Prolactin and Growth Hormone Responses to Hypoglycemia in Patients with Rheumatoid Arthritis and Ankylosing Spondylitis

JOZEF ROVENSKY, RICHARD IMRICH, FRANTISEK MALIS, MARTIN ZLNAY, LADISLAV MACHO, JURAJ KOSKA, and MILAN VIGAS

ABSTRACT.

Objective. Prolactin (PRL) and growth hormone (GH) are pituitary hormones with immunomodulating properties. Their upregulated secretion may play a role in the pathogenesis of chronic inflammatory diseases. We evaluated PRL and GH responses to secretion stimulus in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS).

Methods. Insulin hypoglycemia (0.1 IU/kg) was induced in 15 women with RA, 18 men with AS, and healthy controls matched for age, sex and body mass index. Plasma concentrations of glucose, PRL, GH, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-a) were analyzed.

Results. RA patients had significantly lower area under the curve (AUC) of PRL (p = 0.049) compared to RA controls. During hypoglycemia double or higher increase of plasma PRL occurred in 5 RA (33%) patients and in 8 RA controls (57%). Using the General Linear Model procedure, no significant differences in PRL or GH responses were observed in patients with RA and AS. TNF-a was higher in patients with RA compared to RA controls (p < 0.05). There was no significant difference in TNF-a concentrations between AS patients and AS controls. IL-6 was higher in RA patients compared to controls (p < 0.05) and in AS patients compared to controls (p < 0.01). Significant positive correlation was found between TNF-a levels and AUC of PRL in AS patients (r = 0.46, p = 0.047), but not in the 2 control groups or in RA patients.

Conclusion. Our results indicate no upregulated PRL or GH responses to stimulation in premenopausal women with RA or men with AS. (J Rheumatol 2004;12:2418-21)

Key Indexing Terms:

PROLACTIN
GROWTH HORMONE
RHEUMATOID ARTHRITIS
ANKYLOSING SPONDYLITIS

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From the National Institute of Rheumatic Diseases, Piestany; and the Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovakia.

Supported by grant APVT-21-008602 from the Slovak Ministry of Education.

J. Rovensky, MD, DSc, Professor, National Institute of Rheumatic Diseases; R. Imrich, MD, PhD, Institute of Experimental Endocrinology; F. Malis, MD, CSc; M. Zlnay, MD, National Institute of Rheumatic Diseases; L. Macho, MD, DSc; J. Koska, MD, PhD; M. Vigas, MD, DSc, Institute of Experimental Endocrinology.

Address reprint requests to Prof. J. Rovensky, National Institute of Rheumatic Diseases, Nabr. I. Krasku 4, 921 23 Piestany, Slovakia. E-mail: rovensky@vurch.sk

Submitted February 23, 2004; revision accepted July 8, 2004.

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