Horm Metab Res 1994; 26(6): 288-292
DOI: 10.1055/s-2007-1001685
Originals Clinical

© Georg Thieme Verlag, Stuttgart · New York

Effect of Pyridostigmine on the Hydrocortisone-Mediated Decrease of Circulating Growth Hormone Levels in Acromegaly

A. Giustina1 , A. R. Bussi1 , M. Doga1 , C. Iacobello2 , W. B. Wehrenberg3
  • 1Cattedra di Clinica Medica, University of Brescia, Brescia, Italy
  • 2Chimica, University of Brescia, Brescia, Italy
  • 3Dept. of Health Sciences, University of Wisconsin, Milwaukee, U.S.A.
Further Information

Publication History

1993

1994

Publication Date:
14 March 2008 (online)

Summary

The aims of our study were to investigate the effect of the acetylcholinesterase inhibitor pyridostigmine (PD) administration on growth hormone (GH) secretion in acromegaly and to investigate the effects of PD on GH levels following an iv infusion of hydrocortisone in acromegaly. We studied five adult patients with active acromegaly, three men and two women with a mean age of 60±5 years (range 47-71 years) and a mean BMI of 27 ±0.7 kg/m2 (range 24-28kg/kg/m2). All the patients underwent:1) placebo, 2 tablets po or 2) PD, 120 mg po, at time -60 plus a bolus iv injection of l00 mg hydrocortisone succinate in 2 ml saline at time 0 followed by an iv infusion of 250 mg hydrocortisone succinate in 250 ml saline from 0 to 120 min, or 3) PD, po or 4) placebo, po at time -60 plus a bolus iv injection of 2 ml saline followed by an iv infusion of 250 ml saline from 0 to 120 min. Serum GH values did not significantly change after PD administration compared to those during placebo treatment and with respect to baseline levels. In all of the acromegalic patients during hydrocortisone succinate infusion, GH values clearly decreased with respect to basal levels in varying degrees, with a nadir between 90 and 180 minutes after the beginning of hydrocortisone infusion. After hydrocortisone + PD administration, all five patients showed GH values not significantly different with respect to basal levels and significantly higher with respect to placebo + hydrocortisone from 30 to 180 minutes. Our data show that, in patients with active acromegaly, PD administration does not significantly increase serum GH levels with respect to placebo and that the glucocorticoid-mediated decrease in GH levels is counteracted by the administration of PD. It can be hypothesized that glucocorticoids may cause an increase in somatostatin tone via the cholinergic pathways unmasking the cholinergic stimulating action of PD in acromegaly.

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