Rheumatology
"&
#
#
'
,
" 7& 8/
' '9 : ;
, ' #
#
;
"
#
'
"
" "
&
,
#
#
"
$
)
'- + %# . /
+
1- 2 1 2 1.
+ - "' ". # *#
#
,0
/
-
"
,
4
"
"3
1 5 1-
" #
"
6
* "
7 %%4 %" '
1 7 < % * 6 *+ = * +
%* =* %- 3
7 < % * 6 *+ = * + %* =* %- >
, ,
7 /%2* ?+?32 = %?* + / =? = - %
"
#
#
!
" 1
#
$7
4
*
% % %
w
ie
ev
"
#
"
rR
5
+
(
ee
* '
rP
Fo
% &'
!
Page 1 of 34
Title: Psoriatic Arthritis in Asia
Authors:
Lai-Shan Tam1, Ying-Ying Leung2, Edmund K Li1.
From
1
Department of Medicine & Therapeutics, The Prince of Wales Hospital, The Chinese
Fo
University of Hong Kong; 2Department of Medicine, North District Hospital, Hong
Kong
ee
rP
Address correspondence and reprint requests to:
Dr Edmund K Li
rR
Department of Medicine and Therapeutics, The Prince of Wales Hospital, The
Chinese University of Hong Kong, Shatin, Hong Kong.
ev
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
E-mail: edmundli@cuhk.edu.hk , phone: (852) 2632-3128, fax: (852) 2637-3852
Short title: Psoriatic arthritis (PsA) in Asia
1
Rheumatology
Abstract
Geographic or ethnic differences in the occurrence of disease often provide insights
into causes of disease and possible opportunities for disease prevention. A wide
variation on the incidence and prevalence of psoriatic arthritis (PsA) were reported in
different countries. The prevalence in China appeared to be similar to the rest of the
world, while the incidence and prevalence of PsA was much lower in Japan. Amongst
Fo
patients with psoriasis, 6–42% of Caucasians were reported to have PsA, but figures
were lower from Asian countries (1-9%). Divergent distribution of HLA in different
rP
ethnic groups and other genetic determinants and may account for these prevalence
ee
differences. PsA affects men and women almost equally in Chinese, Japanese and
Iranian similar to their Caucasian counterparts. Polyarthritis developing in the forth
rR
decade was the commonest pattern of arthritis among Chinese, Indians, Iranian,
ev
Kuwaitian Arabs and Malays. Arthritis mutilans and eye lesions have rarely been
reported in Asian countries. Chinese patients with nail disease and distal
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 2 of 34
interphalangeal joints involvement have a significantly higher risk of developing
deformed joints. More data are required on the safety, efficacy and cost effectiveness
of TNF blockers for the treatment of PsA in Asia. Premature atherosclerosis has been
recognized as an important comorbidity in Asian patients with PsA. Increased
2
Page 3 of 34
prevalence of traditional cardiovascular risk factors associated with PsA suggested
that the two conditions may share the same inflammatory pathway. Carotid
intima-media thickness can identify PsA patients with subclinical atherosclerosis who
may benefit from early intervention.
Key words: Psoriatic arthritis, Asia, epidemiology, premature atherosclerosis
Fo
ev
rR
ee
rP
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
3
Rheumatology
Introduction
Psoriatic arthritis (PsA) is an inflammatory arthritis associated with psoriasis. PsA is
characterized by the absence of rheumatoid factor and certain clinical features,
including asymmetric distribution of arthritis, distal interphalangeal involvement
(DIP), enthesitis, dactylitis, spondylitis, and the association with HLA-B27. Based on
these characteristics, PsA has been classified with the HLA-B27 associated
Fo
spondyloarthritis (SpA). Researchers have remarked that ethnic and geographic
differences exist in the prevalence, clinical manifestations and prognosis of SpA (1).
rP
SpA in the nonwhite Caucasians, Asians, and Africans run a different course when
ee
compared with white Caucasians, and the association between B27 and disease is less
strong in some of these populations in whom cross-reacting antigens and other genetic
rR
determinants may be more important (1). Whether there are any ethnic differences in
ev
the prevalence, clinical manifestations and prognosis in PsA have never been studied
in detail, and they may possibly provide further insight into the underlying etiology of
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 4 of 34
this condition. Estimates of prevalence of PsA can also provide information regarding
the burden of the disease and would allow provision for health services for patients
with PsA. Premature atherosclerosis has been recognized as an important
co-morbidity in chronic inflammatory conditions including rheumatoid arthritis (RA)
4
Page 5 of 34
and systemic lupus erythematosus (2, 3). Recent data from Asian countries also
support the hypothesis that inflammation associated with PsA contributes to
accelerated atherosclerosis. In this article, recent advances in research on PsA from
Asians countries are reviewed.
Epidemiology
Fo
PsA was recognized by the American College of Rheumatology (ACR) as a distinct
clinical entity since 1964 (4). However, the first study on prevalence and incidence of
rP
PsA was published only in 1996 (5). The results of a recent systematic review
ee
suggested a wide variation on the incidence and prevalence of PsA in different
countries (5). Based on retrospective and cross-sectional studies, the prevalence of
rR
PsA ranged between 20 to 420 per 100,000 population in Europe and USA. The
ev
incidence of PsA was similar between 5 European and 1 US studies that ranged
between 3.0 to 23.1 per 100,000 population, but data from Asia is limited (5). From
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
population-based surveys in China, the prevalence of PsA appeared to be similar to
the rest of the world, ranging from 10 to 100 per 100,000 population (6). Interestingly,
amongst Japanese, there is a 64 and 180 - fold lower incidence with prevalence
between 0.1 and 1 per 100,000 population as compared to the median incidence and
5
Rheumatology
prevalence of all other studies (7). A multi-ethic study reported that PsA to be
significantly more common among Indians compared to the ethnic distribution of the
Singapore population (8).
