participants between
the hours of 09:00 and 11:00 AM following a 12-h fasting
period. e measurements of serum zinc levels were taken
with an atomic absorption spectrophotometric system
(PerkinElmer, Norwalk, CT, USA). Normal values were
dened as those above 60µg/dL and below 120µg/dL.
SD was graded according to the SD Area and Severity
Index (SDASI), which was modied from the Psoriasis
Area Severity Index (PASI) established by Cömert et
al. [12]. e SDASI was calculated at the time of blood
collection by a single dermatologist. According to this
scoring system, the erythema and desquamation of nine
dierent anatomical sites were graded on a scale between
0 and 3, where 0 = none, 1 = mild, 2 = moderate, and
3 = severe. e score of each site was multiplied by the
constant for the area (forehead [0.1], scalp [0.4], nasolabial
[0.1], eyebrow [0.1], postauricular [0.1], auricular [0.1],
intermammary [0.2], back [0.2], and cheek or chin [0.1]),
and the sum was determined as the SDASI score (range:
0–12.6) [12].
2.1. Statistical analysis
e Number Cruncher Statistical System 2007 program
(NCSS; Kaysville, UT, USA) was used for statistical
analysis. Descriptive data were expressed with mean ±
standard deviation, numeric variables, and percentages. In
the analysis of normally distributed variables, the Shapiro–
Wilk test and graphical analysis were applied to examine
the dierences between the two groups. In the analysis of
normally distributed variables, an independent samples
t-test was applied to examine the dierences between
the two groups. e Pearson chi-square test was used to
compare categorical variables. Correlation analysis was
performed by calculating Pearson and Spearman rank
correlations. Diagnosis and treatment tests (sensitivity,
specicity, positive predictive value, and negative
predictive value) and ROC analysis were used to dene
predictive values. P < 0.05 was considered statistically
signicant.
3. Results
A total of 43 patients with SD and 41 healthy control
subjects were included in the study. No signicant
dierences were observed in the sex ratio or ages between
the patients with SD and healthy controls (P > 0.05). e
mean disease duration among the SD patients was 17.49 ±
21.49 months, ranging from 1 to 120 months. e SDASI
scores of the patients ranged from 0.8 to 6.6, with a mean
of 2.79 ± 1.26.
Statistically signicantly lower serum zinc levels were
noted in SD patients than in the control group (79.16 ±
12.17 vs. 84.88 ± 13.59, respectively; P = 0.045).
e clinical characteristics of the study group are
shown in Table 1.
In ROC curve analysis, the cuto value for serum zinc
levels was assessed as 79 µg/dL with a sensitivity of 58.14%
and a specicity of 73.17%. e positive predictive value
was 69.4 and the negative predictive value was 62.5 (Table
2; Figure). No correlations were found between serum zinc
levels and disease duration (P = 0.658) or SDASI scores (P
= 0.273) (Table 3).
4. Discussion
SD is a chronic inammatory disease of the skin
characterized by erythematous, oily, yellow squames that
are located on sebum-rich areas, such as the face or the
forehead [13]. Although the exact etiology of the disease is
unknown, increased sebum activity, Malassezia infection,
immunological abnormalities, androgens, emotional
stress, diet, lifestyle, and environmental factors are thought
to contribute to the pathogenesis of the disease [14].
e male dominancy of SD and the development of
SD during puberty may indicate a signicant eect of
hormones, namely androgens, in the pathogenesis of the
disease [15].
Sebaceous gland activity is thought to be correlated
with SD development. e level of sebum production
and abnormalities of lipid composition are thought to
play a role in SD development and also provide a suitable
environment for Malassezia growth [16].
