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The genetic epidemiology of tinea versicolor in China

S.-M. He,
1,2
W.-D. Du,
1,2
S. Yang,
1,2
S.-M. Zhou,
1,2
W. Li,
1,2
J. Wang,
1,2
F.-L. Xiao,
1,2
S.-X. Xu,
1,2
and X.-J. Zhang
1,2
1
Department of Dermatology, Institute of Dermatology, First Hospital, Anhui Medical University, Hefei, Anhui Province and
2
Key Laboratory of Gene Resource
Utilization for Genetic Diseases, Ministry of Education, Anhui Province, China
Summary To study the clinical and epidemiological prole of Pityriasis versicolor (PV) and to
determine the possible genetic model for PV in Chinese Han, we investigated 503
patients with PV who were recruited by a questionnaire method. Statistical analysis,
heritability and complex segregation analysis were performed using EPI INFO 6.0, SPSS
10.0, the Falconer method and the SAGE-REGTL programs. In the total 503 PV patients,
the mean age of onset was 22.85 10.36 years. For male and female patients, the
peak ages of initial onset were both 2029 years. A total of 106 (21.1%) patients were
reported to have a positive family history of PV. The mean age of onset in males with
positive family history was earlier than those with negative family history (t = 3.58,
P < 0.01). Higher rate of recurrence and longer duration were seen in the patients
with positive family history than those with negative family history. The heritability of
PV in rst-, second- and third-degree relatives was 48.13%, 40.11% and 27.20%
respectively. Based on the REGTL results, the best model was a polygenic additive
model for PV.
Key words: tinea versicolor, pityriasis versicolor, genetic epidemiology, China.
Introduction
Tinea versicolor (Pityriasis versicolor, PV) is a mild,
chronic common supercial fungal infection of the skin
caused by Malassezia globosa, which belongs to the
resident ora of human skin.
1,2
Generally the Malassezia
is non-pathogenic. However under some predisposing
condition, including exogenous and endogenous, the
fungus can convert from a yeast to a pathogenic
mycelial form.
3,4
Although knowing high temperature
and humidity are a prerequisite for disease expression,
we puzzle why one gets the disease while others
apparently do not under the same circumstance. Fur-
thermore, some positive familial cases were reported in
more than one study,
5,6
while conjugal cases were less
commonly reported, indicating that hereditary factors
seem to play a role in the disease.
Pityriasis versicolor has a worldwide distribution.
Some studies on the prevalence of PV in the general
population have been carried out in the USA, Europe
and Africa.
79
However, there are few genetic epidemi-
ological researches on PV.
10
And also there are no
surveys of a large cohort of Chinese people with PV. The
intention of our study was to review the clinical and
epidemiological prole of PV in China and to determine
a possible genetic model for PV.
Materials and methods
Subjects
A total of 503 outpatients, referred to the First Afliated
Hospital of Anhui Medical University and Anhui Pro-
vincial Hospital and diagnosed with PV in the period
between January and November 2005, were enrolled in
our study. Also 963 normal controls without any skin
disease or autoimmune diseases such as diabetes,
rheumatoid arthritis, lupus or psoriasis were recruited
Correspondence: Xue-Jun Zhang, MD, PhD, Department of Dermatology,
Institute of Dermatology, First Hospital, Anhui Medical University, No. 81,
Meishan Road, Hefei, Anhui 230032, China.
Tel.: +86 551 516 1002. Fax: +86 551 516 1016.
E-mail: ayzxj@vip.sina.com
Accepted for publication 27 June 2007
Original article
2007 The Authors
Journal compilation 2007 Blackwell Publishing Ltd Mycoses 51, 5562 doi:10.1111/j.1439-0507.2007.01437.x
simultaneously with the PV patients. They were from
the same areas, and were matched with the PV patients
for sex and age.
Denitions
The clinical diagnosis of PV was conrmed by the
typical clinical manifestation and the nding of hyphae
and clusters of yeasts in potassium hydroxide micro-
scopic mounts (KOH) of scrapings.
Age of onset was dened as the age when the patient
was diagnosed as PV denitely in hospital for the rst
time.
