ARTICLE
Auteur(s) : Ulker Gul, Müzeyyen Gonul, Ilhan Kaya,
Erkan Aslan
Ankara Numune Education and Research Hospital, 2nd.
Dermatology Clinic, Ankara, Turkey
accepté le 10 Decembre 2008
Psoriasis is a common and chronic inflammatory skin disease
which is characterized by an extremely increased rate of epidermal
turnover, and an activated mononuclear infiltrate in the underlying
dermis [1, 2]. It has been thought of primarily as a genetic
dermatosis. However, environmental and immunological factors
contribute to the ethiopathogenesis of psoriasis [3]. Interaction
between T lymphocytes and keratinocytes, via cytokines, is likely
to play a role in the pathogenesis of psoriasis [2]. Several
factors such as trauma, infections, endocrine factors and stress
may provoke a new episode of the disease [3]. Skin-directed T cells
play a role in the pathogenesis immunologically [1]. T cell
accumulation in skin and the response to immunosuppressive
treatments have implied that psoriasis is an autoimmune disorder.
Associations of psoriasis with other autoimmune disorders have also
been reported [4]. Autoimmune thyroid diseases (ATD) are
organ-specific autoimmune disorders characterized by the presence
of antibodies against the thyroglobulin, thyroid peroxidase, or
thyrotropin receptor autoantigens [5]. Data regarding ATD in
psoriasis are rare. We aimed to investigate if ATD are associated
with psoriasis.
Materials and methods
The study included 105 consecutive patients with psoriasis but
without psoriatic arthritis. The control group consisted of 96 sex
and age matched patients with tinea pedis. Exclusion criteria were
psoriatics or controls with known thyroid impairment, those using
thyroid hormones, anti-thyroid drugs or other drugs affecting
thyroid function, such as lithium, iodine, steroids, dopamine,
anticonvulsant drugs and interferon. All of the patients with
psoriasis were examined dermatologically and Psoriasis Area and
Severity Index (PASI) scores were calculated for each patient. Free
triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating
hormone (TSH) (chemilumminesence microparticle immunoassay-
Abbott), antithyroglobulin (AbTG), and antithyroidperoxidase
antibodies (AbTPO), (electrochemilumminesence immunoassay – Roche)
were measured in all of the subjects. Normal ranges for thyroid
hormones and autoantibodies were accepted as follows: FT3:
1.71-3.71 pg/mL, FT4: 0.70-1.48 ng/mL, TSH:
0.35-4.94 uIU/mL, AbTG: 0-34 IU/mL and AbTPO:
0-115 IU/mL. Thyroid ultrasonography was done to both
psoriasis patients and the control group. The findings of thyroid
ultrasonography were evaluated in five groups; normal
ultrasonographic findings, diffuse hyperplasia, thyroiditis,
nodules and thyroiditis plus nodules. Levels of TSH, FT3, FT4, AbTG
and AbTPO and ultrasonography results of patients and controls were
compared statistically with the Mann-Whitney U Test. The number of
subjects who had increased levels of TSH, FT3, FT4, AbTG and AbTPO
in both groups were compared by the Mann-Whitney U test. Also,
levels of TSH, FT3, FT4, AbTG, AbTPO and ultrasonography outcomes
of patients with psoriasis were compared to sex, disease duration,
PASI scores with Mann-Whitney U test.
Results
The ages and gender of the patients, the duration of psoriasis and
PASI scores are shown in table 1.
The levels of AbTPO, AbTG, FT3, FT4 and TSH could not be
measured and thyroid ultrasonography could not be done in all of
the subjects. The number of subjects in whom these investigations
could be done are shown in table 2. In
the patient group, 6 patients had increased AbTPO levels, 8
patients had increased AbTG levels, 3 patients had both increased
AbTPO and AbTG levels. In the control group, AbTPO levels were
increased in 6 individuals, AbTG levels were increased in 11
individuals and both of them were increased in 6 individuals (table 2). Most of the patients who had
increased AbTG and/or AbTPO were female in both groups. No
statistically significant difference was detected in the number of
the subjects who had increased AbTPO and AbTG between the patient
and control groups. In the patient group, 3 patients were diagnosed
as subclinical hypothyroidism, 2 as non-autoimmune hyperthyroidism,
2 as subclinical hyperthyroidism. Among the subjects in both
groups, no significant difference was found according to presence
of hypothyroidism and hyperthyroidism. However, when levels of TSH,
FT3, FT4, AbTG and AbTPO of patients and controls were compared by
Mann-Whitney U Test, the levels of FT4 were significantly higher in
patients than in controls, even though it was within the normal
range in the majority of cases (p < 0.001) but the levels of
TSH, FT3, AbTPO and AbTG were not statistically different between
two groups. When the levels of TSH, FT3, FT4, AbTG and AbTPO of the
patients with psoriasis were compared according to sex, duration of
disorders, PASI scores, a significant relation was found between
the duration of psoriasis and levels of AbTG. The patients who had
thyroiditis plus nodules in thyroid ultrasonography had
statistically longer disease periods (p < 0.003). The
ultrasonographic findings of the psoriasis patients were as
follows: nodular goiter in 19 patients, thyroiditis plus nodules in
7 patients, thyroiditis in 6 patients and diffuse goiter in 2
patients. In the control group, nodular goiter was diagnosed in 21
subjects, thyroditis plus nodules in 4 subjects, thyroiditis in 3
subjects and diffuse goiter in 2 subjects in thyroid
ultrasonography. No significant difference was found in
ultrasonographic findings between the patient and control groups,
because the number of subjects in each group (according to
ultrasonographic findings) was low.