Malassezia, a fungal component of normal human
skin, is thought to play a role in the pathogenesis of SD
[17]. Since it is a lipid-dependent microorganism, it
is found on sebum-rich areas of the skin, similar to the

1505
AKTAŞ KARABAY and AKSU ÇERMAN / Turk J Med Sci
involvement sites of SD [18]. Malassezia hydrolyzes sebum
triglycerides into unsaturated fatty acids, such as oleic acid
and arachidonic acid, by its lipase [19]. e metabolites of
the yeasts induce inammation with the inltration of NK
cells and macrophages and an increased local production
of inammatory cytokines such as interleukin (IL)-1α, IL-
1β, IL-6, and tumor necrosis factor (TNF)-α in lesional
skin areas. ese metabolites stimulate keratinocyte
dierentiation, leading to abnormalities in the stratum
corneum that result in disruptions of the epidermal barrier
function and inammatory response [20,21].
Some evidence suggests that impairment in
the epidermal barrier function due to altered
corneodesmosomal hydrolysis, lipid disorganization, and
abnormalities in the desquamation process also contribute
to the pathogenesis of SD [20,21].
SD has been reported to be more common in
immunosuppressed patients, particularly those with HIV/
AIDS [13]. e immune or inammatory individual
response to Malassezia was also considered a contributory
factor [16,22]. Moreover, the levels of human leukocyte
antigens (HLAs), including HLA-AW30, HLA-AW31,
HLA-A32, HLA-B12, and HLA-B18, were reported to
be elevated in SD patients [22], in addition to reports of
increased levels of total serum IgA and IgG antibodies [23],
suggesting the potential immune mechanisms involved in
the pathogenesis of the disease.
e genetic components of SD have been studied
in animal models and humans [13]. Zinc nger 750
(ZNF7509) is a transcription factor controlling epidermal
dierentiation and an upstream regulator of MPZL3.
Autosomal dominantly inherited SD-like dermatitis has
been identied in a frameshi mutation in ZNF750 [24].
e functional pathway of ZNF750-MPZL3 has been
suggested to play an important role in the pathogenesis of
SD [25].
Nutritional deciencies, particularly of riboavin,
pyridoxine, niacin, and zinc, can also present as SD-like
dermatitis by an unknown mechanism [9,10]. Although
the exact pathogenesis is still unclaried on the basis of
several studies, SD is considered a multifactorial disease,
with immune, inammatory, and environmental factors
contributing.
Zinc is an essential element for the proper functioning
of several processes in the human body. Among these, zinc
plays a role in a number of skin disorders [26]. In both
acquired and inherited forms of hypozincemia, cutaneous
ndings, including perioricial and acral dermatitis,
alopecia, diaper rash, photosensitivity, nail dystrophy,
angular stomatitis, angular cheilitis, eczematous annular
Table 1. Demographic data of the subjects.
Group Test value
Total SD patients
(n = 43)
Control
(n = 41) P
Age (years) Min–max (median) 19−53 (29.5) 20−44 (28) 19−53 (31) t: –1.703
Mean ± SD 30.60 ± 6.37 29.44 ± 4,90 31.80 ± 7.49 a0.093
Sex Female 38 (45.2) 19 (44.2) 19 (46.3) χ2: 0.039
Male 46 (54.8) 24 (55.8) 22 (53.7) b0.843
Serum zinc levels (µg/dL) Min–max (median) 50−126 (81.5) 50−105 (77) 63−126 (82) t: –2.033
Meant ± SD 81.95 ± 13.12 79.16 ± 12.17 84.88 ± 13.59 a0.045*
aStudent t-test, bPearson chi-square test, *P < 0.05.
SD: Seborrheic dermatitis.
Table 2. Diagnostic scan and ROC curve results of serum zinc levels in seborrheic dermatitis.
Diagnostic scan ROC curve
P
Cut o Sensitivity Specicity Positive
predictive value
Negative
predictive value Area 95% condence
interval
Serum zinc levels (µg/dL) ≤79 58.14 73.17 69.4 62.5 0.623 0.502−0.744 0.044*
*P < 0.05.