Cutaneous fungal infections which were surveyed in
this study included tinea unguium, tinea corporis tinea
cruris, tinea manus tinea pedis.
Methods
After having diagnosed the illness as PV, every patient
(proband) was questioned in detail, using an identical
questionnaire in the outpatient clinic. General condi-
tions (including name, sex, current age), age of onset,
clinical classication, duration and season of onset,
co-existing disease, family history and numbers of
affected rst-, second- and third-degree relatives were
recorded. To increase the accuracy of this investiga-
tion, a parallel mycological examinations were also
made in the relatives of these patients, who all were
positive as well. Additionally, one member from the
probands families was requested to conrm the
answers about family history to reduce the possibility
of recall bias.
Records were put into EPI INFO 6.0 and converted into
the correct format for analysis using Statistical Package
for Social Sciences (SPSS 10.0; SPSS Inc., Chicago, IL,
USA). Statistical procedures used to analyse character-
istics of PV included frequencies, crosstabs and inde-
pendent-samples t-test. A level of P < 0.05 (2-sided)
was considered statistically signicant.
According to Falconers method,
11
we obtained
values for heritability (h
2
) in relatives of probands.
Using the prevalence rate of relatives of the proband and
the general population, heritability was calculated.
Heritabilityh
2
b=r; b x
c
x
r
=a
c
;
V 1=a
2
c
p=a
2
ra
A;
s

v
p
=R; q A=N;
where x
c
and x
r
represent the difference between the
average values of liability and threshold of controls and
relatives respectively; a
c
represents the difference
between the average values of liability of controls and
patients; b is the regression coefcient of relatives and
probands and r is the relationship coefcient. A and N
represent the number of patients and the sample size
respectively. p is equal to 1)q, v is the variance of b and
s is the standard error of h
2
.
A complex segregation analysis was performed to
evaluate possible models of inheritance of PV using SAGE
(Statistical Analysis for Genetic Epidemiology, version
5.0) REGTL programs (segregation analysis of a truncated
trait with logistic probability density function models 1
and 2). REGTL, based on the regression model of Bonney
[12] is a program set up for segregation analysis under a
class A regressive model (with the possibility of includ-
ing a common sibship component that depends on the
proportion of sibs affected) either of a truncated trait
such as age of onset of disease that follows a logistic
distribution (possibly after transformation, model 1), or
of susceptibility to the disease (model 2). The disease is
thus a discrete trait with variable age of onset. Under
model 1, genotype is presumed to inuence age of onset
through location susceptibility (dened as the probabil-
ity of being affected by age innity). Susceptibility may
be different for up to two affection classes. Under model
2, genotype is presumed to inuence susceptibility to the
affected state, but not to affect age of onset.
13
It is
appropriate to use model 1 for analysis of PV. Using a
logistic model, the logarithm of the odds ratio (h) for an
affected member of a certain family was assigned based
on type (y), sex (s), trait of mother (y
m
), trait of father
(y
f
) and assisting variable (x
1
x
n
); thus, the logarithm of
the odds ratio (h) for a particular member i of a family is:
h LogPy
i
1=Py
i
0
b
us
y c
m
y
m
c
f
y
f

1
x
1
. . .
n
x
n
for b
us
, u = alleles PV, ab or bb and s = $ or #.
The a allele was presumed as the susceptibility gene
for PV.
We tested a series of competing models including
Mendelian models (dominant and recessive), an envi-
ronmental model, a non-major-gene model, and a
multigene additive model. The natural logarithm of
likelihood (LnL) of a general unrestricted model was
calculated and compared with the hypothesis-bearing
models specied above with one or more pertinent
parameters restricted. To test a hypothesis about a
specic mode of inheritance, the likelihood ratio test
(LRT) statistic LRT = )2(LnL
general
) LnL
specic
) was
used, where specic indicates the model for a specied
hypothesis. The sampling distribution of this statistic is
well approximated by a v
2
with nk degrees of freedom
S.-M. He et al.
2007 The Authors
56 Journal compilation 2007 Blackwell Publishing Ltd Mycoses 51, 5562
where n and k equal the number of independent
parameters estimated in the general model and the
specic model respectively. When more than one model
was not rejected against the general model, the one with
the lowest Akaike information criteria (AIC)
14
was
considered the best model, where AIC = )2LnL + 2k.
