The Johns Hopkins Lupus Cohort is a longitudinal study, begun by Dr. Petri in 1987, of the incidence and pathogenesis of thrombotic events (TE) and coronary artery disease (CAD) in 225 patients with systemic lupus erythematosus (SLE) (60.2% black, 90.5% female, mean age 36.5 years). In SLE, both TE and CAD are a major cause of morbidity. The usual natural history of TE and CAD is telescoped, so that patients can present with these outcomes in their third and fourth decades. In our cohort study to date, 44 patients, have had past and 10 patients have had prospectively-followed thrombotic events. Thirteen patients (6.6%) have had coronary artery disease. We have prospectively followed our lupus cohort routinely every three months and have amassed a four-year database specifically designed to identify and to follow over time the most important risk factors for TE and CAD. Risk factors to be addressed in the study include: 1) the hypercoagulable state secondary to antiphospholipid antibodies (the lupus anticoagulant and anticardiolipin antibody); 2) premature atherosclerosis, accelerated by prednisone and hypertension; 3) underlying vascular damage from lupus vasculopathy and vasculitis; 4) co-morbid factors, including obesity, smoking, hyperlipidemia, hypertension, sedentary life style, and family history of CAD, and 5) other factors, including sex, age, race, immunogenetics, compliance with medication, and socioeconomic status. The Hopkins Cohort Study is uniquely able to focus on these issues, both because of its population, which reflects a broad racial, educational, and socioeconomic background, and because the four years of data accumulated to date show promising preliminary results. The five years of the proposed study will allow us to address further the incidence of TE and CAD, the importance of identified risk factors both singly and in combination, and to begin to address the issue of intervention to modify and reduce risk factors.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
First Independent Research Support & Transition (FIRST) Awards (R29)
Project #
5R29HL047080-05
Application #
2223402
Study Section
Epidemiology and Disease Control Subcommittee 2 (EDC)
Project Start
1991-09-30
Project End
1996-08-31
Budget Start
1995-09-30
Budget End
1996-08-31
Support Year
5
Fiscal Year
1995
Total Cost
Indirect Cost
Name
Johns Hopkins University
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
045911138
City
Baltimore
State
MD
Country
United States
Zip Code
21218
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Petri, M (1997) Antiphospholipid antibody syndrome: an acquired cause of venous and arterial hypercoagulability. Mt Sinai J Med 64:376-82
Petri, M; Robinson, C (1997) Oral contraceptives and systemic lupus erythematosus. Arthritis Rheum 40:797-803
Petri, M (1997) Hopkins Lupus Pregnancy Center: 1987 to 1996. Rheum Dis Clin North Am 23:1-13
Sullivan, K E; Wooten, C; Schmeckpeper, B J et al. (1997) A promoter polymorphism of tumor necrosis factor alpha associated with systemic lupus erythematosus in African-Americans. Arthritis Rheum 40:2207-11
Petri, M (1997) Pathogenesis and treatment of the antiphospholipid antibody syndrome. Med Clin North Am 81:151-77
Casciola-Rosen, L; Rosen, A; Petri, M et al. (1996) Surface blebs on apoptotic cells are sites of enhanced procoagulant activity: implications for coagulation events and antigenic spread in systemic lupus erythematosus. Proc Natl Acad Sci U S A 93:1624-9
Petri, M; Roubenoff, R; Dallal, G E et al. (1996) Plasma homocysteine as a risk factor for atherothrombotic events in systemic lupus erythematosus. Lancet 348:1120-4
Sullivan, K E; Wisnieski, J J; Winkelstein, J A et al. (1996) Serum complement determinations in patients with quiescent systemic lupus erythematosus. J Rheumatol 23:2063-7
Sullivan, K E; Wooten, C; Goldman, D et al. (1996) Mannose-binding protein genetic polymorphisms in black patients with systemic lupus erythematosus. Arthritis Rheum 39:2046-51

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