1506
AKTAŞ KARABAY and AKSU ÇERMAN / Turk J Med Sci
plaques in areas of friction and pressure, dystrophic nails,
structural hair changes, and diminished growth of both
hair and nails, have been reported [27,28]. Zinc deciency
is reported in some inammatory skin disorders, including
atopic dermatitis [29], oral lichen planus [30], and Behçet’s
disease [31], and in autoimmune bullous diseases such
as pemphigus vulgaris [32], bullous pemphigoid [33],
epidermolysis bullosa [34], and melasma [35]. It is thought
that zinc plays a role in the development of these disorders
via its eects on the immune system [36]. Also, lower
serum zinc levels have been shown to be associated with
the occurrence of acne vulgaris [6,37]. In a recent review,
zinc was reported to be eective in the treatment of acne
vulgaris [26].
Among various functions, zinc plays a role in many
processes that may aect the development of SD [6,38–43].
Zinc aects the regulation of protein, lipid, and nucleic
acid metabolism, acting as a cofactor in metalloenzymes
and transcription factors. Zinc also plays a role in gene
transcription via a zinc-nger motif containing proteins
and factors. It also regulates cell replication, immune
activity, and wound repair. Zinc provides proper immune
activity by preserving macrophage and neutrophil
function and by stimulating NK cell and complement
activity. Zinc also has antiinammatory eects through the
inhibition of IL-6, TNF-α, nitric oxide, and integrin and
toll-like receptor expression by keratinocyte production
[6,41]. Additionally, the zinc nger-transactivating
protein A20 inhibits IL-1b and tumor necrosis factor-α
activation of nuclear factor (NF)-kB [43]. Moreover,
zinc has antiandrogenic activity through the inhibition
of 5α-reductase, which is the enzyme responsible for the
conversion of testosterone to dihydrotestosterone. is
also results in the suppression of sebaceous activity [6,43].
All the biologic processes mentioned above also
occur in the development of SD [9–20]. We believe that
zinc deciency may play a role in the pathogenesis of the
disease through various mechanisms. Additionally, topical
zinc combinations have been reported to be eective in
the treatment of SD [44]. Pierard et al. [44] reported that
topical zinc formulation may be eective in the treatment
of SD through the modulation of epithelial dierentiation,
antiinammatory and antibacterial activity, and the
inhibition of 5α-reductase, which provides antiandrogen
activity [44].
Since most of the mechanisms involved in the
development of SD are related to the functions of zinc, we
hypothesized that SD patients may have zinc deciency or
lower zinc levels. e results of the study demonstrated
that patients who had SD also had lower levels of serum
zinc levels compared with healthy subjects. However,
in the present study, serum zinc levels did not show any
correlation with disease severity, which was presented as
SDASI scores. We believe that there are two reasons for
that: the sample size was small, and the patients included
in the study had mild SD symptoms. It is known that 12.6
is the highest SDASI score that can be measured [12]; the
highest SDASI score assessed in this study group was 6.6,
while the mean score was 2.79 ± 1.26, which might be
considered a very mild presentation of SD.
e patients enrolled in the study had mild or moderate
forms of SD, which could be considered a limitation of
the study. In studies conducted with patients with higher
SDASI scores, the results might vary dramatically, perhaps
demonstrating zinc deciency. Small sample size is another
limitation of the study.
In conclusion, zinc has many properties that aect
inammatory processes, the immune system, and
Figure. ROC curve analysis of serum zinc levels in SD
Table 3. Relationship between serum zinc levels and disease
duration and SDASI.
Serum zinc levels
Disease duration (months) r 0.070c
P 0.658
SDASI r –0.171d
P 0.273
cr = Spearman rank correlation, dr = Pearson rank
correlation.
SDASI: Seborrheic Dermatitis Area and Severity Index.

1507
AKTAŞ KARABAY and AKSU ÇERMAN / Turk J Med Sci
epithelial dierentiation, and it has antifungal properties
and antiandrogenic eects, all of which also contribute
to the pathogenesis of SD. Based on these data and
the reports of SD-like dermatitis development in zinc-
decient individuals, we hypothesized that SD patients
might have lower serum zinc levels than those without
the disease. To date, no data are available on serum zinc
levels in SD. e present study revealed lower zinc levels
in SD patients compared with controls. Further research
on the association of zinc levels and SD will help identify
the pathogenesis of the disease and help develop more
ecacious disease management.
