TY - JOUR T1 - Hypothalamic-Pituitary-Gonadal Axis Hormones and Male Rheumatoid Arthritis: Novel Perspectives JF - The Journal of Rheumatology JO - J Rheumatol SP - 859 LP - 862 DO - 10.3899/jrheum.090092 VL - 36 IS - 5 AU - ALFONSE T. MASI AU - ROBERT T. CHATTERTON AU - JEAN C. ALDAG Y1 - 2009/05/01 UR - http://www.jrheum.org/content/36/5/859.abstract N2 - The female to male (F:M) incidence ratio in rheumatoid arthritis (RA) is almost 3:1, being exaggerated in child-bearing ages (5:1), as opposed to 2:1 in juveniles and older (50+ years) adults1. Female preponderance also occurs in systemic lupus erythematosus (SLE; 9:1), particularly in child-bearing years2, when its age-specific incidence is highest2,3. In RA, however, the incidence is notably higher in postmenopausal than in premenopausal women. The age-specific gender differential in RA is attributable to adult men having significantly delayed disease onset1. Such incidence data imply that gonadal hormones may be protective of RA in younger adult men (testosterone), but may predispose to SLE in women (estrogens)2,3. In this issue of The Journal, Tengstrand, et al4 report a longitudinal study of gonadal hormones in early diagnosed (within 1 year of symptoms) male RA. The baseline hormonal data on RA cases were compared to healthy control values. The longitudinal design over a 2-year duration of therapy permitted analyses of the change in hypothalamic-pituitary-gonadal (HPG) hormones as correlated with the change in RA disease activity. At baseline, the main findings were that the younger (< 50 yrs of age) RA males had lower mean serum levels of total testosterone (T) as well as bioavailable T, i.e., free T or non-sex hormone-binding globulin (SHBG)-bound T than the healthy control subjects. The 2-year interval changes revealed an increased total T level from baseline that was associated significantly with decreased disease activity, as measured by Disease Activity Score 28 (DAS28), but without change in serum luteinizing hormone (LH)4. Cross-sectional (or longitudinal) studies cannot indicate whether observed baseline hormonal alterations reflect a primary risk effect or are secondary to disease severity4,5. Such question of a … Address reprint requests to Dr. Masi; E-mail: amasi{at}uic.edu ER -