Amongst patients with psoriasis, 6–42% from Europe, USA and South Africa were
reported to have PsA (9), but figures were lower from Asian countries. PsA was
observed in 9% of patients with psoriasis in Iran (10) Korea (11) and India (12), 5%
Fo
in China (13), 2% in Turkey (14) and 1% in Japan (15). A Singaporean study also
reported Indians with psoriasis had twice the risk of developing PsA when compared
rP
to Chinese (8), suggesting different ethnicities may affect the development of PsA.
ee
Studies to date on incidence and prevalence for PsA have been limited by small
rR
cross-sectional studies, selective study populations, limited follow-up, and PsA
ev
classification criteria lacking diagnostic sensitivity. More recently, the Classification
of Psoriatic Arthritis (CASPAR) group has developed classification criteria for PsA
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 6 of 34
with a sensitivity of 91.4% and a specificity of 98.7% (16). Population based studies
using this new criteria reported a point prevalence of 150 per 100,000 person (17),
and an incidence between 6 (17) and 7.2 (18) per 100,000 person in Denmark and
USA respectively.
PsA was clinically recognized in less than 10% of psoriasis
6
Page 7 of 34
patients during their lifetime (19). The CASPAR criteria should facilitate
epidemiologic studies of PsA in Asia.
Genetic studies
The reasons for the differences in prevalence may be due to genetic differences,
environmental exposures or a combination of both. Cumulated evidence indicates PsA
Fo
is a diseases caused by the concerted action of multiple disease genes, triggered by
environmental factors. Several studies reported linkage between specific human
rP
leukocyte antigen (HLA) and PsA (20-23). Divergent distribution of HLA was
ee
documented among different reports, suggesting HLA distribution varies with
different ethnic groups. HLA-B16, -B17, -B27 and -Cw6 were associated with PsA in
rR
Caucasians (20), while HLA-A2, -B46, -DR8, and –B27 were associated with PsA in
ev
Japanese (21). A recent study from Taiwan showed HLA-Cw12 to be associated with
PsA, whereas HLA-B58 and -DR17 appeared to be protective (22). In Israeli patients,
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
PsA was associated with HLA-A3, -B13, -B38, -DRB0101, and -DRB0301 (23).
HLA-B27 was not associated with PsA in patients from Israel (23) and Korea (11).
7
Rheumatology
Tumor necrosis factor - α (TNF-α) gene is also mapped within the HLA region, and
its product has been reported as one of the most important cytokines in the
pathogenesis of PsA. There are conflicting reports on the association between
TNF-α-238G/A polymorphism and PsA (24); studies from Japan and Taiwan did not
find any associations (25, 26). In Caucasians, TNF-α and -β gene polymorphism (26),
HLA Cw 0602, class I major histocompatibility complex chain-related gene A (MICA)
- A9,
killer immunoglobulin-like receptor (KIR) 2DS1/S2 (27-30), were associated
Fo
with PsA, and TNF-α and -β gene polymorphism was associated with the presence of
joint erosions in PsA, and progression of joint erosions in early PsA (26). Different
rP
from the Caucasians, TNF-α and -β, HLA Cw 0602, KIR 2DS1/S2, MICA - A9, and
ee
other cytokine gene polymorphism were not associated with PsA in Chinese patients
from Taiwan (31). In addition, PsA patients from Taiwan showed elevated expression
rR
of free HLA class I heavy chains on peripheral blood monocytes compared with
ev
psoriasis patients without arthritis (32). When cytochrome p450 1A1 (CYP 1A1) and
manganese superoxide dismuatse (MnSOD) gene polymorphisms were assessed in
Chinese patients from Taiwan,
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 8 of 34
CYP 1A1 4887A and 4889G were reported to be
associated with PsA, but these were not associated with the manifestations and
severity of PsA (33). MnSOD 1183C polymorphisms may be associated with PsA,
while MnSOD 1183T appeared to be protective from the development of this disease
8
Page 9 of 34
(34). The role of the I-allele of angiotensin-converting enzyme (ACE) gene I/D
polymorphism was controversial in SpA patients from Kuwait (35, 36).
Clinical features of PsA
Five clinical patterns were described by Moll and Wright among patients with PsA
(37): DIP, asymmetrical oligoarticular, symmetric polyarticular, spondylitis, and
Fo
arthritis mutilans. The exact frequency of the patterns is variable but oligoarthritis was
the most commonly reported pattern (37). The clinical features of PsA patients from
rP
Asian countries are summarized in Table 1 together with the largest PsA series from
ee
Toronto for comparison (8, 10-12, 23, 36, 38-42). A number of racial differences in
the clinical presentations of PsA were observed. PsA affects men and women almost
rR
equally in Caucasians (43). Studies from Hong Kong, Singapore (8, 40), Japan (39)
ev
and Iran (10) also reported the same; while others noted a male predominance (11, 12,
23, 38, 41, 44) and 1 study reported a female predominance from Kuwait (36).
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
Polyarthritis developing in the 4th decade was the commonest pattern of arthritis
among Chinese from Hong Kong (40) Singapore (8); Indians (8, 38) ; Iranian (10)
Kuwaitian Arabs (36), Malays (8) and Thai patients (44). On the other hand,
9
Rheumatology
oligoarthritis was the predominant pattern in patients from Israel (23), Japan (39) and
rural India (12). Spondylitis was the most common pattern of PsA in Korea (11) and
Chinese from Taiwan (41). Clinically apparent lumbar spondylitis was significantly
more common in Indians than Chinese from Singapore, 45% was asymptomatic when
present in Chinese and was detectable only on radiological examination (8). Arthritis
multilans was rarely reported in all the studies from Asian regions. The frequency of
distribution of the patterns has also varied in previous Caucasian studies (43), and
Fo
may be explained partly by the different definitions used by individual investigators,
or the changing patterns over time. Those with longer disease duration tend to develop
rP
into the polyarticular pattern (45).
ev
rR
Extra-articular manifestations
ee
The majority (51.2 % to 97.5%) of patients developed arthritis after the onset of
psoriasis, and psoriatic vulgaris was the most common form of psoriasis reported (8,
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 10 of 34
10-12, 23, 38-41). Nail lesions were common in PsA, affecting 30.2 % to 97.0% of
patients, and was significantly more prevalent compared with psoriasis patients
without arthritis in 1 study (10). The prevalence of dactylitis and enthesitis ranged
from 15.4 % to 71.4 % and 7.8 % to 59.1 % respectively. Eye lesions were rarely
10
Page 11 of 34
reported in PsA patients in Asia (1.7% -3.9%) (8, 36, 38, 44).