References
1. Berk T, Scheinfeld N. Seborrheic dermatitis. Pharmacology &
erapeutics 2010; 35 (6): 348-352.
2. Kastarinen H, Oksanen T, Okokon EO, Kiviniemi VV, Airola
K et al. Topical anti-inflammatory agents for seborrhoeic
dermatitis of the face or scalp. Cochrane Database of Systematic
Reviews 2014; 19; (5): CD009446. doi: 10.1002/14651858.
CD009446.pub2
3. Brocard A, Knol AC, Khammari A, Dréno B. Hidradenitis
suppurativa and zinc: a new therapeutic approach. A pilot study.
Dermatology 2007; 214 (4): 325-327. doi: 10.1159/000100883
4. Brocard A, Dréno B. Innate immunity: a crucial target for zinc
in the treatment of inammatory dermatosis. Journal of the
European Academy of Dermatology and Venereology 2011; 25
(10): 1146-1152. doi: 10.1111/j.1468-3083.2010.03934.x
5. Bae YS, Hill ND, Bibi Y, Dreiher J, Cohen AD. Innovative uses
for zinc in dermatology. Dermatologic Clinics 2010; 28 (3):
587-597. doi: 10.1016/j.det.2010.03.006
6. Ozuguz P, Dogruk Kacar S, Ekiz O, Takci Z, Balta I et al.
Evaluation of serum vitamins A and E and zinc levels according to
the severity of acne vulgaris. Cutaneous and Ocular Toxicology
2014; 33 (2): 99-102. doi: 10.3109/15569527.2013.808656
7. Amer M, Bahgat MR, Tosson Z, Abdel Mowla MY, Amer
K. Serum zinc in acne vulgaris. International Journal of
Dermatology 1982; 21 (8): 481-484.
8. Poveda I, Vilarrasa E, Martorell A, García-Martínez FJ, Segura
JM et al. Serum zinc levels in hidradenitis suppurativa: a case-
control study. American Journal of Clinical Dermatology2018;
19 (5): 771-777. doi: 10.1007/s40257-018-0374-5
9. Bukvic Mokos Z, Kralj M, Basta-Juzbasic A, Lakos Jukic I.
Seborrheic dermatitis: an update. Acta Dermatovenerologica
Croatica 2012; 20: 98-104.
10. Valia RG. Etiopathogenesis of seborrheic dermatitis. Indian
Journal of Dermatology, Venereology and Leprology 2006; 72:
253-255.
11. Boyle M, Masson S, Anstee QM. e bidirectional impacts of
alcohol consumption and the metabolic syndrome: cofactors
for progressive fatty liver disease. Journal of Hepatology 2018;
68 (2): 251267. doi: 10.1016/j.jhep.2017.11.006
12. Cömert A, Akbaş B, Kılıç EZ, Akın Ö, Gökçe E et al. Psychiatric
comorbidities and alexithymia in patients with seborrheic
dermatitis: a questionnaire study in Turkey. American Journal
of Clinical Dermatology 201; 14 (4): 335-342. doi: 10.1007/
s40257-013-0019-7
13. Wikramanayake TC, Borda LJ. Seborrheic dermatitis and
dandru: a comprehensive review. Journal of Clinical and
Investigative Dermatology 2015; 3 (2): 10.13188/2373-
1044.1000019. doi: 10.13188/2373-1044.1000019
14. Gupta AK, Bluhm R. Seborrheic dermatitis. Journal of the
European Academy of Dermatology and Venereology 2004; 18
(1): 13-26.