Results
The total of 503 patients with PV consisted of 346
(68.8%) males and 157 (31.2%) females with a
male female ratio of 2.2 : 1. The mean age of the
whole patients was 24.95 11.15 years (range from
62 days to 61 years). The difference of mean age
between male (25.74 11.44 years) and female
(23.21 10.32 years) was signicant in the t-test
(t = 2.36, P < 0.05). The age of onset ranged from
1 month to 61 years (mean SD 22.85 10.36
years). The mean duration was 25.76 42.38 months
for all patients.
Distribution of the number of PV patients by the months
The peak months of onset between July and August are
in hot summer months (Fig. 1).
Relationship between phenotype and sex in PV
The mean age of onset in males and females was
23.45 10.51 and 21.53 9.91 years respectively,
and no statistically signicant difference was found
between two groups (t = 1.94, P > 0.05). Figure 2
shows the distribution by age of onset and sex of PV
patients. The number of males is larger than females in
each age of onset interval. A peak age of onset was seen
between 20 and 29 years for both males and females.
At the same time, the difference in duration between
male and female was also compared as shown in
Table 1. The number of recurrent PV patients in male
was higher than that in female, and longer duration
was seen in male than that in female, but there was no
signicant difference (P > 0.05).
Table 2 shows the frequency of co-existing diseases in
male and female patients with PV. A total of 245
patients with PV suffered from cutaneous fungal
co-infections, in 167 patients hyperhidrosis was found,
97 patients showed acne, 90 patients with seborrrheic
dermatitis and 30 patients with adiposity were seen in
our subjects. In our study, a few patients suffered from
diabetes, tumour and nephropathy. As Table 2 shows,
there is a male preponderance of co-existing other
fungal infestions and hyperhidrosis.
0
20
40
60
80
100
120
140
160
180
Jan Feb Mar Apr May Jun Jul Aug Sep Oct Nov
Months
N
o
.

o
f

P
V

p
a
t
i
e
n
t
s
Figure 1 Distribution by the number of pityriasis versicolor
(PV) patients and the month. The peak number of PV patients
was seen in hot summer months.
0
20
40
60
80
100
120
140
160
09
Age of onset interval (year)
N
o
.

o
f

p
a
t
i
e
n
t
s
Male
Female
1019 2029 3039 4049 5059 60
Figure 2 Distribution in the age of onset and sex of patients with
pityriasis versicolor (PV). The number of males is larger than
females in each age of onset interval. A peak age of onset was
seen between 20 and 29 years for both males and females.
Table 1 The recurrence and duration of
pityriasis versicolor with sex
Sex Initial (%) Recurrence (%) v
2
P-value Duration (months) t P-value
Male 164 (47.4) 182 (52.6) 1.61 >0.05 27.91 45.03 1.69 >0.05
Female 84 (53.5) 73 (46.5) 21.02 35.50
Genetic epidemiology of tinea versicolor in China
2007 The Authors
Journal compilation 2007 Blackwell Publishing Ltd Mycoses 51, 5562 57
Family conditions
Of the 503 probands, there were 106 patients (21.1%)
with a positive family history of PV (66 male and 40
female probands). No conjugal cases were found among
191 married subjects. Of 2145 rst-degree relatives of
probands, 114 had PV, giving a prevalence rate of
5.31%. Corresponding gures for second- and third-
degree relatives are 105 6379 (1.65%) and
32 11 348 (0.28%) respectively. A total of 963 normal
controls were recruited simultaneously. There were
4141 rst-degree relatives of control, of whom 51
suffered from PV with a prevalence rate of 1.23%. The
prevalence rates in the second-, third-degree relative of
controls were 0.8% (98 12 213) and 0.2%
(42 20 778) respectively.