Aortic incompetence was reported in less than 4% of patients with PsA (46). Other
cardiac involvement in PsA included subtle involvement of the atrioventricular node
(47), and diastolic dysfunction (48) in reports from Israel and Turkey respectively. A
recent study from Spain did not find any differences in echocardiographic
abnormalities between PsA and healthy controls (49).
Fo
Predictors for clinical features and prognosis
ee
rP
The association with HLA antigens and disease expression varies in Caucasians PsA
patients (20, 50-52), e.g HLA-B27(20, 50-52), Cw1 (51), Cw2 (20), DRw52 (20), and
rR
DQw3 (50) were associated with back involvement, whereas B38 and B39 were
ev
associated with polyarthritis (20). Studies from Taiwan reported an association
between HLA-B27 and the development of sacroiliitis (22, 41), uveitis (22) but not
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
peripheral arthritis (41). A report from Israel found significant association between
DIP involvement and the presence of HLA-A26 and -B38, while HLA-DRB0301 was
related to spinal involvement (23).
11
Rheumatology
Predictors for progression in Caucasian PsA included five or more swollen joints, a
high medication level at presentation (53), polyarticular onset (54), HLA-B27 in the
presence of HLA-DR7, HLA-B39, and DQw3 in the absence of DR7 (55). Similar to
Caucasians, Chinese PsA patients with positive HLA-B27 tend to develop deformed
joints (p=0.068) as well as having elevated levels of C-reactive protein (p=0.072),
although these results did not attain significance (41). In contrast, Chinese PsA
patients with nail disease and DIP joints involvement had significantly increased risk
Fo
of developing deformed joints (41).
rP
Quality of life and function in PsA
ee
Instruments validated for the assessment of quality of life and function in PsA
rR
included Medical Outcome Survey Short Form 36 (SF-36) (56) and the Health
ev
Assessment Questionnaire (HAQ) (57) respectively. Patients with PsA demonstrated
impaired quality of life and reduced function, comparable to patients with rheumatoid
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 12 of 34
arthritis (RA) (57-59). In a study from Hong Kong, one-third reported PsA related
unemployment and change in job nature (60). Another one third experienced a
reduction in income due to PsA. Multivariate analysis identified higher damaged joint
count, poorer patients' perception of health, poor socioeconomic factor and higher
12
Page 13 of 34
CRP as factors associated with higher HAQ. This study highlighted a significant
social-economic impact in Chinese subjects with PsA. Joint damage was found to be
associated with functional impairment.
Management of PsA
Diagnosis of PsA
Fo
Treatment recommendations for PsA have been recently published by the Group for
rP
Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) (61). The
ee
group recommended that diagnosis of PsA should follow the CASPAR criteria.
However, the sensitivity and specificity may vary with different ethnicities. The
rR
CASPAR criteria for PsA has recently be validated in Chinese populations (62). Data
ev
were collected prospectively from consecutive Han Chinese with PsA and other
chronic inflammatory arthritis. Subjects were classified according to Moll and Wright;
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
or CASPAR criteria. 108 (53 male and 55 female) subjects with PsA were recruited.
Data was compared with 195 controls with RA (n = 154), ankylosing spondylitis (n =
41) and undifferentiated arthritis (n = 1). The sensitivity and specificity of Moll and
Wright criteria were 85.2 % and 100 %. The sensitivity and specificity for the
13
Rheumatology
CASPAR criteria were 98.2 % and 99.5 %, which is similar to reported values in
European populations. The CASPAR criteria performed well in Chinese population
that is very different from populations they were developed, and have a higher
sensitivity in classifying PsA.
Treatment of PsA
Fo
Most rheumatology units in Asia have adopted treatment guidelines from Europe or
USA. The therapeutic strategies outlined in the treatment recommendations were
rP
based on review of literature and expert consensus from mainly North America and
ee
Europe (61). Although this may be appropriate on the whole, there may be subtle
differences in the pharmacokinetics, clinical response, as well as side effects of the
rR
drugs used. Few therapeutic trials on PsA have been performed in Asia, and data on
ev
safety and efficacy of disease modifying anti-rheumatic drugs (DMARDs) and
biologics in PsA from most of these countries are lacking. A survey from 112 PsA
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 14 of 34
patients from Singapore reported that DMARDs were commonly used (67% on
sulphasalazine and 14% on methotrexate (MTX)) (63), and case series from
Singapore and India suggested that MTX may be safe and effective (64, 65).
14
Page 15 of 34
Treatment guideline for the use of tumor necrosis factor-α (TNF-α) blockers in Asian
patients with rheumatic diseases including PsA has been published from Lebanon,
while the guideline from Japan targeted RA patients only (66, 67). The guideline for
the prevention of latent tuberculosis reactivation in rheumatic disease patients given
TNF-α blockers was published from Israel (68). Reports from Israel (69) and Taiwan
(70) suggested that TNF-α blockers were effective and well tolerated in PsA. A
postmarketing surveillance study of 5000 Japanese RA patients treated with
Fo
infliximab showed that infliximab in combination with low-dose MTX was well
tolerated (71). Nonetheless, a study from Korea reported an increased risk of TB
rP
reactivation in RA patients treated with TNF blockers (72), and another report from
ee
Japan noticed a higher risk of pneumocystis pneumonia (73). Etanercept was found to
be cost effective in Japanese patients with RA (74). More data are required on the
rR
safety, efficacy and cost effectiveness of TNF blockers for the treatment of PsA in
Asia.
iew
Co-morbidity-Premature atherosclerosis in PsA
ev
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
Patients with PsA may experience substantial morbidity and unfavorable outcomes at
referral centers (75, 76), although investigators from other center did not report a
15
Rheumatology
Deleted: In a mortality study in PsA
significant increase in mortality in unselected patients (77). Mortality data of Asian
patients from Toronto, the first leading
causes of death were diseases of the
PsA patients were lacking, nonetheless, investigators from Hong Kong and Israel
circulatory (36.2%) system (75). An
increased in death rate of 1.3 due to
have ascertained the prevalence and risk factors for premature atherosclerosis in
cardiovascular diseases (CVD) was noted
compared to general population (75).
patients with PsA.