15. Naldi L, Rebora A. Clinical practice. Seborrheic dermatitis.
New England Journal of Medicine 2009; 360 (4): 387-396. doi:
10.1056/NEJMcp0806464
16. Ostlere LS, Taylor CR, Harris DW, Rustin MH, Wright S et al.
Skin surface lipids in HIV-positive patients with and without
seborrheic dermatitis. International Journal of Dermatology
1996; 35 (4): 276-279.
17. Hay RJ. Malassezia, dandru and seborrhoeic dermatitis: an
overview. British Journal of Dermatology 2011; 165 (Suppl. 2):
2-8. doi: 10.1111/j.1365-2133.2011.10570.x
18. Dawson TL Jr. Malassezia globosa and restricta: breakthrough
understanding of the etiology and treatment of dandru and
seborrheic dermatitis through whole-genome analysis. Journal
of Investigative Dermatology Symposium Proceedings 2007;
12 (2): 15-19. doi: 10.1038/sj.jidsymp.5650049
19. DeAngelis YM, Saunders CW, Johnstone KR, Reeder NL,
Coleman CG et al. Isolation and expression of a Malassezia
globosa lipase gene, LIP1. Journal of Investigative Dermatology
2007; 127 (9): 2138-2146. doi: 10.1038/sj.jid.5700844
20. Warner RR, Schwartz JR, Boissy Y, Dawson TL Jr. Dandru
has an altered stratum corneum ultrastructure that is improved
with zinc pyrithione shampoo. Journal of the American
Academy of Dermatology 2001; 45 (6): 897-903. doi: 10.1067/
mjd.2001.117849
21. Faergemann J, Bergbrant IM, Dohse M, Scott A, Westgate
G. Seborrhoeic dermatitis and Pityrosporum (Malassezia)
folliculitis: characterization of inammatory cells and
mediators in the skin by immunohistochemistry. British
Journal of Dermatology 2001; 144 (3): 549-556.
22. Sampaio AL, Mameri AC, Vargas TJ, Ramos-e-Silva M,
Nunes AP et al. Seborrheic dermatitis. Anais Brasileiros
de Dermatologia 2011; 86: 1061-1071. doi: 10.1590/s0365-
05962011000600002
23. Bergbrant IM, Johansson S, Robbins D, Scheynius A,
Faergemann J et al. An immunological study in patients
with seborrhoeic dermatitis. Clinical and Experimental
Dermatology 1991; 16 (5): 331-338.

1508
AKTAŞ KARABAY and AKSU ÇERMAN / Turk J Med Sci
24. Bhaduri A, Ungewickell A, Boxer LD, Lopez-Pajares V,
Zarnegar BJ et al. Network analysis identies mitochondrial
regulation of epidermal dierentiation by MPZL3 and FDXR.
Developmental Cell 2015; 35 (4): 444-457. doi: 10.1016/j.
devcel.2015.10.023
25. Karakadze MA, Hirt PA, Wikramanayake TC.
egenetic basis of seborrhoeic dermatitis: a review. Journal
of the European Academy of Dermatology and Venereology
2018; 32 (4): 529-536. doi: 10.1111/jdv.14704
26. Cervantes J, Eber AE, Perper M, Nascimento VM, Nouri K et
al. e role of zinc in the treatment of acne: a review of the
literature. Dermatologic erapy 2018; 31 (1): e12576. doi:
10.1111/dth.12576
27. Kumar P, Lal NR, Mondal AK, Mondal A, Gharami RC et al.
Zinc and skin: a brief summary. Dermatology Online Journal
2012; 18 (3): 1.
28. Maverakis E, Fung MA, Lynch PJ, Michael DJ, Ruben B et
al. Acrodermatitis enteropathica and an overview of zinc
metabolism. Journal of the American Academy of Dermatology
2007; 56 (1): 116-124. doi: 10.1016/j.jaad.2006.08.015
29. Kim JE, Yoo SR, Jeong MG, Ko JY, Ro YS. Hair zinc levels and
the ecacy of oral zinc supplementation in patients with atopic
dermatitis. Acta Dermato-Venereologica. 2014; 94 (5): 558-
562. doi: 10.2340/00015555-1772
30. Gholizadeh N, Mehdipour M, Naja S, Bahramian A, Garjani
S et al. Evaluation of the serum zinc level in erosive and non-
erosive oral lichen planus. Journal of Dentistry 2014; 15 (2):
52-56.