Independent-samples t-test was used to determine
whether positive family history of PV had a potential
effect on ages of onset for sex. The mean age of onset
was 19.35 9.60 years in males with positive family
history, which was earlier than in males with negative
family history (24.42 10.50 years) (t = 3.58,
P < 0.01). However, there was no signicant difference
between the mean age of onset in females with and
without family history (t = 1.52, P > 0.05, Table 3). It
was not seen that both parents had PV in our study. The
mean age of onset of male probands with or without one
parent having PV was 16.01 6.43 and
24.21 10.56 years respectively, and the mean age
of onset of female probands was 17.66 10.50 and
22.30 9.65 years respectively. The difference was
signicant with the t-test (male: t = 4.31, P < 0.01;
female: t = 2.21, P < 0.05) in the above named groups
(Table 4).
Higher recurrence rate and longer duration were seen
in the patients with positive family history than with
negative family history (Table 5). This difference was
statistically signicant (P < 0.05).
Analysis of heritability
According to Falconers method, the heritability (h
2
) of
PV in rst-, second- and third-degree relatives of
probands was 48.13 3.41%, 40.11 5.63%,
27.20 14.48% respectively (Table 6). The prevalence
Table 2 Frequency of co-existing disease
in patients with pityriasis versicolor
between different sex
Co-existing disease Total (%)
Sex
v
2
P-value Male (%) Female (%)
Cutaneous fungal infections 245 (48.7) 184 (53.18) 61 (38.85) 8.87 0.003
Hyperhidrosis 167 (33.2) 133 (38.44) 34 (21.66) 13.72 0.001
Acne 97 (19.3) 65 (18.79) 32 (20.38) 0.18 0.67
Seborrrheic dermatitis 90 (18.1) 67 (19.63) 24 (15.29) 1.21 0.27
Adiposity 30 (6.0) 20 (5.78) 10 (6.37) 0.07 0.80
Diabetes 2 (0.4) 2 (0.58) 0 (0) 0.91 0.47
Tumour 1 (0.2) 1 (0.29) 0 (0) 0.46 0.69
Nephropathy 1 (0.2) 1 (0.29) 0 (0) 0.46 0.69
Tuberculosis 1 (0.2) 0 (0) 1 (0.64) 2.21 0.31
Table 3 Age of onset, sex and family
history distribution in patients with tinea
versicolor
Sex
With family history Without family history
t P-value N (%) Age of onset n (%) Age of onset
Male 66 (62.3) 19.35 9.60 280 (70.5) 24.42 10.50 3.58 <0.01
Female 40 (37.7) 19.48 11.15 117 (29.5) 22.23 9.41 1.52 >0.05
Table 4 Comparison of parents with or without pityriasis versi-
color (PV) on the age of onset
Sex
Age of onset
t P-value Parents with PV Parents without PV
Male 16.01 6.43 24.21 10.56 4.31 < 0.01
Female 17.66 10.50 22.30 9.65 2.21 < 0.05
Table 5 The recurrence and duration of
pityriasis versicolor in two groups
Family history Initial (%) Recurrent (%) v
2
P-value Duration (months) t P-value
Positive 43 (40.6) 63 (59.4) 4.10 <0.05 36.98 54.20 3.09 <0.05
Negative 205 (51.6) 192 (48.4) 22.76 38.14
S.-M. He et al.
2007 The Authors
58 Journal compilation 2007 Blackwell Publishing Ltd Mycoses 51, 5562
rate in rst-degree relatives was higher than that in
second-degree relatives and third-degree relatives.
Therefore, obviously, there is a clear hereditary ten-
dency in PV pathogenesis.
Complex segregation analysis
To explore the possible genetic model of PV, we
performed complex segregation analysis using the REGTL
program. Based on the REGTL results (Table 7), by both
LRT and AIC, the best model was an additive model for
PV (P > 0.05, AIC is the lowest).
Discussion
Although PV is reported worldwide, it is more fre-
quently observed in hot summer periods and humid
tropical regions with the prevalence as high as 20
50%.
1517
There are only few studies available on the
prevalence of PV in the general population in temperate
regions, such as Sweden, the USA, Turkey, Adana, with
the prevalence ranging from 0.3% to 3.5% respec-
tively.
7,8,18,19
The role of sex in propensity to development of PV is
still unclear. In Madras, the male female ratio was
3.3 : 1.
