Vous êtes sur la page 1sur 5

Rheumatology 2009;48:14731477 Advance Access publication 27 August 2009

doi:10.1093/rheumatology/kep230

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:

Downloaded from http://rheumatology.oxfordjournals.org/ by guest on June 19, 2012

Psoriatic arthritis, Asia, Epidemiology, Premature atherosclerosis.

Introduction
PsA is an inflammatory arthritis associated with psoriasis. PsA is characterized by the absence of RF and certain clinical features, including asymmetric distribution of arthritis, DIP involvement, enthesitis, dactylitis, spondylitis and the association with HLAB27. On the basis of these characteristics, PsA has been classified with the HLA-B27-associated SpAs. Researchers have remarked that ethnic and geographic differences exist in the prevalence, clinical manifestations and prognosis of SpA [1]. SpA in the non-white Caucasians, Asians and Africans runs a different course when 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 determinants may be more important [1]. None of the studies has ever studied in detail whether there are any ethnic differences in the prevalence, clinical manifestations and prognosis in PsA, but they may possibly provide further insight into the underlying aetiology of 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 RA and SLE [2, 3]. Data from Asian countries also support the hypothesis that inflammation associated with PsA contributes to accelerated atherosclerosis. We review recent advances in research on PsA from Asian countries.

Epidemiology
PsA was recognized by the ACR as a distinct clinical entity since 1964 [4]. However, the first study on prevalence and incidence of PsA was published only in 1996 [5]. The results of a recent
Department of Medicine and Therapeutics, The Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin and 2Department of Medicine, North District Hospital, Hong Kong, China. Submitted 12 May 2009; revised version accepted 30 June 2009. Correspondence to: Edmund K. Li, Department of Medicine and Therapeutics, The Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong, China. E-mail: edmundli@cuhk.edu.hk
1

systematic review suggested a wide variation on the incidence and prevalence of PsA in different countries [5]. On the basis of retrospective and cross-sectional studies, the prevalence of PsA ranged between 20 and 420 per 100 000 population in Europe and USA, respectively. The incidence of PsA was similar between five European studies and one US study that ranged between 3 and 23.1 per 100 000 population, but data from Asia are limited [5]. From 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, among Japanese, there is a 64- and 180-fold lower incidence with prevalence between 0.1 and 1 per 100 000 population as compared with the median incidence and prevalence of all other studies [7]. A multi-ethnic study reported that PsA was significantly more common among Indians than the ethnic distribution of the Singapore population [8]. Among patients with psoriasis, 642% 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 the patients with psoriasis in Iran [10], Korea [11] and India [12]; 5% in China [13]; 2% in Turkey [14] and 1% in Japan [15]. A Singaporean study also reported that Indians with psoriasis had twice the risk of developing PsA when compared with Chinese [8], suggesting that different ethnicities may affect the development of PsA. Studies to date on incidence and prevalence for PsA have been limited by small cross-sectional studies, selective study populations, limited follow-up and PsA classification criteria lacking diagnostic sensitivity. The Classification of Psoriatic Arthritis (CASPAR) group has developed classification criteria for PsA with a sensitivity of 91.4% and a specificity of 98.7% [16]. Population-based studies using these new criteria reported a point prevalence of 150 per 100 000 persons [17], and an incidence between 6 [17] and 7.2 [18] per 100 000 persons in Denmark and USA, respectively. PsA was clinically recognized in <10% of the psoriasis patients during their lifetime [19]. The CASPAR criteria should help with epidemiological studies of PsA in Asia.

Genetic studies
Reasons for differences in prevalence may be due to genetic differences, environmental exposures or a combination of both.
1473

The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

1474

Lai-Shan Tam et al.


Caucasian 46 104:116 36 68 31 16 2 12 16 Thai 20:8 31 68 27 46 Arab 47 19:32 39 90 10 20 0 0 Jewish 58 30:20 40 24 76 36 63
Nail lesions significantly increased compared with patients without arthritis. bAll values shown are the mean age of onset, except the entry for Rajendran et al. in which only the range is provided.

