psa in asia

7/27/2019 PsA in Asia

1/5

Review

Psoriatic arthritis in Asia

Lai-Shan Tam1, Ying-Ying Leung2 and Edmund K. Li1

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 PsA was reported in different countries. The prevalence in

China was similar to the rest of the world, whereas the incidence and prevalence of PsA was much lower in Japan. Among patients with

psoriasis, 642% of the Caucasians were reported to have PsA, but figures were lower from Asian countries (19%). Divergent distribution of

HLA in different ethnic groups and other genetic determinants may account for these differences in prevalence. PsA affects men and women

almost equally in Chinese, Japanese and Iranians, which is similar to their Caucasian counterparts. Polyarthritis developing in the fourth

decade was the commonest pattern of arthritis among Chinese, Indians, Iranians, Kuwaiti Arabs and Malays. Arthritis mutilans and eye

lesions have rarely been reported in Asian countries. Chinese patients with nail disease and DIP 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 co-morbidity in Asian patients with PsA. Increased prevalence

of traditional cardiovascular risk factors associated with PsA suggested that the two conditions may share the same inflammatory pathway.

Carotid intimamedia thickness can identify PsA patients with subclinical atherosclerosis who may benefit from early intervention.

KEY WORDS: Psoriatic arthritis, Asia, Epidemiology, Premature atherosclerosis.

Introduction

PsA is an inflammatory arthritis associated with psoriasis. PsA ischaracterized by the absence of RF and certain clinical features,including asymmetric distribution of arthritis, DIP involvement,enthesitis, dactylitis, spondylitis and the association with HLA-B27. On the basis of these characteristics, PsA has been classifiedwith the HLA-B27-associated SpAs. Researchers have remarkedthat ethnic and geographic differences exist in the prevalence,clinical manifestations and prognosis of SpA [1]. SpA in thenon-white Caucasians, Asians and Africans runs a differentcourse when compared with white Caucasians, and the association

between B27 and disease is less strong in some of these popula-tions in whom cross-reacting antigens and other genetic determi-nants may be more important [1]. None of the studies has everstudied in detail whether there are any ethnic differences in theprevalence, clinical manifestations and prognosis in PsA, but theymay possibly provide further insight into the underlying aetiologyof this condition. Estimates of prevalence of PsA can also provideinformation regarding the burden of the disease and would allowprovision for health services for patients with PsA. Prematureatherosclerosis has been recognized as an important co-morbidityin chronic inflammatory conditions including RA and SLE [2, 3].Data from Asian countries also support the hypothesis thatinflammation associated with PsA contributes to acceleratedatherosclerosis. We review recent advances in research on PsAfrom Asian countries.

Epidemiology

PsA was recognized by the ACR as a distinct clinical entity since1964 [4]. However, the first study on prevalence and incidence ofPsA was published only in 1996 [5]. The results of a recent

systematic review suggested a wide variation on the incidenceand prevalence of PsA in different countries [5]. On the basis ofretrospective and cross-sectional studies, the prevalence of PsAranged between 20 and 420 per 100 000 population in Europeand USA, respectively. The incidence of PsA was similar betweenfive European studies and one US study that ranged between 3and 23.1 per 100 000 population, but data from Asia are limited[5]. From population-based surveys in China, the prevalence ofPsA appeared to be similar to the rest of the world, ranging from10 to 100 per 100 000 population [6]. Interestingly, amongJapanese, there is a 64- and 180-fold lower incidence with preva-

lence between 0.1 and 1 per 100 000 population as compared withthe median incidence and prevalence of all other studies [7]. Amulti-ethnic study reported that PsA was significantly morecommon among Indians than the ethnic distribution of theSingapore population [8].

Among patients with psoriasis, 642% from Europe, USA andSouth Africa were reported to have PsA [9], but figures were lowerfrom Asian countries. PsA was observed in 9% of the patientswith psoriasis in Iran [10], Korea [11] and India [12]; 5% in China[13]; 2% in Turkey [14] and 1% in Japan [15]. A Singaporeanstudy also reported that Indians with psoriasis had twice therisk of developing PsA when compared with Chinese [8], suggest-ing that different ethnicities may affect the development of PsA.

