Objective. To compare the incidence and risk factors for thromboembolic events in systemic lupus erythematosus (SLE) patients of different ethnic backgrounds.Methods. SLE patients who were newly diagnosed or were referred within 6 months of diagnosis between 1996 and 2002 were prospectively followed up for the occurrence of thromboembolic events. Cumulative hazard and risk factors for thromboembolism were evaluated and compared among patients of different ethnic origins.Results. We studied 625 patients who fulfilled the American College of Rheumatology criteria for SLE (89% women): 258 Chinese, 140 African Americans, and 227 Caucasians. The mean ؎ SD age at SLE diagnosis was 35.7 ؎ 14 years. After a followup of 3,094 patientyears, 48 arterial events and 40 venous events occurred in 83 patients. The overall incidence of arterial and venous thromboembolism was 16/1,000 patient-years and 13/1,000 patient-years, respectively. The cumulative hazard of arterial events at 60 months after the diagnosis of SLE was 8.5%, 8.1%, and 5.1% for the Chinese, African Americans, and Caucasians, respectively. The corresponding cumulative risk of venous events was 3.7%, 6.6%, and 10.3%, respectively (P ‫؍‬ 0.008 for Chinese versus Caucasians, by log rank test). Smoking, obesity, antiphospholipid antibodies, and use of antimalarial agents and exogenous estrogens were less frequent in the Chinese patients. In Cox regression models, low levels of high-density lipoprotein (HDL) cholesterol, Chinese ethnicity, oral ulcers, and serositis predicted arterial events, whereas male sex, low levels of HDL cholesterol, antiphospholipid antibodies, non-Chinese ethnicity, obesity, renal disease, and hemolytic anemia predicted venous events.Conclusion. There are ethnic differences in the incidence of arterial and venous thromboembolism in patients with SLE that cannot be fully explained by the clinical factors studied. Further evaluation of other genetic and immunologic factors is warranted.Premature atherosclerosis is a major cause of mortality and late morbidity in patients with systemic lupus erythematosus (SLE) (1-3). In several cohort studies, it was found that atherosclerotic cardiovascular and cerebrovascular diseases are more common causes of late deaths than active SLE itself (1,(4)(5)(6). More recent studies have demonstrated that subclinical coronary heart disease and carotid plaque were present in a significantly higher proportion of SLE patients than in age-and sex-matched control subjects with similar risk factors (7,8). The etiology of accelerated atherosclerosis in SLE is multifactorial and cannot be fully explained by traditional risk factors (9).Compared with individuals without SLE, the risk of myocardial infarction in SLE patients is 2-50 times higher, and the risk of stroke is 2-10 times higher (2,9,10). The prevalence of symptomatic coronary heart disease in SLE patients has been reported to be 6-20%, The Hopkins Lupus Cohort is supported by NIH grants R01-AR-43727 and M01-RR-00052 (to the outpatient Clinical Research Center).

Objective. To evaluate the prevalence of the metabolic syndrome in patients with rheumatoid arthritis (RA), ankylosing spondylitis (AS), and psoriatic arthritis (PsA). Methods. Consecutive patients with RA, AS, or PsA who attended our outpatient arthritis clinics between July and November 2009 were recruited for a study of atherosclerotic risk factors and the metabolic syndrome, defined according to the 2009 joint statements using the Asian criteria for central obesity. Results. Nine hundred thirty patients were studied (699 with RA, 122 with AS, and 109 with PsA; 70% women, mean ؎ SD age 51.1 ؎ 12.7 years). The mean ؎ SD disease duration for patients with RA, AS, and PsA was 5.3 ؎ 5.4, 6.0 ؎ 5.6, and 3.6 ؎ 3.1 years, respectively. The prevalence of metabolic syndrome was significantly higher in PsA (38%) than RA (20%) or AS (11%; P < 0.001). The odds ratios (ORs) for the metabolic syndrome compared to age-and sex-matched controls were 0.98 (95% confidence interval [95% CI] 0.78 -1.23, P ‫؍‬ 0.88), 0.59 (95% CI 0.30 -1.15, P ‫؍‬ 0.12), and 2.68 (95% CI 1.60 -4.50, P < 0.001), respectively, for RA, AS, and PsA. Patients with PsA had a significantly higher prevalence of impaired fasting glucose (30%; P < 0.001), low high-density lipoprotein (HDL) cholesterol (33%; P < 0.001), high triglycerides level (21%; P ‫؍‬ 0.008), central obesity (65%; P < 0.001), and high blood pressure (56%; P ‫؍‬ 0.045). In a logistic regression model, the adjusted OR for the metabolic syndrome in PsA was 2.44 (95% CI 1.48 -4.01, P < 0.001) relative to RA or AS. The adjusted ORs for central obesity, impaired fasting glucose, hypertriglyceridemia, and low HDL cholesterol were also significantly higher in PsA patients. Conclusion. Patients with PsA, but not RA or AS, have a significantly higher prevalence of the metabolic syndrome compared to the general population. Among the 3 diseases studied, PsA has the highest prevalence of the metabolic syndrome and is associated with the highest cardiovascular risk.