TABLE 1. Summary of clinical features of PsA from Asian countries compared with the Toronto series

n 22

Moll and Wright [37] described five clinical patterns among patients with PsA: DIP, asymmetrical oligoarticular, symmetric polyarticular, spondylitis and 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 Asian countries are summarized in Table 1 together with the largest PsA series from Toronto for comparison [8, 1012, 23, 36, 3842]. A number of racial differences in the clinical presentations of PsA were observed. PsA affects men and women almost equally in Caucasians [43]. Studies from Hong Kong, Singapore [8, 40], Japan [39] and Iran [10] also reported the same, whereas others noted a male predominance [11, 12, 23, 38, 41, 44] and one study reported a female predominance from Kuwait [36]. Polyarthritis developing in the fourth decade was the commonest 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 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% of cases were asymptomatic when present in Chinese and

Tam et al. [40], n 102

Rajendran et al. [38], n 116

Ethnicity Mean age, years Male:female Age of onset of PsA, yearsb Arthritis after psoriasis, % Polyarthritis, % Oligoarthritis, % Spondyloarthritis, % DIP, % Arthritis mutilans, %

Indian 41 78:38 1065 51 48 37 11 2.6 0.86

Chinese 49 48:54 40 62 34 28 30 8 1

Chinese 29:22 38 73 41 14 39 6 4

n 51

Indian 12:10 36 73 41 9 50 0 0

Clinical features of PsA

Thumboo et al. [8], n 80

Malay 4:3 33 86 43 14 43 0 0

n7

Cumulated evidence indicates that PsA is a disease caused by the concerted action of multiple disease genes, triggered by environmental factors. Several studies reported linkage between specific HLA and PsA [2023]. Divergent distribution of HLA was documented in different reports, suggesting that HLA distribution varies with different ethnic groups. HLA-B16, -B17, -B27 and -Cw6 were associated with PsA in Caucasians [20], whereas HLA-A2, -B46, -DR8 and -B27 were associated with PsA in Japanese [21]. A recent study from Taiwan showed that HLA-Cw12 was associated with PsA, whereas HLA-B58 and -DR17 appeared to be protective [22]. In Israeli patients, 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]. TNF-a 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 about the association 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], HLA Cw 0602, Class I MHC chain-related gene A (MICA)-A9 and killer immunoglobulin-like receptor (KIR) 2DS1/S2 [2730] were associated with PsA, and TNF-a and - gene polymorphisms were significantly associated with presence of joint erosions in PsA and progression of joint erosions in early PsA [26]. Different from the Caucasians, TNF-a and - , HLA Cw 0602, KIR 2DS1/S2, MICA-A9 and other cytokine gene polymorphism were not associated with PsA in Chinese patients from Taiwan [31]. In addition, PsA patients from Taiwan showed elevated expression of free HLA Class I heavy chains on peripheral blood monocytes compared with 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, 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, whereas MnSOD 1183T appeared to be protective from the development of this disease [34]. The role of the I-allele of angiotensinconverting enzyme gene I/D polymorphism was controversial in SpA patients from Kuwait [35, 36].

Yamamoto et al. [39], n 21 Al-Awadhi et al. [36], n 51 Deesomchok et al. [44], n 28 Elkayam et al. [23], n 50

Gladman et al. [42], n 220

Japanese 42 12:9 81 24 48 10 14 5

Downloaded from http://rheumatology.oxfordjournals.org/ by guest on June 19, 2012

Tsai et al. [41], n 41 Prasad et al. [12], n 40 Jamshidi et al. [10]a, n 29

Iranian 43 17:12 48

Baek et al. [11], n 32

Korean 40 19:13 35 69 6 31 50 6 0

17 14

Indian 3468 34:6 98 43 18 18 0

Chinese 41 28:13 30 51 34 27

PsA in Asia the condition was detectable only on radiological examination [8]. Arthritis mutilans 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 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 into the polyarticular pattern [45].