20
Similar results were reported from a couple of
Table 6 Prevalence rate of pityriasis versicolor in relatives of
probands, normal controls and heritability (h
2
s) in relatives of
probands
Number of
subjects
Number of
patients
Prevalence
rate (%) h
2
s(%)
Proband
Father 503 47 9.34
Mother 503 11 2.19
Sibs 891 47 5.27
Children 248 9 3.63
First degree
relatives
2145 114 5.31 48.13 3.41
Second degree
relatives
6379 105 1.65 40.11 5.63
Third degree
relatives
11348 32 0.28 27.20 14.48
Control
Father 963 21 2.18
Mother 963 8 0.83
Sibs 1726 17 0.98
Children 489 5 1.02
First degree relatives 4141 51 1.23
Second degree
relatives
12213 98 0.8
Third degree
relatives
20778 42 0.2
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Genetic epidemiology of tinea versicolor in China
2007 The Authors
Journal compilation 2007 Blackwell Publishing Ltd Mycoses 51, 5562 59
investigations
9,21
while others indicate that the inci-
dence of this infection is higher in women.
6,2224
The
male preponderance found in our study was evident
with a male female ratio of 2.2 : 1 and the number of
male was larger than female in each age of onset
interval. The higher prevalence of the disease in males
correlated with the higher sebaceous activity in males
than in females, suggesting that the activity of hor-
mones, especially androgens, could be important pre-
disposing factors of PV.
9
In fact, the true sex incidence
may be difcult to obtain, because most of the patients
have only cosmetic complains which may be due to
extra attention to beauty and skin hygiene. This might
partially explain the higher incidence of infection in
women in some studies. PV can arise at any age, but
most cases occurring during adolescence and young
adulthood.
25,26
This may be because of hormonal
changes and or increases in sebum secretion.
27
It is
uncommon in children and the elderly.
4,28
Our youn-
gest patient was a 1-year-old boy and the oldest was a
man aged 61 years. The mean age of onset (mean SD
22.85 10.36 years) of PV was consistent with that in
previous reports.
7
Similar to other investigations, the
highest prevalence of PV in our study was observed in
2029 year-old group with the mean age of onset
(22.85 10.36 years), suggesting that the peak of the
infection is coincided with ages when the sebum
production is in the highest level.
4,2830
The mean age
of initial onset in females (21.53 9.91 years) was
earlier than that in males (23.45 10.51 years), but
this difference was not statistically signicant. The
nding that the difference in onset age between the
sex is not statistically signicant is similar to that
reported by Roberts [5].
We also analysed the frequency of co-existing
diseases in patients with PV. From Table 2, cutaneous
fungal infections, hyperhidrosis, acne, seborrrheic der-
matitis, adiposity, diabetes, tumour and nephropathy
had been seen. We could demonstrate that there was a
male preponderance of complicating cutaneous fungal
co-infections and hyperhydrosis. The result may pos-
sibly partially be explained by the following reasons.
Firstly, the activity of hormones, especially androgens,
may be important predisposing factors leading to PV
which belongs to supercial fungal infections,
9
and
may play roles in a certain extent in the pathogenesis
of cutaneous fungal infections including tinea ungui-
um, tinea corporis tinea cruris, tinea manus tinea
pedis. Secondly, male often sweat more than female
because of the difference in physiological functions
between sexes. PV occurs when the yeast converts to
its mycelial form due to certain predisposing factors.
These factors can be further classied as exogenous or
endogenous.
4,31
Exogenous factors arousing the emer-
gence of PV involve high ambient temperature and
moisture, a possible reason why the disease is more
prevalent in the tropics than in temperate zone.
According to Borelli [32], climate has the greatest
impact on appearance, spread and relapse of PV.
Another exogenous factor may be occlusion of the skin
by clothing, cosmetics, creams and lotions.
4,33
Other-
wise, endogenous factors also contribute to the devel-
opment of PV. The lack of conjugal cases combined
with a positive family history suggests that hereditary
factors seem to play a role in the disease.
4
Further-
more, hyperhidrosis, malnutrition, immunosuppres-
sants, increased plasma cortisol level, Cushings
syndrome, diabetes, pregnancy and oral contraceptives
have all been implicated as endogenous fac-
tors.