Objective. To examine autoantibody clusters and their associations with clinical features and organ damage accrual in patients with systemic lupus erythematosus (SLE).Methods. The study group comprised 1,357 consecutive patients with SLE who were recruited to participate in a prospective longitudinal cohort study. In the cohort, 92.6% of the patients were women, the mean ؎ SD age of the patients was 41.3 ؎ 12.7 years, 55.9% were Caucasian, 39.1% were African American, and 5% were Asian. Seven autoantibodies (anti-doublestranded DNA [anti-dsDNA], anti-Sm, anti-Ro, anti-La, anti-RNP, lupus anticoagulant (LAC), and anticardiolipin antibody [aCL]) were selected for cluster analysis using the K-means cluster analysis procedure.Results. Three distinct autoantibody clusters were identified: cluster 1 (anti-Sm and anti-RNP), cluster 2 (anti-dsDNA, anti-Ro, and anti-La), and cluster 3 (anti-dsDNA, LAC, and aCL). Patients in cluster 1 (n ‫؍‬ 451), when compared with patients in clusters 2 (n ‫؍‬ 470) and 3 (n ‫؍‬ 436), had the lowest incidence of proteinuria (39.7%), anemia (52.8%), lymphopenia (33.9%), and thrombocytopenia (13.7%). The incidence of nephrotic syndrome and leukopenia was also lower in cluster 1 than in cluster 2. Cluster 2 had the highest female-to-male ratio (22:1) and the greatest proportion of Asian patients. Among the 3 clusters, cluster 2 had significantly more patients presenting with secondary Sjögren's syndrome (15.7%). Cluster 3, when compared with the other 2 clusters, consisted of more Caucasian and fewer African American patients and was characterized by the highest incidence of arterial thrombosis (17.4%), venous thrombosis (25.7%), and livedo reticularis (31.4%). By using the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index, the greatest frequency of nephrotic syndrome (8.9%) was observed in patients in cluster 2, whereas cluster 3 patients had the highest percentage of damage due to cerebrovascular accident (12.8%) and venous thrombosis (7.8%). Osteoporotic fracture (11.9%) was also more common in cluster 3 than in cluster 2.Conclusion. Autoantibody clustering is a valuable tool to differentiate between various subsets of SLE, allowing prediction of subsequent clinical course and organ damage.

We conducted the current study to determine the clinical determinants of survival and the survival rates in an unselected cohort of Chinese patients with new-onset systemic lupus erythematosus (SLE), including all age-groups. Patients were those newly diagnosed as having SLE or referred within 6 months of diagnosis to the departments of medicine, geriatrics, and pediatrics at Tuen Mun Hospital, Hong Kong, between 1991 and 2003. Patients under the care of all specialists were included for analysis. We obtained demographic data, presenting and cumulative clinical features, disease activity, and serial damage scores. For patients who died or were lost to follow-up, data were censored at the last clinic visit. Survival over time was studied by the Kaplan-Meier method, and factors predictive of mortality were evaluated by the Cox proportional hazard model. We studied 285 new-onset SLE patients (92% women). All were ethnic Chinese and fulfilled at least 4 of the American College of Rheumatology criteria for SLE. The mean age of SLE onset was 30.0 +/- 13.5 years. Fifty (18%) patients had first onset of SLE before the age of 16 years (childhood onset), and 22 (8%) had disease onset after the age of 50 years (late onset); 213 (75%) patients had disease onset between the ages of 16 and 50 years (adult onset). Twenty-nine (10%) patients died (4 from the childhood-onset group, 6 from the late-onset group, and 19 from the adult-onset group) and 18 (6%) patients were lost to follow-up. The overall 5-, 10-, and 15-year survival rates were 92%, 83%, and 80%, respectively. Survival was significantly worse in late-onset patients: 5-, 10-, and 15-year survival rates were 66%, 44%, and 44%, respectively; p < 0.0001. Infection was the main cause of death (55%), followed by cardiovascular (17%) and cerebrovascular complications (14%). Unfavorable factors for survival on univariate analysis were increasing age, damage scores at 1 year, and the use of high-dose corticosteroids. Cox regression revealed that damage scores at 1 year and hematologic manifestations were independent predictors of mortality. Long-term survival of Chinese SLE patients is comparable to that reported for white patients in the 1990s. Late-onset SLE patients have the worst prognosis. Early damage predicts mortality.