Although m
In a study by Kimhi et al. from Israel (78), the prevalence of traditional CVD risk
factors including smoking, altered lipid profile, hypertension and diabetes mellitus
Fo
(DM) were similar between 30 PsA patients and age-matched controls, although the
body mass index (BMI) was significantly increased in the patient group. On the
rP
Deleted: ,
contrary, Han et al. from the US (79) reported a higher prevalence ratio of type II DM,
Deleted: using a large administrative
database,
ee
hyperlipidaemia and hypertension in PsA patients compared with controls. To address
Deleted: In addition, PsA patients had
the central question if individuals with PsA have an increased prevalence of CVD risk
rR
significantly increased systolic and
diastolic blood pressures, insulin
factors, a study from Hong Kong compared CVD risk factors between 102
resistance and inflammatory markers
(high-sensitive C-reactive protein (hsCRP)
ev
consecutive PsA patients and 82 controls (40). The BMI of PsA patients was
and white cell count) compared to
controls. Higher HDL cholesterol and
significantly higher than healthy controls. PsA patients had a higher prevalence of
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 16 of 34
apolipoprotein (Apo) A1 levels; and
lower total cholesterol (TC) and low
DM and hypertension, but a lower prevalence of low high density lipoprotein (HDL)
density lipoprotein cholesterol (LDL)
levels; and a lower TC/HDL ratio were
cholesterol after adjusting for the BMI. Further adjustment for hsCRP level rendered
observed in PsA. However, the Apo B
level was higher in PsA patients.
the differences in the prevalence of hypertension and DM non-significant between the
Deleted: ; the TC, and sugar levels; and
white cell count
PsA and controls. These data support the hypothesis that PsA may be associated with
Deleted: ; while the differences in other
parameters remained significant
16
Page 17 of 34
Deleted: , dyslipidaemia
obesity, hypertension and insulin resistance because of the shared inflammatory
pathway.
Early diagnosis of atherosclerosis in PsA might trigger more aggressive prophylaxis.
Increased intima-media thickness (IMT) of the carotid artery, a sign of early
atherosclerosis (80) has been reported in PsA patients from Spain and Israel (78,
81-83). Increased IMT significantly correlated with traditional risk factors including
Fo
age (78, 82), BMI (78), uric acid (83), triglycerides (82), TC and LDL cholesterol
levels (81); and disease related parameters including age at the time of PsA diagnosis
rP
(81), disease duration (78, 81), spine involvement (78), erythrocyte sedimentary rate
Deleted: ¶
ee
(ESR) (78), and fibrinogen (78) levels. A study from Hong Kong reported an
¶
Whether subclinical atherosclerosis as
increased prevalence of subclinical atherosclerosis in Chinese, defined as the average
rR
determined by carotid ultrasound can
refine CV risk assessment in patients with
of IMT measures above the 95th percentile of healthy controls (84). Using logistic
PsA will be of great interest.
Deleted: IMT was measured using
ev
regression analysis, independent explanatory variables associated with subclinical
carotid ultrasonography in 82 consecutive
PsA patients and 82 healthy controls
atherosclerosis in PsA included increased sugar and total triglyceride levels. The
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
Framingham risk score (FRS) was similar in PsA patients with or without subclinical
atherosclerosis. Twenty-six (35%) of 74 patients had subclinical atherosclerosis
despite having a low cardiovascular risk according to the FRS. These studies
suggested that carotid IMT can identify PsA patients with subclinical atherosclerosis
17
matched on age, sex, and ethnicity.
Rheumatology
who may benefit from early intervention.
Deleted: ¶
Characterized by their capacity to
transform into mature endothelial cells,
Conclusions
endothelial progenitor cells (EPCs)
participate in ongoing endothelial repair,
while an imbalance between endothelial
damage and repair may lead to an
A wide variation on the incidence and prevalence of PsA have been reported in
increase in cardiovascular events (85). A
study from Israel reported no significant
different countries, ranging from 10 to 100 per 100,000 population in China to 1 per
difference between numbers of EPCs
between healthy controls, patients with
100,000 population in Japan. Amongst Asian patients with psoriasis, 1–9% was
Fo
reported to have PsA. Divergent distribution of HLA in different ethnic groups and
EPCs in the cardiovascular morbidity of
psoriasis and PsA.¶
other genetic determinants may account for these prevalence differences. Polyarthritis
developing in the 4th decade was the commonest pattern of arthritis among Asian PsA
ee
patients, while arthritis mutilans and eye lesions were rarely reported. More data are
rR
required on the safety, efficacy and cost effectiveness of TNF blockers for the
treatment of PsA in Asia. An increased prevalence of traditional CVS risk factors and
ev
subclinical atherosclerosis has been reported in patients with PsA, including Asian
patients. CVS risk factors should be routinely monitored and treated aggressively in
iew
high risk patients.
psoriasis and PsA (86). The results of this
study do not support a significant role for
rP
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 18 of 34
18
Page 19 of 34
References
1.
Lau CS, Burgos-Vargas R, Louthrenoo W, Mok MY, Wordsworth P, Zeng QY.
Features of spondyloarthritis around the world. Rheum Dis Clin North Am
1998;24(4):753-70.