Studies to date on incidence and prevalence for PsA have beenlimited by small cross-sectional studies, selective study popula-tions, limited follow-up and PsA classification criteria lacking

diagnostic sensitivity. The Classification of Psoriatic Arthritis(CASPAR) group has developed classification criteria for PsAwith a sensitivity of 91.4% and a specificity of 98.7% [16].Population-based studies using these new criteria reported apoint prevalence of 150 per 100 000 persons [17], and an incidencebetween 6 [17] and 7.2 [18] per 100 000 persons in Denmark andUSA, respectively. PsA was clinically recognized in


2/5

Cumulated evidence indicates that PsA is a disease caused by theconcerted action of multiple disease genes, triggered by environ-mental factors. Several studies reported linkage between specificHLA and PsA [2023]. Divergent distribution of HLA wasdocumented in different reports, suggesting that HLA distri-bution varies with different ethnic groups. HLA-B16, -B17, -B27and -Cw6 were associated with PsA in Caucasians [20], whereasHLA-A2, -B46, -DR8 and -B27 were associated with PsA in

Japanese [21]. A recent study from Taiwan showed thatHLA-Cw12 was associated with PsA, whereas HLA-B58 and-DR17 appeared to be protective [22]. In Israeli patients, PsAwas associated with HLA-A3, -B13, -B38, -DRB0101 and-DRB0301 [23]. HLA-B27 was not associated with PsA in patientsfrom Israel [23] and Korea [11].

TNF-a gene is also mapped within the HLA region, and itsproduct has been reported as one of the most important cytokinesin the pathogenesis of PsA. There are conflicting reports about theassociation between TNF-a-238G/A polymorphism and PsA [24];studies from Japan and Taiwan did not find any associations [25,26]. In Caucasians, TNF-a and - gene polymorphism [26], HLACw 0602, Class I MHC chain-related gene A (MICA)-A9 andkiller immunoglobulin-like receptor (KIR) 2DS1/S2 [2730] wereassociated with PsA, and TNF-a and - gene polymorphisms weresignificantly associated with presence of joint erosions in PsA andprogression of joint erosions in early PsA [26]. Different fromthe Caucasians, TNF-a and -, HLA Cw 0602, KIR 2DS1/S2,MICA-A9 and other cytokine gene polymorphism were notassociated with PsA in Chinese patients from Taiwan [31]. Inaddition, PsA patients from Taiwan showed elevated expressionof free HLA Class I heavy chains on peripheral blood monocytescompared with psoriasis patients without arthritis [32]. Whencytochrome p450 1A1 (CYP 1A1) and manganese superoxidedismuatse (MnSOD) gene polymorphisms were assessed inChinese patients from Taiwan, CYP 1A1 4887A and 4889Gwere reported to be associated with PsA, but these were not asso-ciated with the manifestations and severity of PsA [33]. MnSOD1183C polymorphisms may be associated with PsA, whereasMnSOD 1183T appeared to be protective from the developmentof this disease [34]. The role of the I-allele of angiotensin-

converting enzyme gene I/D polymorphism was controversial inSpA patients from Kuwait [35, 36].

Clinical features of PsA

Moll and Wright [37] described five clinical patterns amongpatients with PsA: DIP, asymmetrical oligoarticular, symmetricpolyarticular, spondylitis and arthritis mutilans. The exactfrequency of the patterns is variable but oligoarthritis was themost commonly reported pattern [37]. The clinical features ofPsA patients from Asian countries are summarized in Table 1together with the largest PsA series from Toronto for comparison[8, 1012, 23, 36, 3842]. A number of racial differences in theclinical presentations of PsA were observed. PsA affects men andwomen almost equally in Caucasians [43]. Studies from HongKong, Singapore [8, 40], Japan [39] and Iran [10] also reportedthe same, whereas others noted a male predominance [11, 12, 23,38, 41, 44] and one study reported a female predominancefrom Kuwait [36].