31. Saglam K, Serce AF, Yilmaz MI, Bulucu F, Aydin A et al.
Trace elements and antioxidant enzymes in Behcet’s disease.
Rheumatology International 2002; 22 (3): 93-96. doi: 10.1007/
s00296-002-0195-x
32. Yazdanpanah, MJ, Ghayour-Mobarhan M, Taji A, Javidi Z,
Pezeshkpoor F et al. Serum zinc and copper status in Iranian
patients with pemphigus vulgaris. International Journal of
Dermatology 2011; 50 (11): 1343-1346. doi: 10.1111/j.1365-
4632.2011.04968.x
33. Tasaki M, Hanada K, Hashimoto I. Analyses of serum copper
and zinc levels and copper/zinc ratios in skin diseases. Journal
of Dermatology 1993; 20 (1): 21-24.
34. Ingen-Housz-Oro S, Blanchet-Bardon C, Vrillat M, Dubertret
L. Vitamin and trace metal levels in recessive dystrophic
epidermolysis bullosa. Journal of the European Academy of
Dermatology and Venereology 2004; 18 (6): 649-653. doi:
10.1111/j.1468-3083.2004.01067.x
35. Rostami MM, Safavi AN, Iranparvar AM, Maleki N, Aghabalaei
DM. Evaluation of the serum zinc level in adult patients with
melasma: is there a relationship with serum zinc deciency and
melasma? Journal of Cosmetic Dermatology 2018; 17 (3): 417-
422. doi: 10.1111/jocd.12392
36. Wessels I, Maywald M, Rink L. Zinc as a gatekeeper of
immune function. Nutrients 2017; 9 (12): E1286. doi: 10.3390/
nu9121286
37. Rostami Mogaddam M, Safavi Ardabili N, Maleki N, Soaee
M. Correlation between the severity and type of acne
lesions with serum zinc levels in patients with acne vulgaris.
BioMed Research International 2014; 2014: 474108. doi:
10.1155/2014/474108
38. Azzouni F, Godoy A, Li Y, Mohler J. e 5 alpha-reductase
isozyme family: a review of basic biology and their role in
human diseases. Advances in Urology 2012; 2012: 530121. doi:
10.1155/2012/530121
39. Chow SC. Immunomodulation by statins: mechanisms
and potential impact on autoimmune diseases. Archivum
Immunologiae et erapiae Experimentalis 2009; 57 (4): 243-
251. doi: 10.1007/s00005-009-0038-5
40. Gupta M, Mahajan VK, Mehta KS, Chauhan PS. Zinc therapy
in dermatology: a review. Dermatology Research and Practice
2014; 2014: 709152. doi: 10.1155/2014/709152
41. Kitamura H, Morikawa H, Kamon H, Iguchi M, Hojyo S et
al. Toll-like receptor-mediated regulation of zinc homeostasis
inuences dendritic cell function. Nature Immunology 2006; 7
(9): 971-977. doi: 10.1038/ni1373
42. Sardana K, Chugh S, Garg VK. e role of zinc in acne and
prevention of resistance: have we missed the “base” eect?
International Journal of Dermatology 2014; 53 (1): 125-127.
doi: 10.1111/ijd.12264
43. Sugimoto Y, Lopez-Solache I, Labrie F, Luu-e V. Cations
inhibit specically type I 5 alpha-reductase found in human
skin. Journal of Investigative Dermatology 1995; 104 (5): 775-
778.
44. Pierard GE, Pierard-Franchimont C. Eect of a topical
erythromycin-zinc formulation on sebum delivery. Evaluation
by combined photometric-multi-step samplings with Sebutape.
Clinical and Experimental Dermatology 1993; 18 (5): 410-413.