4,5,29,3436
Our result is similar to the above
investigations.
Pityriasis versicolor is neither contagious, nor due to
poor hygiene,
16,31
because the hygiene of the clothing
(good or poor) or the habit of wearing shoes (always,
sometimes or never) had no signicant inuence on
the prevalence of PV.
9
The susceptibility to PV may be
genetically transferred, and that conjugal cases are
seldom found are in agreement with the impression
that PV is not contagious disease.
6
The lack of
conjugal cases combined with the common appearance
of PV in more than one member of a family suggests a
genetic component to susceptibility. A strong positive
family history of PV was investigated in western
countries, ranging from 5.8% to 39% of families.
5,6,10
Roberts reported a positive family history in consan-
guineous relations obtained in ve of 85 patients
(5.8%).
5
Faergemann and Fredriksson [6] reported a
positive family history in 18.8% of patients with a
sample size of 48. A similar result was surveyed from
Burke [29]. Hafez [10] also found a positive family
history of 39% in their prospective series of 300
patients. In our study, a positive family history of PV
was elucidated 21.1%. We divided all the PV patients
into those with positive and negative family history,
then compared their ages of initial onset. We found
that the mean age of initial onset was
19.35 9.60 years in males with positive family
history, which was earlier than that in males
(24.42 0.50 years) with negative family history
(t = 3.58, P < 0.01). However, there was no signi-
cant difference in females. We also found that patients
with positive family history recurred easily and had
longer duration of PV than patients with negative
family history. Even within the tropic countries,
S.-M. He et al.
2007 The Authors
60 Journal compilation 2007 Blackwell Publishing Ltd Mycoses 51, 5562
susceptibility can vary,
37
and among those prone to
infection, recurrence is almost inevitable.
There were 114 affected patients among 2145
rst-degree relatives (5.31%), 105 among 6379
second-degree relatives (1.65%) and 32 among
11 348 third-degree relatives (0.28%). According to
Falconers method,
11
we calculated the heritability of
PV in the rst-degree relatives to be 48.13%, second-
to be 40.11%, third- to be 27.20% respectively. Based
on the distribution of the disease in rst-, second- and
third-degree relatives, it seems that this susceptibility is
due to multifactorial inheritance.
10
At present, some
researchers agree that the pathogenesis of PV is
intimately related to heredity. However, Hafez [10]
described a genetic model of PV in 300 patients with
PV. This model showed a genetic susceptibility which
was inconsistent with any of the single gene defects
but fulls the criteria of multifactorial (genetic-envi-
ronmental) inheritance. We set up a genetic model of
PV using the method of complex segregation analysis.
The results suggest that the genetic model of PV does
not t a single-gene recessive or dominant mode of
inheritance. The environmental and non-transmitted
genetic models of inheritance are all rejected. This
reveals that inheritance of PV follows the polygenetic
additive model and that heredities play an important
role in the pathogenesis of PV, but excludes the
possibility of single-gene inheritance. In multifactorial
conditions, the risk is highest in the closest relatives,
and falls with more distant relationships. Our study
has conrmed the above viewpoint. As heritability is
lower than 70%, environmental factors may still play
an important role. The result agrees with the report,
which suggests the genetic model fulls the criteria of
multifactorial (genetic-environmental) inheritance.
10
Thus, environmental factors such as infection, high
temperature and humidity may serve as precipitat-
ing aggravating factors involving in the pathogenesis
of PV.
This is the rst time that the epidemiological prole
of PV has been reviewed at a larger scale in China.
Our ndings showed that most patients are adolescent
and young adulthood, and there seems to be a male
preponderance. Compared with the female patients,
male patients were likely to be affected by cutaneous
fungal infections and hyperhydrosis. The positive
family history has a potential impact on the age of
onset in male and frequence of onset. By analyses of
the prevalence of relatives of the probands with PV,
heritability and the possible genetic model for PV, it
is speculated that the effect of genetic factors is
important.
Acknowledgements
We thank all the patients concerned for their voluntary
participation in the present study. We thank all the
dermatologist of Anhui Provincial Hospital.
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