 |
|
|
 |
Lower Adrenocortical and Adrenomedullary Responses to Hypoglycemia in Premenopausal
Women with Systemic Sclerosis
RICHARD IMRICH, JOZEF LUKAC, JOZEF ROVENSKY, ZOFIA RADIKOVA, ADELA PENESOVA, RICHARD KVETNANSKY, MIROSLAVA HUCKOVA, MILAN VIGAS, LADISLAV MACHO, and JURAJ KOSKA ABSTRACT. Objectives. To evaluate function of the hypothalamic-pituitary-adrenal (HPA) axis, adrenomedullary hormonal system (AMHS), and sympathetic noradrenergic system (SNS) in premenopausal women with systemic sclerosis (SSc). Methods. Insulin-induced hypoglycemia (0.1 IU/kg) was performed in 17 longterm, glucocorticoid-naive SSc patients with low disease activity and in 18 healthy women matched for age and body mass index (BMI). Concentrations of glucose, adrenocorticotrophic hormone (ACTH), cortisol, androstenedione (ASD), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), 17a-hydroxyprogesterone (17OHP), epinephrine (EPI), norepinephrine (NE), interleukin 1ß (IL-1ß), IL-6, and tumor necrosis factor-a (TNF-a) were analyzed in plasma. Results. Basal plasma levels of cortisol, ASD, 17OHP, DHEAS, IL-1ß, IL-6, and TNF-a were not significantly different in SSc compared to controls. Patients had higher basal ACTH (6.76 ± 1.0 pmol/l in SSc vs 4.14 ± 0.45 pmol/l in controls; p < 0.05), lower basal DHEA (9.02 ± 1.64 nmol/l in SSc vs 17.0 ± 2.8 nmol/l in controls; p < 0.05), and lower basal NE (1.61 ± 0.26 nmol/l in SSc vs 2.57 ± 0.38 nmol/l in controls; p < 0.05). Patients had comparable responses of glucose and ACTH to hypoglycemia. General linear model for repeated measurements, with BMI and age as covariates, revealed that the responses of 17OHP (p < 0.05), ASD (p < 0.05), DHEA (p < 0.01), EPI (p < 0.001), and NE (p < 0.001) to hypoglycemia were lower in SSc compared to controls. Cortisol response to hypoglycemia tended to be lower in SSc patients (p = 0.06) compared to controls. Conclusion. Our data indicate decreased adrenocortical and adrenomedullary functions in premenopausal women with SSc. Whether the observed changes in the neuroendocrine system are secondary to chronic disease deserves further investigation. (J Rheumatol 2006;33:2235-41) Key Indexing Terms:
SYSTEMIC SCLEROSIS From the Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava; and the National Institute of Rheumatic Diseases, Piestany, Slovakia. Supported by grant APVT-21-008602 and by a grant from the Ministry of Health of Slovak Republic. R. Imrich, MD, PhD, Institute of Experimental Endocrinology; J. Lukac, MD, PhD; J. Rovensky, MD, DSc, Professor; National Institute of Rheumatic Diseases; Z. Radikova, MD, PhD; A. Penesova, MD, PhD; R. Kvetnansky, DSc; M. Huckova, MSc; M. Vigas, MD, DSc; L. Macho, MD, DSc; J. Koska, MD, PhD, Institute of Experimental Endocrinology. Address reprint requests to Dr. R. Imrich, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlarska 3, 833 06 Bratislava, Slovakia. E-mail: richard.imrich@savba.sk Accepted for publication June 15, 2006.
|