2.
Roman MJ, Shanker BA, Davis A, Lockshin MD, Sammaritano L, Simantov R,
et al. Prevalence and correlates of accelerated atherosclerosis in systemic lupus
Fo
erythematosus. N Engl J Med 2003;349(25):2399-406.
3.
Roman MJ, Moeller E, Davis A, Paget SA, Crow MK, Lockshin MD, et al.
rP
Preclinical carotid atherosclerosis in patients with rheumatoid arthritis. Ann Intern
Med 2006;144:249 - 256.
ee
4. O'Neill T, Silman AJ. Psoriatic arthritis. Historical background and epidemiology.
Baillieres Clin Rheumatol 1994;8(2):245-61.
ev
5.
rR
Alamanos Y, Voulgari PV, Drosos AA. Incidence and prevalence of psoriatic
arthritis: a systematic review. J Rheumatol 2008;35(7):1354-8.
6.
Zeng QY, Chen R, Darmawan J, Xiao ZY, Chen SB, Wigley R, et al. Rheumatic
diseases in China. Arthritis Res Ther 2008;10(1):R17.
7.
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
Hukuda S, Minami M, Saito T, Mitsui H, Matsui N, Komatsubara Y, et al.
Spondyloarthropathies in Japan: nationwide questionnaire survey performed by the
19
Rheumatology
Japan Ankylosing Spondylitis Society. J Rheumatol 2001;28(3):554-9.
8.
Thumboo J, Tham SN, Tay YK, Chee T, Mow B, Chia HP, et al. Patterns of
psoriatic arthritis in Orientals. J Rheumatol 1997;24(10):1949-53.
9.
Gladman DD. Psoriatic arthritis. Dermatol Ther 2009;22(1):40-55.
10. Jamshidi F, Bouzari N, Seirafi H, Farnaghi F, Firooz A. The prevalence of
psoriatic arthritis in psoriatic patients in Tehran, Iran. Arch Iran Med
2008;11(2):162-5.
Fo
11. Baek HJ, Yoo CD, Shin KC, Lee YJ, Kang SW, Lee EB, et al. Spondylitis is the
most common pattern of psoriatic arthritis in Korea. Rheumatol Int 2000;19(3):89-94.
rP
12. Prasad PV, Bikku B, Kaviarasan PK, Senthilnathan A. A clinical study of
ee
psoriatic arthropathy. Indian J Dermatol Venereol Leprol 2007;73(3):166-70.
13. Fan X, Yang S, Sun LD, Liang YH, Gao M, Zhang KY, et al. Comparison of
rR
clinical features of HLA-Cw*0602-positive and -negative psoriasis patients in a Han
ev
Chinese population. Acta Derm Venereol 2007;87(4):335-40.
14. Kundakci N, Tursen U, Babiker MO, Gurgey E. The evaluation of the
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 20 of 34
sociodemographic and clinical features of Turkish psoriasis patients. Int J Dermatol
2002;41(4):220-4.
15. Kawada A, Tezuka T, Nakamizo Y, Kimura H, Nakagawa H, Ohkido M, et al. A
survey of psoriasis patients in Japan from 1982 to 2001. J Dermatol Sci
20
Page 21 of 34
2003;31(1):59-64.
16. Taylor W, Gladman D, Helliwell P, Marchesoni A, Mease P, Mielants H.
Classification criteria for psoriatic arthritis: development of new criteria from a large
international study. Arthritis Rheum 2006;54(8):2665-73.
17. Pedersen OB, Svendsen AJ, Ejstrup L, Skytthe A, Junker P. The occurrence of
psoriatic arthritis in Denmark. Ann Rheum Dis 2008;67(10):1422-6.
18. Wilson FC, Icen M, Crowson CS, McEvoy MT, Gabriel SE, Kremers HM. Time
Fo
trends in epidemiology and characteristics of psoriatic arthritis over 3 decades: a
population-based study. J Rheumatol 2009;36(2):361-7.
rP
19. Wilson FC, Icen M, Crowson CS, McEvoy MT, Gabriel SE, Kremers HM.
ee
Incidence and clinical predictors of psoriatic arthritis in patients with psoriasis: A
population-based study. Arthritis Rheum 2009;61(2):233-239.
rR
20. Gladman DD, Anhorn KA, Schachter RK, Mervart H. HLA antigens in psoriatic
arthritis. J Rheumatol 1986;13(3):586-92.
ev
21. Muto M, Nagai K, Mogami S, Nakano J, Sasazuki T, Asagami C. HLA antigens
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
in Japanese patients with psoriatic arthritis. Tissue Antigens 1995;45(5):362-4.
22. Liao HT, Lin KC, Chang YT, Chen CH, Liang TH, Chen WS, et al. Human
leukocyte antigen and clinical and demographic characteristics in psoriatic arthritis
and psoriasis in Chinese patients. J Rheumatol 2008;35(5):891-5.
21
Rheumatology
23. Elkayam O, Segal R, Caspi D. Human leukocyte antigen distribution in Israeli
patients with psoriatic arthritis. Rheumatol Int 2004;24(2):93-7.
24. Rahman P, Siannis F, Butt C, Farewell V, Peddle L, Pellett F, et al. TNFalpha
polymorphisms and risk of psoriatic arthritis. Ann Rheum Dis 2006;65(7):919-23.
25. Hamamoto Y, Tateno H, Ishida T, Muto M. Lack of association between
promoter polymorphism of the tumor necrosis factor-alpha gene and psoriatic arthritis
in Japanese patients. J Invest Dermatol 2000;115(6):1162-4.
Fo
26. Balding J, Kane D, Livingstone W, Mynett-Johnson L, Bresnihan B, Smith O, et
al. Cytokine gene polymorphisms: association with psoriatic arthritis susceptibility
rP
and severity. Arthritis Rheum 2003;48(5):1408-13.
ee
27. Gonzalez S, Martinez-Borra J, Torre-Alonso JC, Gonzalez-Roces S, Sanchez del
Rio J, Rodriguez Perez A, et al. The MICA-A9 triplet repeat polymorphism in the
rR
transmembrane region confers additional susceptibility to the development of
ev
psoriatic arthritis and is independent of the association of Cw*0602 in psoriasis.