Polyarthritis developing in the fourth decade was the common-est pattern of arthritis among Chinese from Hong Kong [40],Singaporians [8], Indians [8, 38], Iranians [10], Kuwaiti Arabs[36], Malays [8] and Thai patients [44]. On the other hand,oligoarthritis was the predominant pattern in patients fromIsrael [23], Japan [39] and rural India [12]. Spondylitis was themost common pattern of PsA in Korea [11] and Chinese fromTaiwan [41]. Clinically apparent lumbar spondylitis was signifi-cantly more common in Indians than Chinese from Singapore,45% of cases were asymptomatic when present in Chinese and T

ABLE

1.

SummaryofclinicalfeaturesofPsA

from

AsiancountriescomparedwiththeToronto

series

Rajendran

etal.[38],

Tam

etal.[40],

Thumboo

etal.[8],n

80

Baek

e

tal.[11],

Jamshidi

etal.[10]a,

Prasad

etal.[12],

Tsai

etal.[41],

Al-Awadhi

etal.[36],

Deesomchok

etal.[44],

Elkayam

etal.[23],

Yamamoto

etal.[39],

Gladman

etal.[42],

n

116

n

102

n

51

n

22

n

7

n

32

n

29

n

40

n4

1

n

51

n

28

n

50

n

21

n

220

Ethnicity

Indian

Chinese

Chinese

Indian

Malay

Korean

Iranian

Indian

Chine

se

Arab

Thai

Jewish

Japanese

Caucasian

Meanage,years

41

49

40

43

3468

41

47

58

42

46

Male:female

78:38

48:54

29:22

12:10

4:3

19:13

17:12

34:6

28:13

19:32

20:8

30:20

12:9

104:116

AgeofonsetofPsA,yearsb

1065

40

38

36

33

35

30

39

31

40

36

Arthritisafterpsoriasis,

%

51

62

73

73

86

69

98

51

81

68

Polyarthritis,

%

48

34

41

41

43

6

48

90

68

24

24

31

Oligoarthritis,

%

37

28

14

9

14

31

43

10

27

76

48

16

Spondyloarthritis,

%

11

30

39

50

43

50

17

18

34

20

46

36

10

2

DIP,

%

2.6

8

6

0

0

6

14

18

27

0

63

14

12

Arthritismutilans,

%

0.8

6

1

4

0

0

0

0

0

5

16

aNaillesionssignificantlyincreasedcomparedwith

patientswithoutarthritis.

bAllvaluesshownarethemeanageofonset,excepttheentryforRajendranetal.inwh

ichonlytherangeisprovided.

1474 Lai-Shan Tam et al.


3/5

the condition was detectable only on radiological examination[8]. Arthritis mutilans was rarely reported in all the studiesfrom Asian regions. The frequency of distribution of the pat-terns has also varied in previous Caucasian studies [43], andmay be explained partly by the different definitions used byindividual investigators or the changing patterns over time.Those with longer disease duration tend to develop into thepolyarticular pattern [45].

Extra-articular manifestations

Almost all (51.297.5%) patients developed arthritis after theonset of psoriasis, and psoriatic vulgaris was the most commonform of psoriasis reported [8, 1012, 23, 3841]. Nail lesions werecommon in PsA, affecting 30.297% of the patients, and weresignificantly more prevalent compared with psoriasis patientswithout arthritis in one study [10]. The prevalence of dactylitisand enthesitis ranged from 15.4 to 71.4% and from 7.8 to59.1%, respectively. Eye lesions were rarely reported in PsApatients in Asia (1.73.9%) [8, 36, 38, 44].

Aortic incompetence was reported in


4/5

controls, although the BMI was significantly increased in thepatient group. On the contrary, Han et al. [79] from the USAreported a higher prevalence ratio of type II DM, hyperlipidaemiaand hypertension in PsA patients compared with controls. Toaddress the central question that if individuals with PsA have anincreased prevalence of CVD risk factors, a study from HongKong compared CVD risk factors between 102 consecutive PsApatients and 82 controls [40]. The BMI of the PsA patients was

significantly higher than healthy controls. PsA patients had ahigher prevalence of DM and hypertension, but a lower preva-lence of low high density lipoprotein cholesterol after adjusting forthe BMI. Further adjustment for high sensitive C-reactive proteinlevel rendered the differences in the prevalence of hypertensionand DM non-significant between the PsA and controls. Thesedata support the hypothesis that PsA may be associated withobesity, hypertension and insulin resistance because of theshared inflammatory pathway.