1475

Management of PsA Diagnosis of PsA


Treatment recommendations for PsA have been recently published by the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis [61]. The group recommended that diagnosis of PsA should follow the CASPAR criteria. However, the sensitivity and specificity may vary with different ethnicities. The CASPAR criteria for PsA have recently been validated in Chinese populations [62]. Data were collected prospectively from Han Chinese with PsA and other patients with chronic inflammatory arthritis. Subjects were classified according to Moll and Wright or CASPAR criteria. A total of 108 (53 males and 55 females) subjects with PsA were recruited. Data were compared with 195 controls with RA (n 154), AS (n 41) and undifferentiated arthritis (n 1). The sensitivity and specificity of Moll and Wright criteria were 85.2 and 100%, respectively, whereas 98.2 and 99.5%, respectively, for the CASPAR criteria, which is similar to the reported values in European populations. The CASPAR criteria performed well in Chinese population, i.e. very different from populations they were developed, and have a higher sensitivity in classifying PsA.

Extra-articular manifestations
Almost all (51.297.5%) patients developed arthritis after the onset of psoriasis, and psoriatic vulgaris was the most common form of psoriasis reported [8, 1012, 23, 3841]. Nail lesions were common in PsA, affecting 30.297% of the patients, and were significantly more prevalent compared with psoriasis patients without arthritis in one study [10]. The prevalence of dactylitis and enthesitis ranged from 15.4 to 71.4% and from 7.8 to 59.1%, respectively. Eye lesions were rarely reported in PsA patients in Asia (1.73.9%) [8, 36, 38, 44]. Aortic incompetence was reported in <4% of the patients with PsA [46]. Other cardiac involvement in PsA included subtle involvement of the atrioventricular node [47] and diastolic dysfunction [48] from Israel and Turkey, respectively. A study from Spain did not find any differences in echocardiographic abnormalities between PsA and healthy controls [49].

Downloaded from http://rheumatology.oxfordjournals.org/ by guest on June 19, 2012

Treatment of PsA
Most rheumatology units in Asia have adopted treatment guidelines from Europe or USA. The therapeutic strategies outlined in the treatment recommendations were based on review of literature and expert consensus mainly from North America and Europe [61]. Although the therapeutic strategy may be appropriate on the whole, there may be subtle differences in the pharmacokinetics, clinical response, as well as side effects of the drugs used. Few therapeutic trials on PsA have been done in Asia, and data for safety and efficacy of DMARDs and biologics in PsA from most of these countries are lacking. A survey from 112 PsA patients from Singapore reported that DMARDs were commonly used (67% on SSZ and 14% on MTX) [63], and case series from Singapore and India suggested that MTX may be safe and effective [64, 65]. Treatment guideline for the use of TNF-a blockers in Asian patients with rheumatic diseases including PsA has been published from Lebanon, whereas 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-a blockers was published from Israel [68]. Reports from Israel [69] and Taiwan [70] suggested that TNF-a blockers were effective and well tolerated in PsA. A post-marketing surveillance study of 5000 Japanese RA patients treated with 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 reactivation in RA patients treated with TNF blockers [72], and another report from 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 safety, efficacy and cost effectiveness of TNF blockers for the treatment of PsA in Asia.

Predictors for clinical features and prognosis


The association of HLA antigens with disease expression varies in Caucasian PsA patients [20, 5052], e.g. HLA-B27 [20, 5052], -Cw1 [51], -Cw2 [20], -DRw52 [20] and -DQw3 [50] were associated with involvement of the back, whereas HLA-B38 and -B39 were associated with polyarthritis [20]. Studies from Taiwan reported an association between HLA-B27 and the development of sacroiliitis [22, 41] and uveitis [22], but not peripheral arthritis [41]. A study from Israel found significant association between DIP involvement and the presence of HLA-A26 and -B38, whereas HLA-DRB0301 was related to spinal involvement [23]. Predictors for progression in Caucasian PsA included five or more swollen joints, a high medication level at presentation [53], polyarticular onset [54] and HLA-B27 in the presence of HLA-DR7 and -B39, and HLA-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 have elevated levels of CRP (P 0.072), although these results did not attain significance [41]. By contrast, Chinese PsA patients with nail disease and DIP joints involvement had significantly increased risk of developing deformed joints [41].