Arthritis Rheum 1999;42(5):1010-6.
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 22 of 34
28. Nelson GW, Martin MP, Gladman D, Wade J, Trowsdale J, Carrington M.
Cutting edge: heterozygote advantage in autoimmune disease: hierarchy of
protection/susceptibility conferred by HLA and killer Ig-like receptor combinations in
psoriatic arthritis. J Immunol 2004;173(7):4273-6.
22
Page 23 of 34
29. Gladman DD, Cheung C, Ng CM, Wade JA. HLA-C locus alleles in patients
with psoriatic arthritis (PsA). Hum Immunol 1999;60(3):259-61.
30. Al-Heresh AM, Proctor J, Jones SM, Dixey J, Cox B, Welsh K, et al. Tumour
necrosis factor-alpha polymorphism and the HLA-Cw*0602 allele in psoriatic
arthritis. Rheumatology (Oxford) 2002;41(5):525-30.
31. Chang YT, Chou CT, Yu CW, Lin MW, Shiao YM, Chen CC, et al. Cytokine
gene polymorphisms in Chinese patients with psoriasis. Br J Dermatol
Fo
2007;156(5):899-905.
32. Lan CC, Tsai WC, Wu CS, Yu CL, Yu HS. Psoriatic patients with arthropathy
rP
show significant expression of free HLA class I heavy chains on circulating
ee
monocytes: a potential role in the pathogenesis of psoriatic arthropathy. British
Journal of Dermatology 2004;151(1):24-31.
rR
33. Yen JH, Tsai WC, Lin CH, Ou TT, Hu CJ, Liu HW. Cytochrome p450 1Al gene
polymorphisms
2004;33(1):19-23.
in
patients
with
psoriatic
ev
arthritis.
Scand
J
Rheumatol
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
34. Yen JH, Tsai WC, Lin CH, Ou TT, Hu CJ, Liu HW. Manganese superoxide
dismutase gene polymorphisms in psoriatic arthritis. Dis Markers 2003;19(6):263-5.
35. Shehab DK, Al-Jarallah KF, Al-Awadhi AM, Al-Herz A, Nahar I, Haider MZ.
Association of angiotensin-converting enzyme (ACE) gene insertion-deletion
23
Rheumatology
polymorphism with spondylarthropathies. J Biomed Sci 2008;15(1):61-7.
36. Al-Awadhi AM, Hasan EA, Sharma PN, Haider MZ, Al-Saeid K.
Angiotensin-converting enzyme gene polymorphism in patients with psoriatic arthritis.
Rheumatol Int 2007;27(12):1119-23.
37. Moll JM, Wright V. Psoriatic arthritis. Semin Arthritis Rheum 1973;3(1):55-78.
38. Rajendran CP, Ledge SG, Rani KP, Madhavan R. Psoriatic arthritis. J Assoc
Physicians India 2003;51:1065-8.
Fo
39. Yamamoto T, Yokozeki H, Nishioka K. Clinical analysis of 21 patients with
psoriasis arthropathy. J Dermatol 2005;32(2):84-90.
rP
40. Tam LS, Tomlinson B, Chu TT, Li M, Leung YY, Kwok LW, et al.
ee
Cardiovascular risk profile of patients with psoriatic arthritis compared to
controls--the role of inflammation. Rheumatology (Oxford) 2008;47(5):718-23.
rR
41. Tsai YG, Chang DM, Kuo SY, Wang WM, Chen YC, Lai JH. Relationship
ev
between human lymphocyte antigen-B27 and clinical features of psoriatic arthritis. J
Microbiol Immunol Infect 2003;36(2):101-4.
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 24 of 34
42. Gladman DD, Shuckett R, Russell ML, Thorne JC, Schachter RK. Psoriatic
arthritis (PSA)--an analysis of 220 patients. Q J Med 1987;62(238):127-41.
43. Gladman DD, Antoni C, Mease P, Clegg DO, Nash P. Psoriatic arthritis:
epidemiology, clinical features, course, and outcome. Ann Rheum Dis 2005;64 Suppl
24
Page 25 of 34
2:ii14-7.
44. Deesomchok U, Tumrasvin T. Clinical comparison of patients with ankylosing
spondylitis, Reiter's syndrome and psoriatic arthritis. J Med Assoc Thai
1993;76(2):61-70.
45. McHugh NJ, Balachrishnan C, Jones SM. Progression of peripheral joint disease
in
psoriatic
arthritis:
a
5-yr
prospective
study.
Rheumatology
(Oxford)
2003;42(6):778-83.
Fo
46. Wright V, Moll JMH. Psoriatic arthritis. In seronegative polyarthritis. Amsterdam:
North Holland Publishing Co.; 1976: 169-235.
rP
47. Feld J, Weiss G, Rosner I, Rozenbaum M, Laor A, Rimar D, et al.
ee
Electrocardiographic findings in psoriatic arthritis: a case-controlled study. J
Rheumatol 2008;35(12):2379-82.
48. Saricaoglu
H,
Gullulu
S,
rR
Bulbul Baskan E,
Cordan
J,
Tunali
S.
ev
Echocardiographic findings in subjects with psoriatic arthropathy. J Eur Acad
Dermatol Venereol 2003;17(4):414-417.
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
49. Gonzalez-Juanatey C, Amigo-Diaz E, Miranda-Filloy JA, Testa A, Revuelta J,
Garcia-Porrua C, et al. Lack of Echocardiographic and Doppler Abnormalities in
Psoriatic Arthritis Patients Without Clinically Evident Cardiovascular Disease or
Classic Atherosclerosis Risk Factors. Seminars in Arthritis and Rheumatism
25
Rheumatology
2006;35(5):333-339.