Early diagnosis of atherosclerosis in PsA might trigger moreaggressive prophylaxis. Increased intimamedia thickness (IMT)of the carotid artery, a sign of early atherosclerosis [80], has beenreported in PsA patients from Spain and Israel [78, 8183].Increased IMT significantly correlated with traditional risk factorsincluding age [78, 82], BMI [78], uric acid [83], triglycerides [82],total cholesterol and low density lipoprotein cholesterol levels [81];and disease-related parameters including age at the time of PsAdiagnosis [81], disease duration [78, 81], spine involvement [78],ESR [78] and fibrinogen [78] levels. A study from Hong Kongreported an increased prevalence of subclinical atherosclerosis inChinese, defined as the average of IMT measures above the 95thpercentile of healthy controls [84]. Using logistic regressionanalysis, independent explanatory variables associated with sub-clinical atherosclerosis in PsA including increased sugar and totaltriglyceride levels. The Framingham risk score (FRS) was similarin PsA patients with or without subclinical atherosclerosis.Twenty-six (35%) of the 74 patients had subclinical atherosclero-sis despite having a low cardiovascular risk according to the FRS.These studies suggested that carotid IMT can identify PsApatients with subclinical atherosclerosis who may benefit fromearly intervention.

Conclusions

A wide variation on the incidence and prevalence of PsA hasbeen reported in different countries, ranging from 10 to 100 per100 000 population in China to 1 per 100 000 population in Japan.Amongst Asian patients with psoriasis, 19% were reported tohave PsA. Divergent distribution of HLA in different ethnicgroups and other genetic determinants may account for theseprevalence differences. Polyarthritis developing in the fourthdecade was the commonest pattern of arthritis among AsianPsA patients, whereas arthritis mutilans and eye lesions wererarely reported. More data are required on the safety, efficacyand cost effectiveness of TNF blockers for the treatment of PsAin Asia. An increased prevalence of traditional cardiovascular

system risk factors and subclinical atherosclerosis has beenreported in patients with PsA, including Asian patients. Suchrisk factors should be routinely monitored and treated aggres-sively in high-risk patients.

Rheumatology key messages

Divergent distribution of HLA may account for the prevalencedifferences in PsA.

An increased prevalence of subclinical atherosclerosis has beenreported in Asian patients with PsA.

Disclosure statement: The authors have declared no conflicts ofinterest.

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:

75370.

2 Roman MJ, Shanker BA, Davis A et al. Prevalence and correlates of accelerated

atherosclerosis in systemic lupus erythematosus. N Engl J Med 2003;349:2399406.

3 Roman MJ, Moeller E, Davis A et al. Preclinical carotid atherosclerosis in patients

with rheumatoid arthritis. Ann Intern Med 2006;144:24956.

4 ONeill T, Silman AJ. Psoriatic arthritis. Historical background and epidemiology.

Baillieres Clin Rheumatol 1994;8:24561.

5 Alamanos Y, Voulgari PV, Drosos AA. Incidence and prevalence of psoriatic arthritis:

a systematic review. J Rheumatol 2008;35:13548.

6 Zeng QY, Chen R, Darmawan J et al. Rheumatic diseases in China. Arthritis Res

Ther 2008;10:R17.

7 Hukuda S, Minami M, Saito T et al. Spondyloarthropathies in Japan: nationwide

questionnaire survey performed by the Japan Ankylosing Spondylitis Society.

J Rheumatol 2001;28:5549.

8 Thumboo J, Tham SN, Tay YK et al. Patterns of psoriatic arthritis in orientals.

J Rheumatol 1997;24:194953.

9 Gladman DD. Psoriatic arthritis. Dermatol Ther 2009;22:4055.

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;11:1625.

11 Baek HJ, Yoo CD, Shin KC et al. Spondylitis is the most common pattern of psoriatic

arthritis in Korea. Rheumatol Int 2000;19:8994.

12 Prasad PV, Bikku B, Kaviarasan PK, Senthilnathan A. A clinical study of psoriatic

arthropathy. Indian J Dermatol Venereol Leprol 2007;73:16670.

