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Winthrop University Hospital

Steve Carsons, MD

Winthrop Titles/Positions

Chief, Division of Rheumatology, Clinical Immunology and Allergy

Director, Clinical and Translational Research

Academic Faculty Appointments

Professor of Medicine, Stony Brook University School of Medicine

Address

120 Mineola Boulevard, Mineola, NY 11501

Phone

516-663-4751

Fax

516-663-2946

Email

scarsons@winthrop.org

Brief Resume

Dr. Carsons received his M.D. degree from New York Medical College and subsequently trained in Internal Medicine and Rheumatology at Maimonides Medical Center and SUNY Downstate Medical Center (Brooklyn, NY) Dr. Carsons completed an NIH postdoctoral fellowship at Downstate where he was the Renee Carhart Amory Research fellow of the New York Arthritis Foundation. Dr. Carsons was the physician-in-charge of Clinical Immunology at Long Island Jewish Medical Center from 1982-1989 and Chief of the Division of Rheumatology, Clinical Immunology and Allergy at Winthrop University Hospital from 1989 to present. Dr. Carsons is certified by the American Board of Internal Medicine, the subspecialty board of Rheumatology and the subspecialty board of Diagnostic Laboratory Immunology.

Description of Research Interests/Activities

Dr. Carsons' research has focused on modulation of inflammation in rheumatic disease including the effect of biochemical modulation of extracellular matrix proteins on inflammatory cell function and the role of circulating matrix proteins on inflammatory cell function and the role of circulating matrix proteins as biomarkers in rheumatic disease. In collaboration with Dr. Frances Santiago-Schwartz, he demonstrated that natural inhibitors of TNF-? found in rheumatoid arthritis synovial fluid were able to modulate human dendritic cell development and maturation. Current research in collaboration with Dr. Allison Reiss has discovered that COX-2 inhibitors accelerate macrophage development into foam cells, a potentially important mechanism of accelerated vascular disease in individuals taking these medications. Dr. Carsons’ clinical research involves assessing the outcome of systemic manifestations and therapeutic interventions in autoimmune disorders including Sjögren's syndrome.

Areas of Experience

Rheumatology, Allergy & Immunology

Clinical Practice and Interests

Dr. Carsons' clinical practice is located in the Institutes of Care building, 120 Mineola Boulevard and can be contacted at 516-663-2097. His clinical interests include Sjšgren's syndrome, rheumatoid arthritis and systemic vasculitis.

Selected Publications

Carsons, SE, Lavietes, BB, Diamond, HS, Berkowitz, E: Carbohydrate heterogeneity of fibronectins: synovial fluid fibronectin resembles the form secreted by cultured synoviocytes but differs from the plasma form. J. Clin. Invest. 80: 1342-1349, 1987

Wolf, J, and Carsons, SE. Fibronectin mediates anchorage-dependent focus formation in cultured human synoviocytes. Semin. Arth. Rheum. 21:387-392, 1992

Carsons, SE, Clausen, H., and Wolf, J. Expression of a developmentally regulated epitope on fibronectins from the synovial fluid of rheumatic disease patients. J. Rheumatol. 21:1888-91,1994.

Carsons SE. Extradomain-positive fibronectins in arthritis: Wolf in Sheep’s clothing. Rheumatology (editorial) 2001,40:721-723.

Santiago-Schwarz F, Anand, P, Liu S, Carsons SE. Dendritic cells in rheumatoid arthritis: Progenitor cells and soluble factors contained in RA synovial fluid yield a subset of myeloid DCs which preferentially activate TH1 inflammatory type responses. J. Immunol. 2001,167:1758-1768

Vitali C, Bombardieu S, Jonsson R, Moutsopoulos HM, Alexander EL, Carsons SE, Daniels T, Fox PC, Fox R, Kassan S, Pillemer S, Talal N, Weisman MH. Classification Criteria for Sjogren’s Syndrome: A revised version of the European criteria proposed by the American-European Consensus Group. Ann. Rheum. Dis. 2002, 61:554-558.

Chan ESL, Zhang H, Fernandez P, Edelman SD, Pillinger MH, Ragolia LR, Palaia T, Carsons SE, Reiss AB. Effect of cyclooxygenase inhibition on cholesterol efflux in THP-1 human macrophages: a possible mechanism for increased cardiovascular risk. Arth. Res. Ther. 2007, 9:4
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