Quality of life and function in PsA


Instruments validated for the assessment of quality of life and function in PsA included Medical Outcome Survey Short Form 36 (SF-36) [56] and the HAQ [57], respectively. Patients with PsA showed impaired quality of life and reduced function, comparable with those who had RA [5759]. In a study from Hong Kong, a third reported PsA-related unemployment and change in job nature [60]. Another 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 CRP as factors associated with higher HAQ. This study highlighted a significant socio-economic effect in Chinese subjects with PsA. Joint damage was found to be associated with functional impairment.

Co-morbidity of premature atherosclerosis in PsA


Patients with PsA may experience substantial morbidity and unfavourable outcomes at referral centres [75, 76], although investigators from other centre did not report a significant increase in mortality in unselected patients [77]. Mortality data of Asian PsA patients were lacking, nonetheless, investigators from Hong Kong and Israel have ascertained the prevalence and risk factors for premature atherosclerosis in patients with PsA. In a study by Kimhi et al. [78] from Israel, the prevalence of traditional cardiovascular diseases (CVD) risk factors including smoking, altered lipid profile, hypertension and diabetes mellitus (DM) was similar between 30 PsA patients and age-matched

1476

Lai-Shan Tam et al.

controls, although the BMI was significantly increased in the patient group. On the contrary, Han et al. [79] from the USA reported a higher prevalence ratio of type II DM, hyperlipidaemia and hypertension in PsA patients compared with controls. To address the central question that if individuals with PsA have an increased prevalence of CVD risk factors, a study from Hong Kong compared CVD risk factors between 102 consecutive PsA patients and 82 controls [40]. The BMI of the PsA patients was significantly higher than healthy controls. PsA patients had a higher prevalence of DM and hypertension, but a lower prevalence of low high density lipoprotein cholesterol after adjusting for the BMI. Further adjustment for high sensitive C-reactive protein level rendered the differences in the prevalence of hypertension and DM non-significant between the PsA and controls. These data support the hypothesis that PsA may be associated with obesity, hypertension and insulin resistance because of the shared inflammatory pathway. Early diagnosis of atherosclerosis in PsA might trigger more aggressive prophylaxis. Increased intimamedia thickness (IMT) of the carotid artery, a sign of early atherosclerosis [80], has been reported in PsA patients from Spain and Israel [78, 8183]. Increased IMT significantly correlated with traditional risk factors including 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 PsA diagnosis [81], disease duration [78, 81], spine involvement [78], ESR [78] and fibrinogen [78] levels. A study from Hong Kong reported an increased prevalence of subclinical atherosclerosis in Chinese, defined as the average of IMT measures above the 95th percentile of healthy controls [84]. Using logistic regression analysis, independent explanatory variables associated with subclinical atherosclerosis in PsA including increased sugar and total triglyceride levels. The Framingham risk score (FRS) was similar in PsA patients with or without subclinical atherosclerosis. Twenty-six (35%) of the 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 who may benefit from early intervention.

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*0602positive 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 sociodemographic 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 populationbased 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 psoriatic arthritis. 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 polymorphism 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.

Downloaded from http://rheumatology.oxfordjournals.org/ by guest on June 19, 2012

Conclusions
A wide variation on the incidence and prevalence of PsA has been reported in different countries, ranging from 10 to 100 per 100 000 population in China to 1 per 100 000 population in Japan. Amongst Asian patients with psoriasis, 19% were reported to have PsA. Divergent distribution of HLA in different ethnic groups and other genetic determinants may account for these prevalence differences. Polyarthritis developing in the fourth decade was the commonest pattern of arthritis among Asian PsA patients, whereas arthritis mutilans and eye lesions were rarely reported. More data are required on the safety, efficacy and cost effectiveness of TNF blockers for the treatment of PsA in Asia. An increased prevalence of traditional cardiovascular system risk factors and subclinical atherosclerosis has been reported in patients with PsA, including Asian patients. Such risk factors should be routinely monitored and treated aggressively in high-risk patients.

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.

Disclosure statement: The authors have declared no conflicts of interest.

PsA in Asia
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. Angiotensinconverting 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 with psoriatic 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 echocardiographic 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 Dis 2003;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.

1477

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 intimamedia 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, GonzalezGay 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.

Downloaded from http://rheumatology.oxfordjournals.org/ by guest on June 19, 2012

Vous aimerez peut-être aussi