13 Fan X, Yang S, Sun LD et al. Comparison of clinical features of HLA-Cw*0602-

positive and -negative psoriasis patients in a Han Chinese population. Acta Derm

Venereol 2007;87:33540.

14 Kundakci N, Tursen U, Babiker MO, Gurgey E. The evaluation of the socio-

demographic and clinical features of Turkish psoriasis patients. Int J Dermatol

2002;41:2204.

15 Kawada A, Tezuka T, Nakamizo Y et al. A survey of psoriasis patients in Japan from

1982 to 2001. J Dermatol Sci 2003;31:5964.

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;54:266573.

17 Pedersen OB, Svendsen AJ, Ejstrup L, Skytthe A, Junker P. The occurrence of

psoriatic arthritis in Denmark. Ann Rheum Dis 2008;67:14226.

18 Wilson FC, Icen M, Crowson CS, McEvoy MT, Gabriel SE, Kremers HM. Time

trends in epidemiology and characteristics of psoriatic arthritis over 3 decades: a

population-based study. J Rheumatol 2009;36:3617.

19 Wilson FC, Icen M, Crowson CS, McEvoy MT, Gabriel SE, Kremers HM. Incidence

and clinical predictors of psoriatic arthritis in patients with psoriasis: a population-

based study. Arthritis Rheum 2009;61:2339.

20 Gladman DD, Anhorn KA, Schachter RK, Mervart H. HLA antigens in psoriatic

arthritis. J Rheumatol 1986;13:58692.

21 Muto M, Nagai K, Mogami S, Nakano J, Sasazuki T, Asagami C. HLA antigens in

Japanese patients with psoriatic arthritis. Tissue Antigens 1995;45:3624.22 Liao HT, Lin KC, Chang YT et al. Human leukocyte antigen and clinical and

demographic characteristics in psoriatic arthritis and psoriasis in Chinese patients.

J Rheumatol 2008;35:8915.

23 Elkayam O, Segal R, Caspi D. Human leukocyte antigen distribution in Israeli

patients with psoriatic arthritis. Rheumatol Int 2004;24:937.

24 Rahman P, Siannis F, Butt C et al. TNFalpha polymorphisms and risk of psoriatic

arthritis. Ann Rheum Dis 2006;65:91923.

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;115:11624.

26 Balding J, Kane D, Livingstone W et al. Cytokine gene polymorphisms: association

with psoriatic arthritis susceptibility and severity. Arthritis Rheum 2003;48:140813.

27 Gonzalez S, Martinez-Borra J, Torre-Alonso JC et al. The MICA-A9 triplet repeat

polymorphism in the transmembrane region confers additional susceptibility to the

development of psoriatic arthritis and is independent of the association of Cw*0602 in

psoriasis. Arthritis Rheum 1999;42:10106.

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 psoriaticarthritis. J Immunol 2004;173:42736.

29 Gladman DD, Cheung C, Ng CM, Wade JA. HLA-C locus alleles in patients with

psoriatic arthritis (PsA). Hum Immunol 1999;60:25961.

30 Al-Heresh AM, Proctor J, Jones SM et al. Tumour necrosis factor-alpha polymorph-

ism and the HLA-Cw*0602 allele in psoriatic arthritis. Rheumatology 2002;41:

52530.

31 Chang YT, Chou CT, Yu CW et al. Cytokine gene polymorphisms in Chinese patients

with psoriasis. Br J Dermatol 2007;156:899905.

32 Lan CC, Tsai WC, Wu CS, Yu CL, Yu HS. Psoriatic patients with arthropathy show

significant expression of free HLA class I heavy chains on circulating monocytes: a

potential role in the pathogenesis of psoriatic arthropathy. Br J Dermatol 2004;151:

2431.

33 Yen JH, Tsai WC, Lin CH, Ou TT, Hu CJ, Liu HW. Cytochrome p450 1Al gene

polymorphisms in patients with psoriatic arthritis. Scand J Rheumatol 2004;33:

1923.

34 Yen JH, Tsai WC, Lin CH, Ou TT, Hu CJ, Liu HW. Manganese superoxide dismutase

gene polymorphisms in psoriatic arthritis. Dis Markers 2003;19:2635.