50. Salvarani C, Macchioni PL, Zizzi F, Mantovani W, Rossi F, Baricchi R, et al.
Clinical subgroups and HLA antigens in Italian patients with psoriatic arthritis. Clin
Exp Rheumatol 1989;7(4):391-6.
51. Torre Alonso JC, Rodriguez Perez A, Arribas Castrillo JM, Ballina Garcia J,
Riestra Noriega JL, Lopez Larrea C. Psoriatic arthritis (PA): a clinical, immunological
and radiological study of 180 patients. Br J Rheumatol 1991;30(4):245-50.
Fo
52. Marsal S, Armadans-Gil L, Martinez M, Gallardo D, Ribera A, Lience E.
Clinical, radiographic and HLA associations as markers for different patterns of
rP
psoriatic arthritis. Rheumatology (Oxford) 1999;38(4):332-7.
ee
53. Gladman DD, Farewell VT, Nadeau C. Clinical indicators of progression in
psoriatic arthritis: multivariate relative risk model. Journal of Rheumatology
1995;22(4):675-9.
ev
rR
54. Queiro-Silva R, Torre-Alonso JC, Tinture-Eguren T, Lopez-Lagunas I. A
polyarticular onset predicts erosive and deforming disease in psoriatic arthritis.
Annals of the Rheumatic Diseases 2003;62(1):68-70.
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 26 of 34
55. Gladman DD, Farewell VT, Kopciuk KA, Cook RJ. HLA markers and
progression in psoriatic arthritis. J Rheumatol 1998;25(4):730-3.
56. Husted JA, Gladman DD, Farewell VT, Long JA, Cook RJ. Validating the SF-36
26
Page 27 of 34
health survey questionnaire in patients with psoriatic arthritis. J Rheumatol
1997;24(3):511-7.
57. Husted JA, Tom BD, Farewell VT, Schentag CT, Gladman DD. Description and
prediction of physical functional disability in psoriatic arthritis: a longitudinal analysis
using a Markov model approach. Arthritis Rheum 2005;53(3):404-9.
58. Husted JA, Gladman DD, Farewell VT, Cook RJ. Health-related quality of life of
patients with psoriatic arthritis: a comparison with patients with rheumatoid arthritis.
Fo
Arthritis Rheum 2001;45(2):151-8.
59. Sokoll KB, Helliwell PS. Comparison of disability and quality of life in
rP
rheumatoid and psoriatic arthritis. J Rheumatol 2001;28(8):1842-6.
ee
60. Leung YY, Tam LS, Kun EW, Li EK. Impact of illness and variables associated
with functional impairment in Chinese patients with psoriatic arthritis. Clin Exp
Rheumatol 2008;26(5):820-6.
ev
rR
61. Ritchlin CT, Kavanaugh A, Gladman DD, Mease PJ, Helliwell P, Boehncke WH,
et al. Treatment recommendations for psoriatic arthritis. Ann Rheum Dis
2008:ard.2008.094946.
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
62. Leung YY, Ho KW, Kun EW, Tam LS, E.K. L. Evaluation of the CASPAR
criteria verse Moll and Wright criteria for Psoriatic Arthritis in Chinese. [Abstract]
Ann Rheum Dis 2009;in press.
27
Rheumatology
63. Howe HS, Zhao L, Song YW, Springer L, Edmonds J, Gu J, et al. Seronegative
spondyloarthropathy--studies from the Asia Pacific region. Ann Acad Med Singapore
2007;36(2):135-41.
64. Lim JT, Tham SN. Methotrexate in the treatment of psoriasis at the National Skin
Centre, Singapore. Ann Acad Med Singapore 1994;23(6):848-51.
65. Singh YN, Verma KK, Kumar A, Malaviya AN. Methotrexate in psoriatic
arthritis. J Assoc Physicians India 1994;42(11):860-2.
Fo
66. Uthman I, Mroueh K, Arayssi T, Nasr F, Masri AF. The use of tumor necrosis
factor neutralization strategies in rheumatologic disorders other than rheumatoid
rP
arthritis in Lebanon. Semin Arthritis Rheum 2004;33(6):422-3.
ee
67. Koike R, Takeuchi T, Eguchi K, Miyasaka N. Update on the Japanese guidelines
for the use of infliximab and etanercept in rheumatoid arthritis. Mod Rheumatol
2007;17(6):451-8.
ev
rR
68. Elkayam O, Balbir-Gurman A, Lidgi M, Rahav G, Weiler-Ravel D. [Guidelines
of the Israeli association of rheumatology for the prevention of tuberculosis in patients
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 28 of 34
treated with TNF-alpha blockers]. Harefuah 2007;146(3):235-7, 244.
69. Braun-Moscovici Y, Markovits D, Rozin A, Toledano K, Nahir AM,
Balbir-Gurman A. Anti-tumor necrosis factor therapy: 6 year experience of a single
center in northern Israel and possible impact of health policy on results. Isr Med
28
Page 29 of 34
Assoc J 2008;10(4):277-81.
70. Chou CT. The clinical application of etanercept in Chinese patients with
rheumatic diseases. Mod Rheumatol 2006;16(4):206-13.
71. Takeuchi T, Tatsuki Y, Nogami Y, Ishiguro N, Tanaka Y, Yamanaka H, et al.
Postmarketing surveillance of the safety profile of infliximab in 5000 Japanese
patients with rheumatoid arthritis. Ann Rheum Dis 2008;67(2):189-94.
72. Seong SS, Choi CB, Woo JH, Bae KW, Joung CL, Uhm WS, et al. Incidence of
Fo
tuberculosis in Korean patients with rheumatoid arthritis (RA): effects of RA itself
and of tumor necrosis factor blockers. J Rheumatol 2007;34(4):706-11.
rP
73. Harigai M, Koike R, Miyasaka N. Pneumocystis pneumonia associated with
ee
infliximab in Japan. N Engl J Med 2007;357(18):1874-6.
