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Serum Levels of Pregnenolone and 17-hydroxypregnenolone in Patients with Rheumatoid Arthritis and Systemic Lupus Erythematosus: Relation to Other Adrenal Hormones
DANIELA VOGL, WERNER FALK, MONIKA DORNER, JÜRGEN SCHÖLMERICH, and RAINER H. STRAUB
ABSTRACT. Methods. We measured serum levels of adrenal hormones such as pregnenolone, 17OHPreg, dehydroepiandrosterone (DHEA), DHEA sulfate (DHEAS), progesterone (P), 17-hydroxyprogesterone (17OHP), androstenedione (ASD), and cortisol in 24 healthy controls, 24 patients with RA, and 24 patients with SLE. Results. Serum levels of pregnenolone were similar in RA and SLE patients as compared to healthy controls irrespective of prior prednisolone therapy. In all RA and SLE patients (including those with prior prednisolone treatment), serum levels of all measured hormones except pregnenolone were significantly lower as compared to controls. In RA patients without prior prednisolone treatment, serum levels of 17OHPreg, DHEA, cortisol, and ASD were similar to controls, and serum levels of P, 17OHP, and DHEAS were significantly lower as compared to controls. In SLE patients without prior prednisolone treatment, serum levels of 17OHPreg and cortisol were similar, and serum levels of P, 17OHP, ASD, DHEA, and DHEAS were significantly lower as compared to controls. Conclusion. The primary hormone of the adrenal steroid cascade, pregnenolone, is almost normal in RA and SLE irrespective of corticosteroid treatment. In patients with RA, we believe that there is a near normal P450scc reaction and a normal double step P450c17 reaction. In SLE patients, the P450scc reaction also seems normal but the second step of the P450c17 reaction seems to be inhibited. In both diseases, cortisol levels remain relatively stable at the expense of other adrenal hormones. This study revealed distinct changes of steroid pathways that are related to the disease entities. (J Rheumatol 2003;30:269-75) Key Indexing Terms:
RHEUMATOID ARTHRITIS
From the Department of Internal Medicine I, Laboratory of Neuroendocrinoimmunology, University Medical Center Regensburg, Regensberg, Germany. R.H. Straub was supported by a grant from the Deutsche Forschungsgemeinschaft (DFG Str 511/10-1 and DFG Str 511/11-1). D. Vogl, Research Assistant; W. Falk, PhD, Professor, Chemist; M. Dorner, Doctoral Student of Dental Medicine; J. Schölmerich, MD, Professor, Head of the Department; R.H. Straub, MD, Professor, Rheumatologist, Department of Internal Medicine I, University Medical Center Regensburg. Address reprint requests to Dr. R.H. Straub, Department of Internal Medicine I, University Medical Center, D-93042 Regensburg, Germany. E-mail: rainer.straub@klinik.uni-regensburg.de Submitted April 2, 2002; revision accepted July 24, 2002. |