1476 Lai-Shan Tam et al.


5/5

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

polymorphism with spondylarthropathies. J Biomed Sci 2008;15:617.

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;27:111923.

37 Moll JM, Wright V. Psoriatic arthritis. Semin Arthritis Rheum 1973;3:5578.

38 Rajendran CP, Ledge SG, Rani KP, Madhavan R. Psoriatic arthritis. J Assoc

Physicians India 2003;51:10658.

39 Yamamoto T, Yokozeki H, Nishioka K. Clinical analysis of 21 patients with psoriasis

arthropathy. J Dermatol 2005;32:8490.

40 Tam LS, Tomlinson B, Chu TT et al. Cardiovascular risk profile of patients withpsoriatic arthritis compared to controlsthe role of inflammation. Rheumatology

2008;47:71823.

41 Tsai YG, Chang DM, Kuo SY, Wang WM, Chen YC, Lai JH. Relationship between

human lymphocyte antigen-B27 and clinical features of psoriatic arthritis. J Microbiol

Immunol Infect 2003;36:1014.

42 Gladman DD, Shuckett R, Russell ML, Thorne JC, Schachter RK. Psoriatic arthritis

(PSA)an analysis of 220 patients. Q J Med 1987;62:12741.

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. 2):ii147.

44 Deesomchok U, Tumrasvin T. Clinical comparison of patients with ankylosing

spondylitis, Reiters syndrome and psoriatic arthritis. J Med Assoc Thai 1993;76:

6170.

45 McHugh NJ, Balachrishnan C, Jones SM. Progression of peripheral joint disease in

psoriatic arthritis: a 5-yr prospective study. Rheumatology 2003;42:77883.

46 Wright V, Moll JMH. Psoriatic arthritis. Seronegative polyarthritis. Amsterdam: North

Holland Publishing, 1976:169235.

47 Feld J, Weiss G, Rosner I et al. Electrocardiographic findings in psoriatic arthritis: a

case-controlled study. J Rheumatol 2008;35:237982.48 Saricaoglu H, Gullulu S, Bulbul Baskan E, Cordan J, Tunali S. Echocardiographic

findings in subjects with psoriatic arthropathy. J Eur Acad Dermatol Venereol 2003;

17:4147.

49 Gonzalez-Juanatey C, Amigo-Diaz E, Miranda-Filloy JA et al. Lack of echocardio-

graphic and Doppler abnormalities in psoriatic arthritis patients without clinically

evident cardiovascular disease or classic atherosclerosis risk factors. Semin

Arthritis Rheum 2006;35:3339.

50 Salvarani C, Macchioni PL, Zizzi F et al. Clinical subgroups and HLA antigens in

Italian patients with psoriatic arthritis. Clin Exp Rheumatol 1989;7:3916.

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;30:24550.

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 psoriatic

arthritis. Rheumatology 1999;38:3327.

53 Gladman DD, Farewell VT, Nadeau C. Clinical indicators of progression in psoriatic

arthritis: multivariate relative risk model. J Rheumatol 1995;22:6759.

54 Queiro-Silva R, Torre-Alonso JC, Tinture-Eguren T, Lopez-Lagunas I. A polyarticular

onset predicts erosive and deforming disease in psoriatic arthritis. Ann Rheum Dis2003;62:6870.

55 Gladman DD, Farewell VT, Kopciuk KA, Cook RJ. HLA markers and progression in

psoriatic arthritis. J Rheumatol 1998;25:7303.

56 Husted JA, Gladman DD, Farewell VT, Long JA, Cook RJ. Validating the SF-36

health survey questionnaire in patients with psoriatic arthritis. J Rheumatol 1997;

24:5117.

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;53:4049.

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.

Arthritis Rheum 2001;45:1518.

59 Sokoll KB, Helliwell PS. Comparison of disability and quality of life in rheumatoid and

psoriatic arthritis. J Rheumatol 2001;28:18426.

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;26:8206.

61 Ritchlin CT, Kavanaugh A, Gladman DD et al. Treatment recommendations for

psoriatic arthritis. Ann Rheum Dis. Advance Access published October 24, 2008,

doi: ard.2008.094946.