Table 1 The features of the groups of patients and
controls
|
Age
|
Sex
|
PASI
|
Duration of psoriasis (month)
|
|
min
|
max
|
med
|
female
|
male
|
mean
|
min
|
max
|
mean
|
|
Psoriasis
|
9
|
84
|
42
|
57
|
49
|
4.9 ± 4.8
|
1
|
600
|
99.6 ± 120.0
|
|
Control
|
11
|
66
|
40
|
55
|
41
|
|
|
|
|
Table 2 The number of subjects in both groups according
to levels of FT3, FT4, TSH, AbTG, Ab TPO and ultrasonographic
findings
|
|
|
|
|
|
|
|
D
|
N
|
I
|
D
|
N
|
I
|
D
|
N
|
I
|
N
|
I
|
N
|
I
|
N
|
T
|
T+n
|
n
|
Dif
|
|
Psoriasis N: 106
|
3
|
95
|
5
|
0
|
96
|
7
|
4
|
94
|
3
|
85
|
11
|
93
|
9
|
66
|
6
|
7
|
19
|
2
|
|
N: 88
|
N: 95
|
N: 95
|
N: 93
|
N: 94
|
N: 67
|
|
Control N: 96
|
0
|
82
|
6
|
1
|
93
|
1
|
0
|
89
|
6
|
76
|
17
|
82
|
12
|
37
|
3
|
4
|
21
|
2
|
Discussion
The etiopathogenesis of psoriasis still remains obscure although
many developments are recorded in the treatment and pathogenesis of
psoriasis [6]. Local or topical anti-thyroid preparations have been
succesfully used in the treatment of psoriasis, although the
mechanism of action is unclear. It has been thought that
propylthiouracil increases the number of total and
suppressor/cytotoxic T cells and reduces activated lymphocytes in
psoriatic plaques [7, 8].
Increased serum total T4 and FT3 levels in psoriatic patients
have been reported previously [6]. We found that FT4 levels were
significantly higher in patients with psoriasis. This increase did
not correlate with PASI scores, sex, age of the patients and
duration of psoriasis. Thyroid hormone receptors are expressed in
human skin and are thought to be involved in the regulation of
epidermal proliferation and differentiation. Thyroid hormones cause
an increase in epidermal growth factor (EGF). EGF plays an
important role in cell proliferation. In psoriasis, increased
histochemical expression of the EGF receptor has been reported in
the epidermis [9]. This altered process of EGF receptor production
may be involved in the onset of psoriasis vulgaris [10]. Also,
another suggestion may be that increased T4 levels result from
psoriasis. Increased levels of T4 in non-thyroidal illness have
been reported. About 80% of the extrathyroidal T3 pool is produced
from T4 by monodeiodination with 5’-deiodinase enzyme in peripheral
tissues. The activity of the 5’-deiodinase enzyme may diminish in
some patients with nonthyroidal disease [11]. 5’-deiodinase enzyme
activity is regulated by proinflammatory cytokines such as
interleukin (IL) -1β, IL-6 and tumor necrosis factor (TNF) [12].
Cytokines like TNF, IL-1, IL-6, IL-7, IL-8, IL-15, IL-18, IL-19,
IL-20 and IL-23 are directly involved in psoriasis [13]. The reason
for the increased T4 levels in psoriasis may be related to the
increase in some cytokines in psoriasis.
ATD may be seen among patients with systemic autoimmune diseases
such as systemic lupus erythematosus, Sjogren’s syndrome or
rheumatoid arthritis [14, 15]. A few studies have shown a high
prevalence of thyroid autoimmunity in patients with psoriatic
arthritis [16, 17]. There are no data about an association of
psoriasis and ATD except a few case reports [18-20]. We found both
that levels of AbTPO and AbTG in patients with psoriasis and AbTPO
and AbTG positivities were not significantly different between the
two groups.
Neither the levels of Ab TPO and AbTG and nor the positivities
of Ab TPO and TG differed according to age, sex, duration of
disorders and PASI scores of psoriatic patients. Nodules and
thyroiditis findings in thyroid ultrasonography were significantly
higher in patients with psoriasis who had longer disease duration.
The increase of thyroiditis and nodules in ultrasonography in
patients with longer psoriasis durations may be due to an increase
in the age of those psoriatic patients. The frequency of thyroid
nodules increases with age [5].
To our knowledge, this is the first study that investigated ATD
in psoriatic patients without psoriatic arthritis. Our study showed
that the serum levels of thyroid autoantibodies did not change, but
FT4 levels can increase in psoriatic patients. The patients with
increased FT4 should be followed up with treatment of the psoriasis
and screening of the thyroid hormone levels to differentiate from
actual thyroid disorders. If it is needed, detailed investigations
should be done. Because the number of patients with thyroid
disorders were very small in our study, further studies are needed
to explain the relationship between psoriasis and thyroid hormones
and thyroid autoantibodies.
Acknowledgements
Conflict of interest: none. Financial support: none.
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