Location via proxy:   [ UP ]  
[Report a bug]   [Manage cookies]                

Ps A in Asia

...Read more
For Peer Review              !" ## "  $  %&’" & # # () *’ + , # ’- +%#. / , 0 - " " # +1- 21 21.  / - " " 3 +- "’". # *# 4 , 1 51- " 6 # 5"7&8/   ’’’ 9: ;" ,’ #  "" # ;"  & "    , # ’ *" 7 %%4%- "’1 7 <%* 6 *+=*+ %*=*%- 3 7 <%* 6 *+=*+ %*=*%- > , , 7 /%2*?+?32 = %?*+ /=?=- %"## !"1  #$ 7 4* %%% Rheumatology
For Peer Review 1 Title: Psoriatic Arthritis in Asia Authors: Lai-Shan Tam 1 , Ying-Ying Leung 2 , Edmund K Li 1 . From 1 Department of Medicine & Therapeutics, The Prince of Wales Hospital, The Chinese University of Hong Kong; 2 Department of Medicine, North District Hospital, Hong Kong Address correspondence and reprint requests to: Dr Edmund K Li Department of Medicine and Therapeutics, The Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong. E-mail: edmundli@cuhk.edu.hk , phone: (852) 2632-3128, fax: (852) 2637-3852 Short title: Psoriatic arthritis (PsA) in Asia Page 1 of 34 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 48 49 50 51 52 53 54 55 56 57 58 59 60
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
Keep reading this paper — and 50 million others — with a free Academia account
Used by leading Academics
Donna M Goldstein
University of Colorado, Boulder
Amlan Ray
Annamalai University
Rodrigo Toniol
Universidade Federal do Rio de Janeiro (UFRJ)
Chiara Moretti
Università degli Studi di Milano-Bicocca