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The Journal of Clinical Endocrinology & Metabolism Vol. 86, No. 11 5465-5470
Copyright © 2001 by The Endocrine Society


Other Original Articles

Fetal Antigen 1 in Healthy Adults and Patients with Pituitary Disease: Relation to Physiological, Pathological, and Pharmacological GH Levels

M. Andersen, C. H. Jensen, R. K. Støving, J. B. Larsen, H. D. Schrøder, B. Teisner and C. Hagen

Departments of Endocrinology (M.A., R.K.S., C.H.), Immunology (C.H.J., B.T.), and Pathology (J.B.L., H.D.S.), Odense University Hospital, DK-5000 Odense C, Denmark

Address all correspondence and requests for reprints to: Marianne Andersen, M.D., Ph.D., Department of Endocrinology, Odense University Hospital, 5000 Odense C, Denmark. E-mail: m.andersen{at}dadlnet.dk

Abstract

Immunohistochemical analysis of the distribution of human fetal antigen 1 (FA1) in adult human tissues has demonstrated a strong association between FA1 and (neuro)endocrine structures. In the anterior pituitary gland FA1 was colocalized with GH, and the present study was performed to evaluate a possible relationship between GH and FA1. FA1 and GH levels were measured during a 24-h period at 20-min intervals. In contrast to the known GH peaks during 24-h sampling, there was no detectable FA1 peak. The FA1 responses to placebo were not significantly different from the responses to the combination of pyridostigmine and GHRH. No significant difference was found between basal FA1 (nanograms per ml) levels [median (minimum–maximum)] in healthy adults [n = 40; 28.6 ng/ml (12.5–72.0)], acromegalic patients [n = 11; 31.0 ng/ml (21.6–56.3)], and patients with GH deficiency [n = 22; 32.1 ng/ml (13.4–108.7)].

FA1 levels were significantly reduced, in the six of seven acromegalic GH responders to octreotide, from [median (minimum–maximum)] 30.6 ng/ml (20.0–43.1) to 20.3 (13.9–30.2; P < 0.02). There was no significant change during placebo. FA1 levels were significantly increased compared with placebo values during 3 months of GH therapy. The increase in FA1 levels was significantly higher than the change during placebo (P < 0.003).

In conclusion, a common secretory and stimulatory pathway for FA1 and GH in healthy adults has been ruled out. However, we found that pharmacologically induced changes in GH levels during weeks to months had a corresponding direct or indirect effect on FA1 levels in patients with GH deficiency or acromegaly. However, a direct effect of octreotide on FA1 levels, independent of GH levels, has not been ruled out.




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