74. Tanno M, Nakamura I, Ito K, Tanaka H, Ohta H, Kobayashi M, et al. Modeling
rR
and cost-effectiveness analysis of etanercept in adults with rheumatoid arthritis in
ev
Japan: a preliminary analysis. Mod Rheumatol 2006;16(2):77-84.
75. Wong K, Gladman DD, Husted J, Long JA, Farewell VT. Mortality studies in
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
psoriatic arthritis: results from a single outpatient clinic. I. Causes and risk of death.
Arthritis Rheum 1997;40(10):1868-72.
76. Gladman DD, Farewell VT, Wong K, Husted J. Mortality studies in psoriatic
arthritis: results from a single outpatient center. II. Prognostic indicators for death.
29
Rheumatology
Arthritis Rheum 1998;41(6):1103-10.
77. Shbeeb M, Uramoto KM, Gibson LE, O'Fallon WM, Gabriel SE. The
epidemiology of psoriatic arthritis in Olmsted County, Minnesota, USA, 1982-1991. J
Rheumatol 2000;27(5):1247-50.
78. Kimhi O, Caspi D, Bornstein NM, Maharshak N, Gur A, Arbel Y, et al.
Prevalence and risk factors of atherosclerosis in patients with psoriatic arthritis. Semin.
Arthritis Rheum. 2007;36(4):203-9.
Fo
79. Han C, Robinson DW, Jr., Hackett MV, Paramore LC, Fraeman KH, Bala MV.
Cardiovascular disease and risk factors in patients with rheumatoid arthritis, psoriatic
rP
arthritis, and ankylosing spondylitis. J Rheumatol 2006;33(11):2167-72.
ee
80. Persson J, Formgren J, Israelsson B, Berglund G. Ultrasound-determined
intima-media thickness and atherosclerosis. Direct and indirect validation.
Arterioscler Thromb 1994;14(2):261-4.
ev
rR
81. Gonzalez-Juanatey C, Llorca J, Amigo-Diaz E, Dierssen T, Martin J,
Gonzalez-Gay MA. High prevalence of subclinical atherosclerosis in psoriatic
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 30 of 34
arthritis patients without clinically evident cardiovascular disease or classic
atherosclerosis risk factors. Arthritis Rheum 2007;57(6):1074-80.
82. Eder L, Zisman D, Barzilai M, Laor A, Rahat M, Rozenbaum M, et al.
Subclinical atherosclerosis in psoriatic arthritis: a case-control study. J Rheumatol
30
Page 31 of 34
2008;35(5):877-82.
83. Gonzalez-Gay MA, Vazquez-Rodriguez TR, Gonzalez-Juanatey C, Llorca J.
Subclinical Atherosclerosis in Patients with Psoriatic Arthritis. J Rheumatol
2008;35(10):2070-2071.
84. Tam LS, Shang Q, Li EK, Tomlinson B, Chu TT, Li M, et al. Subclinical carotid
atherosclerosis
in
patients
with
psoriatic
arthritis.
Arthritis
Rheum
2008;59(9):1322-31.
Fo
85. Hill JM, Zalos G, Halcox JP, Schenke WH, Waclawiw MA, Quyyumi AA, et al.
Circulating endothelial progenitor cells, vascular function, and cardiovascular risk. N
rP
Engl J Med 2003;348(7):593-600.
ee
86. Ablin JN, Goldstein Z, Aloush V, Matz H, Elkayam O, Caspi D, et al. Normal
levels and function of endothelial progenitor cells in patients with psoriatic arthritis.
Rheumatol Int 2009;29(3):257-62.
ev
rR
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
31
Rheumatology
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
Page 32 of 34
Table 1. Summary of clinical features of PsA from Asian countries compared with the Toronto series
Rajendran
Tam et al
Thumboo et al (8)
Baek et
Jamshidi
Prasad
Tsai et al
Al-Awadhi
Deesomc
Elkayam
Yamamoto
Gladman et
et al (38)
(40)
(n=80)
al (11)
et al (10)
et al
(41)
et al (36)
-hok et al
et al (23)
et al (39)
al (42)
Fo
(n=116)
(n=102)
(n=51)
(n=22)
Indian
Chinese
Chinese
Indian
Malay
Mean age (yrs)
41
49
-
-
Male : Female
78:38
48:54
29:22
Age of onset of PsA (yrs)
Ethnicity
(44)
(12)
(n=7)
(n=32)
(n=29)
(n=40)
(n=41)
(n=51)
(n=28)
(n=50)
(n=21)
(n=220)
Korean
Iranian
Indian
Chinese
Arabs
Thai
Jewish
Japanese
Caucasian
-
40
43
34-68
41
47
-
58
42
46
12:10
4:3
19:13
17:12
34:6
28:13
19:32
20:8
30:20
12:9
104:116
33
35
-
69
rP
ee
10-65
40
38
36
Arthritis after skin (%)
51
62
73
73
86
30
39
31
40
-
36
-
98
Polyarthritis (%)
48
34
41
41
43
-
-
-
81
68
48
-
-
90
68
24
24
31
43
-
10
27
76
48
16
50
rR
51
Oligoarthritis (%)
37
28
14
9
14
31
Spondyloarthritis (%)
11
30
39
50
43
17
18
34
20
46
36
10
2
DIP (%)
2.6
8
6
0
0
6
14
18
27
0
-
63
14
12
Arthritis mutilans (%)
0.86
1
4
0
0
0
-
0
0
-
-
5
16
6
DIP= Distal interphalangeal. * Nail lesion significantly increased compared to patients without arthritis.
-
ev
-
iew
32
Page 33 of 34
Conflict of Interest
The authors have declared no conflicts of interest.
Fo
ev
rR
ee
rP
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Rheumatology
33
Rheumatology
Key Messages:
Divergent distribution of HLA may account for the prevalence differences in
PsA.
An increased prevalence of subclinical atherosclerosis has been reported in Asian
patients with PsA.
Fo
ev
rR
ee
rP
iew
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
Page 34 of 34
34