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Low Serum Levels of DHEAS in Untreated Polymyalgia Rheumatica/Giant Cell Arteritis
JAVIER NARVÁEZ, BERTA BERNAD, CESAR DÍAZ TORNÉ, JAIME VILASECA MOMPLET, JORDI ZARAGOZA MONTPEL, JOAN M. NOLLA, and JOSÉ VALVERDE-GARCÍA ABSTRACT. Objective. To address a controversy regarding the existence of a relative adrenal hypofunction in patients with untreated polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) we evaluated baseline serum levels of ACTH, cortisol, and DHEAS in a cohort of patients with recent onset PMR/GCA not previously treated with glucocorticoids, in comparison with healthy controls. Possible correlations between baseline DHEAS levels and laboratory measures of disease activity were also explored. Methods. Basal serum levels of these hormones were prospectively investigated in 25 patients with active untreated disease and compared with those of 25 age- and sex-matched control subjects. Results. Of the 25 patients, 19 had isolated PMR and 6 had biopsy-proven GCA + PMR. Basal levels of cortisol and ACTH in PMR/GCA patients did not differ from control subjects; in relation to inflammatory status, lower than expected basal production of cortisol was observed in active untreated PMR/GCA. Baseline serum DHEAS levels were significantly lower in all patients compared with controls. In these patients, a significant correlation was found between baseline DHEAS values and laboratory measures of disease activity. The percentage of DHEAS reduction and the severity of inflammatory response were higher in women than in men. Conclusion. Patients with PMR/GCA with new-onset active disease before steroid treatment have inappropriately normal cortisol levels regarding the ongoing inflammation, and significantly lower levels of DHEAS compared to the age- and sex-matched healthy control subjects. These data support the existence of a relative adrenal hypofunction in PMR and GCA. (First Release June 15 2006; J Rheumatol 2006;33:1293–8) Key Indexing Terms:
POLYMYALGIA RHEUMATICA
From the Department of Rheumatology, Hospital Universitari de Bellvitge–Institut D'investigació Biomèdica De Bellvitge (IDIBELL); and Department of Internal Medicine and Laboratory of Clinical Biochemistry, Clinica Delfos, Barcelona, Spain. J. Narváez, MD, PhD; B. Bernad, MD; C. Díaz Torné, MD, Department of Rheumatology, Hospital Universitari de Bellvitge–IDIBELL; J. Vilaseca Momplet, MD, PhD, Department of Internal Medicine; J. Zaragoza Montpel, MD, Laboratory of Clinical Biochemistry, Clinica Delfos; J.M. Nolla, MD, PhD; J. Valverde-García, MD, PhD, Department of Rheumatology, Hospital Universitari de Bellvitge-IDIBELL. Address reprint requests to Dr. F.J. Narváez-García, Department of Rheumatology (Planta 10-2), Hospital Universitario de Bellvitge, Feixa LLarga s/n, Hospitalet de Llobregat, Barcelona 08907, Spain. E-mail: 31577edd@comb.es Accepted for publication February 13, 2006.
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