Systemic lupus erythematosus in three ethnic groups: III A comparison of characteristics early in the natural history of the LUMINA cohort

Abstract

H and AA patients have more active SLE, at an earlier age of onset, and a less favorable socioeconomic-demographic structure (worse among the H than AA) which predispose them to a less favorable natural history.

Systemic lupus erythematosus in a multiethnic US cohort (LUMINA): XXV. Smoking, older age, disease activity, lupus anticoagulant, and glucocorticoid dose as risk factors for the occurrence of venous thrombosis in lupus patients

“…As previously described (7,8), LUMINA (LUpus in MInorities, NAture versus nurture) is a longitudinal study of outcome in SLE and includes patients from 3 ethnic groups living in the US: Hispanics from Texas and Puerto Rico, African Americans, and Caucasians. The study is being conducted in 3 geographic areas (Alabama, Texas, and Puerto Rico) and at 3 institutions (The University of Alabama at Birmingham, The University of Texas Health Science Center at Houston, and The University of Puerto Rico Medical Sciences Campus).…”

Systemic lupus erythematosus in three ethnic groups: IX. Differences in damage accrual

“…The constitution of this cohort, the variables obtained prior to, at, and after enrollment in the cohort, and the frequency and nature of the study visits have been described in detail previously (23)(24)(25)(26)(27)(28). Briefly, patients with SLE according to the American College of Rheumatology (ACR) criteria (4,29,30) who had disease duration of Յ5 years at enrollment, were living within the catchment area of the participating institutions (The University of Alabama at Birmingham, The University of Texas-Houston Health Science Center, and The University of Texas Medical Branch at Galveston), and were of defined Hispanic (Mexican American or Central American), African American, or Caucasian ethnicity were eligible to participate.…”

“…Socioeconomic/ demographic variables included age, sex, ethnicity (same as that of the 4 grandparents), education, marital status, occupation, housing (ownership and density), income (above and below the federally defined poverty level, adjusted for the number of members in the household [31]), health insurance, health behaviors (smoking, drinking, not exercising), and access to health care. Clinical and immunologic variables included SLE onset type (acute versus insidious), number of ACR criteria met at TD, presence of autoantibodies (antinuclear antibodies by indirect immunofluorescence [IIF]; antidouble-stranded DNA by IIF against Crithidia luciliae; antiSmith, anti-small nuclear RNP, anti-Ro, and anti-La by immunodiffusion; anti-phospholipid G and anti-phospholipid M antibodies by enzyme-linked immunosorbent assay; and lupus anticoagulant by the statclot test) (24,25). Also recorded were disease activity according to the Systemic Lupus Activity Measure (SLAM) (32,33) and damage caused by the disease or its treatments according to the SDI (34).…”

“…It is unclear, however, how damage accrues in these population groups compared with the Caucasian population. To sort out the genetic and socioeconomic/demographic factors associated with poor outcome in SLE, a cohort of patients with disease duration of Յ5 years, from the 3 major ethnic groups inhabiting the US (Hispanic, African American, and Caucasian) was constituted and is being followed up longitudinally (23)(24)(25)(26)(27)(28). We are now reporting on the accrual of damage, overall and by ethnic group, in the cohort.…”

Interferon regulatory factor-5 is genetically associated with systemic lupus erythematosus in African Americans

“…1 It has an earlier onset, more severe disease manifestations and a four times higher prevalence in African Americans compared to Caucasians in the United States. 2,3 The diagnosis of SLE requires the presence of 4 of 11 defined criteria of the American College of Rheumatology (ACR), lacking a defined etiology. 4,5 Both genetic and environmental factors have been suggested as causative agents for the pathogenesis and variable clinical manifestations of SLE.…”