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BRIEF REPORT |
Longitudinal Studies Section (M.M., S.Bas., A.B., L.F.) and Translational Research and Medical Support Section (S.Bas., S.M.L.), Clinical Research Branch, National Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, Maryland 21225; Department of Medicine, Division of Endocrinology, Johns Hopkins University School of Medicine, Bayview Medical Center (S.Bas.), Baltimore, Maryland; Tuscany Regional Health Agency (F.L.,), 50134 Florence, Italy; Geriatric Rehabilitation, Azienda Sanitaria di Firenze (S.Ban.), 50125 Florence, Italy; and Department of Internal Medicine and Biomedical Sciences, Section of Geriatrics, University of Parma (G.P.C., G.V.), 43100 Parma, Italy
Address all correspondence and requests for reprints to: Dr. Luigi Ferrucci, National Institute on Aging, National Institutes of Health, National Institute on Aging, Advanced Studies in Translational Research on Aging at Harbor Hospital, 3001 South Hanover Street, Baltimore, Maryland 21225. E-mail: ferruccilu{at}grc.nia.nih.gov.
Context: An age-associated decline in testosterone (T) levels and an increase in proinflammatory cytokines contribute to chronic diseases in older men. Whether and how these changes are related is unclear.
Objective: We hypothesized that T and inflammatory markers are negatively correlated in older men.
Design: This was a cross-sectional study.
Setting: A population-based sample of older men was studied.
Participants and Measures: After excluding participants taking glucocorticoids or antibiotics or those with recent hospitalization, 467 men, aged 65 yr or older, had complete determinations of total T, bioavailable T, SHBG, albumin, IL-6, soluble IL-6 receptor (sIL-6r), TNF-
, IL-1ß, and C-reactive protein.
Results: After adjusting for potential confounders, sIL-6r was significantly and inversely correlated with total T (r = 0.20; P < 0.001) and bioavailable T (r = 0.12; P < 0.05). T was not correlated with any other inflammatory marker.
Conclusions: These preliminary findings suggest an inverse relationship between T and sIL-6r. Longitudinal studies are needed to establish the causality of this association.
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