62 Leung YY, Ho KW, Tam LS et al. Evaluation of the CASPAR criteria versus Moll and

Wright criteria for psoriatic arthritis in Chinese [Abstract]. Ann Rheum Dis 2009;68

(Suppl. 3):663.

63 Howe HS, Zhao L, Song YW et al. Seronegative spondyloarthropathystudies from

the Asia Pacific region. Ann Acad Med Singapore 2007;36:13541.

64 Lim JT, Tham SN. Methotrexate in the treatment of psoriasis at the National Skin

Centre, Singapore. Ann Acad Med Singapore 1994;23:84851.

65 Singh YN, Verma KK, Kumar A, Malaviya AN. Methotrexate in psoriatic arthritis.

J Assoc Physicians India 1994;42:8602.

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 arthritis

in Lebanon. Semin Arthritis Rheum 2004;33:4223.

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:

4518.

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

treated with TNF-alpha blockers]. Harefuah 2007;146:2357, 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 Assoc J 2008;10:

27781.

70 Chou CT. The clinical application of etanercept in Chinese patients with rheumatic

diseases. Mod Rheumatol 2006;16:20613.

71 Takeuchi T, Tatsuki Y, Nogami Y et al. Postmarketing surveillance of the safety

profile of infliximab in 5000 Japanese patients with rheumatoid arthritis. Ann

Rheum Dis 2008;67:18994.72 Seong SS, Choi CB, Woo JH et al. Incidence of tuberculosis in Korean patients with

rheumatoid arthritis (RA): effects of RA itself and of tumor necrosis factor blockers.

J Rheumatol 2007;34:70611.

73 Harigai M, Koike R, Miyasaka N. Pneumocystis pneumonia associated with

infliximab in Japan. N Engl J Med 2007;357:18746.

74 Tanno M, Nakamura I, Ito K et al. Modeling and cost-effectiveness analysis of

etanercept in adults with rheumatoid arthritis in Japan: a preliminary analysis. Mod

Rheumatol 2006;16:7784.

75 Wong K, Gladman DD, Husted J, Long JA, Farewell VT. Mortality studies in psoriatic

arthritis: results from a single outpatient clinic. I. Causes and risk of death. Arthritis

Rheum 1997;40:186872.

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. Arthritis

Rheum 1998;41:110310.

77 Shbeeb M, Uramoto KM, Gibson LE, OFallon WM, Gabriel SE. The epidemiology of

psoriatic arthritis in Olmsted County, Minnesota, USA, 19821991. J Rheumatol

2000;27:124750.

78 Kimhi O, Caspi D, Bornstein NM et al. Prevalence and risk factors of atherosclerosis

in patients with psoriatic arthritis. Semin Arthritis Rheum 2007;36:2039.79 Han C, Robinson DW Jr, Hackett MV, Paramore LC, Fraeman KH, Bala MV.

Cardiovascular disease and risk factors in patients with rheumatoid arthritis, psoriatic

arthritis, and ankylosing spondylitis. J Rheumatol 2006;33:216772.

80 Persson J, Formgren J, Israelsson B, Berglund G. Ultrasound-determined intima-

media thickness and atherosclerosis. Direct and indirect validation. Arterioscler

Thromb 1994;14:2614.

81 Gonzalez-Juanatey C, Llorca J, Amigo-Diaz E, Dierssen T, Martin J, Gonzalez-

Gay MA. High prevalence of subclinical atherosclerosis in psoriatic arthritis patients

without clinically evident cardiovascular disease or classic atherosclerosis risk

factors. Arthritis Rheum 2007;57:107480.

82 Eder L, Zisman D, Barzilai M et al. Subclinical atherosclerosis in psoriatic arthritis: a

case-control study. J Rheumatol 2008;35:87782.

83 Gonzalez-Gay MA, Vazquez-Rodriguez TR, Gonzalez-Juanatey C, Llorca J.

Subclinical atherosclerosis in patients with psoriatic arthritis. J Rheumatol 2008;35:

20701.

84 Tam LS, Shang Q, Li EK et al. Subclinical carotid atherosclerosis in patients with

psoriatic arthritis. Arthritis Rheum 2008;59:132231.

PsA in Asia 1477

psa in asia

Documents